Switra kc032 gdg

“EVALUATION OF THE EFFICACY OF KAKODUMBARADIGHANAVATI (INTERNAL) AND

AYORAJADILEPA (EXTERNAL) IN THE MANAGEMENT OF SWITRA” By

BASAVARADDI.H.VENKARADDIYAVAR Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial

Ayurved

KUnd

Dr. V.

Dr

DepartmPost Graduate S

D.G. MELMALAGI AYUR

fulfillment of the degree of

a Vachaspati M.D. In

ayachikitsa er the Guidance of Varadacharyulu

M.D. (Ayu) (Osm)

. R.V. Shettar M.D. (Ayu)

ent of Kayachikitsa tudies & Research Center VEDIC MEDICAL COLLEGE, GADAG

2003-2006

Ayurmitra

TAyComprehended

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTER GADAG, 582 103

This is to certify that the dissertation entitled “EVALUATION OF THE EFFICACY OF

KAKODUMBARADIGHANAVATI (INTERNAL) AND AYORAJADILEPA (EXTERNAL) IN

THE MANAGEMENT OF SWITRA” is a bonafide research work done by

BASAVARADDI.H.VENKARADDIYAVAR in partial fulfillment of the requirement for the post

graduation degree of “Ayurveda Vachaspati M.D. (Kayachikitsa)” Under Rajeev Gandhi

University of Health Sciences, Bangalore, Karnataka.

Dr. V. VARADACHARYULUM.D. (Ayu) (Osm)

GuideProfessor & HOD

Dept. of Kayachikitsa

PGS&RC

Date:

Place: Gadag

Dr. R. V. Shettar

M.D. (Ayu)

Co- Guide

Lecturer in Kayachikitsa

DGMAMC, PGS&RC, Gadag

Date:

Place: Gadag

J.S.V.V. SAMSTHE’S

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTER GADAG, 582 103

Endorsement by the H.O.D, principal/ head of the institution

This is to certify that the dissertation entitled “EVALUATION OF THE EFFICACY OF


THE MANAGEMENT OF SWITRA” is a bonafide research work done by BASAVARADDI. H.

VENKARADDIYAVAR under the guidance of Dr. V. Varadacharyulu M.D. (Ayu) (Osm),

Professor & HOD and Co- Guidance of Dr. R. V. Shettar, M.D. (Ayu) Lecturer in

Kayachikitsa, in partial fulfillment of the requirement for the post graduation degree of

“Ayurveda Vachaspati M.D. (Kayachikitsa)” Under Rajeev Gandhi University of Health

Sciences, Bangalore, Karnataka.

.

DP

(Dr. G. B. Patil) Principal,

DGM Ayurvedic Medical College, Gadag

Date: Place:

(Dr. V. Varadacharyulu)Professor & HOD

Dept. of Kayachikitsa PGS&RC

ate: lace: Gadag

Declaration by the candidate

I here by declare that this dissertation / thesis entitled “EVALUATION OF THE EFFICACY OF


THE MANAGEMENT OF SWITRA” is a bonafide and genuine research work carried out by

me under the guidance of Dr. V. Varadacharyulu M.D.(Ayu) and Co - Guidance of Dr.R. V.

Shettar Lecturer, in Kayachikitsa, DGMAMC, PGS&RC, Gadag.

Date

Place

BASAVARADDI.H.VENKARADDIYAVAR

Copy right

Declaration by the candidate

I here by declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall

have the rights to preserve, use and disseminate this dissertation/ thesis in print or electronic

format for the academic / research purpose.

Date

Place


© Rajiv Gandhi University of Health Sciences, Karnataka

Acknowledgement

At the onset, my devotional pranamas to his Holiness Sri. Jagadguru Abhinava

Shivanada Swamiji, Shivananda math, Gadag whose blessings gave me enough strength to

complete this work as per my expectations.

I express my deep gratitude to my guide Dr. V. Varadacharyulu M.D.(Ayu), Gold

Medalist, Professor & H.O.D., for his timely advises and encouragement in every step of my

success.

I express my gratefulness to my co-guide Dr. R.V. Shettar, M.D (Ayu) lecturer in

Kayachikitsa, for his time to time help and critical suggestions associated with expert

guidance at the completion of this dissertation.

I express my thankfulness to beloved principal Dr. G. B. Patil, Principal for his

encouragement as well as providing all necessary facilities for this research work.

I lay my deep love and affection to my respected parents Shri Hanamaraddi

Venkaraddiyavar, Smt Lakshmidevi who are the prime reasons for my success.

I express my sincere thanks to Dr. K. Shiva Rama Prasad, Dr. M.C. Patil, Dr.

Shashidar. H. Doddamani, Dr. P. Shivaramudu, Dr. Danappagoudar, Dr. Mulkipatil Dr.

Kuber Sankh, Dr. Santhosh Belavadi, Dr. Jagadish Mitti. Dr.Shashidhar Nidagundi. and Mr.

Nandakumar for his help in statistical analysis of results.

I express my sincere thanks to Dr.Jagadish Shirol MD(Gen med.) and Dr.Ravindra

Wadoni (MD, Dermatology) for their valuable suggestions at times. I pay my tribute to late

Dr. Sarangmath whose inspiration made me to do post graduation studies.

I extend my immense gratitude to Dr.M.V.Malagoudar, Dr.G.S.Hiremath,

Dr.R. K.Gacchinmath, Dr.S.A.Patil, Dr.B. G. Swami, Dr.Reddar, Dr.Yarageri(RMO)

Dr.K.S. Paraddi, Dr.U.V. Purad and other teaching staff who helped me during my work.

I am gratefull to my brothers, Brother in law Dr. B.LYaragatti and other family

members. I express my deep affectionate love to my wife Smt. Dr. Aruna who co-operated

me throughout this work. I also extend my gratitude towards Sri. Kencharaddy, Smt.

Susheela, and Mr. Dayanand

I would like to express my sincere thanks to Mr. V. M. Mundinamani, Librarian and

Asst. Mr. S. B. Sureban for providing valuable books in time throughout the study and

Mr.Tippanagouda, Lab Technician for his support.

I take this moment to express my thanks to my friends and Prashanth Gokhale.

Basavaraj Channappagoudar, Kariyappa, Manju, Basavaraj for their moral support. And all

my Post Graduate Seniors Koteshwar, D.P. Joshi, Santoji, Jaggal, V.S. Hiremath,

Pattanashetty, Santosh, Subin, Febin, Satheesh, Chetan, Mangala, and my Colleagues

Kalmath, Udaykumar, Ratnakumar, Menakshi, Shaila, Hugar, Chandramouli, Jayaraj,

Shakuntala, Kendadmath, Ganti, Pradeep, Bingi, Sajjan, Lingareddi, Jagadeesh, Vijay, Akki,

Hakkandi, Ashwin, Umesh,.Gavi, Krishna, Sarvi, Ashok, Siba, Sharanu, Suvarna, Anitha

and others. I am very much thankful to Smt. P. K. Belavadi, Mr. M. M. Joshi, Mr. Sarvi, Mr.

Shankar, Mr. Biradar, Mr. Kallanagoudar, Mr. Dasar and Smt. Sarangamath.

And most sincere thanks to my patients who cooperated at my dissertation; with out

whom the study was not possible.

Place: Date:

Basavaraddi.H.Venkaraddiyavar

Kakodumbaradighanavati (internal) and

Ayorajadilepa (external) in Switra – Abstract Switra is most blemishing disease compared to other dermatological problems, is

a medico-social problem since the time immemorial in India. Switra is characterised by

Aparisravi swetha varna mandala i.e. non exudative skin lesions which are hypo-

pigmentary disease. Vitiligo lesions over face, particularly embracing and cause

frustration. Last decade has witnessed an increasing interest in psychological affect of the

various skin diseases, and quality of life in patients suffering from disease.

Twak (Skin) is indicator of status of Rasa Dhatu. Ayurveda suggested good

remedies like kushtagna and varnya drugs to cure the disease. All patients advised to

exposure to sunlight after the local application. The trial drug Kakodumbaradi Ghanavati

internal and Ayorajadilepa external are considered for the evaluation in Switra. The

clinical study was undertaken on 30 patients in a single group. Ayurveda emphasized diet

as an important etiological factor in Switra.

The hypothesis on the action of Kakodumbaradi Ghanavati (internal) has

Kushtagna, krimighna, varnya, Switraghna prabhava along with deepana, pachana,

Bruhana, Balya and Vrushya properties and Ayorajadilepa is verified its external action

to introduce potentially melanin pigmentation in this observational study. To assess the

effect of treatment, color, number of mandalas, VASI Score, hyper-pigmentation of

margin and serum copper levels were considered.

The results of the study are based upon the assessment of the subjective and

objective criteria considered in the study. Mainly the objective parameters are considered

to show the evidences of the relief in the study. The result encourages the Ayurvedic

fraternity even though the cure is only 6.67% (2 Patients) in the time bound study. Study

reveals well responded listed as 26.66% (8) patients along with the 37.66% of moderately

responded patients. In the study many causes made hindrances of the melanin re-

pigmentation and 8 i.e. 26.66% patients fall under poor response. Only one patient i.e.

3.34% noticed as the no response patient in the entire study. Subjective parameters viz.

“Rookshata, Parusha, Daha, Kandu, Guruta” are not significant in the study but all

objective parameters are highly significant as par statistical evaluation.

“EVALUATION OF THE EFFICACY OF

KAKODUMBARADIGHANAVATI (INTERNAL) AND

AYORAJADILEPA (EXTERNAL) IN THE MANAGEMENT OF

SWITRA”

By


Chapter Content Pages

1 Introduction 1 to 8

2 Objectives 9 to 13

3 Review of literature 14 to 76

4 Methodology 77 to 88

5 Results 89 to 118

6 Discussion 119 to 131

7 Conclusion 132 to 132

8 Summary 133 to 134

9 Bibliographic References 1 to 7

10 Annex – Case sheet 1 to 8

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra – Contents

1

Tables of



AYORAJADILEPA (EXTERNAL) IN THE MANAGEMENT OF SWITRA”

By


SNo Topic Page

1 Skin layers according to Charaka, Susruta and Vagbhata 23

2 Skin layers comparison according to Dr. Ghanekar 24

3 Skin colour according to Vagbhata 28

4 Chaya nirupana - Panchabhuta sambandha 29

5 Classification of Viruddha Ahara by different authors 37

6 Mithya Ahara Hetu for Kushtha 38

7 Mithya Vihara Hetu for Kushtha 39

8 Achara Hetu for Kushtha 40

9 Poorvaroopa according to different authors 44

10 Depicting lakshana according to Dosha 45

11 Clinical features according to various texts 46

12 Colouration of skin as Dosha dislodged in Dhatu 47

13 Switra bhedas - various authors 48

14 Switra and Kushta lakshana sadharmya and vaidharmyata 49

15 Causes of localized hypo pigmentation 56

16 Clinical criteria for classification of Vitiligo 60

17 Pharmacological properties of Kakodumbaradi Ghanavati 76

18 Pharmacological properties of Ayourajadi lepa 76

19 Demographic Data of trail in Switra with Kakodumbaradi Ghanavati &

Ayorajadilepa

90

20 Distribution of patients by Age- gender in Switra with Kakodumbaradi 91


2

Ghanavati & Ayorajadilepa

21 Result of patients by Age in Switra with Kakodumbaradi Ghanavati &

Ayorajadilepa

92

22 Distribution and Result of patients by Gender in Switra with Kakodumbaradi

Ghanavati and Ayorajadilepa

93

23 Distribution & Results of patients by Religion in Switra with Kakodumbaradi


95

24 Distribution & Result of patients by occupation in Switra with Kakodumbaradi


96

25 Distribution and Results of patients by Economic status in Switra with

Kakodumbaradi Ghanavati and Ayorajadilepa

98

26 Distribution and Result of patients by diet in Switra with Kakodumbaradi


99

27 Data of patients by presenting complaints in study 100

28 Distribution of patients by presenting complaints in Switra 101

29 Distribution and Result of patients by Mode of onset in Switra with


102

30 Distribution and Result of patients by Family history in Switra with


104

31 Distribution and Result of patients by Chronicity in Switra with


105

32 Distribution and Result of patients by Incidence of initial site of onset in Switra

withKakodumbaradi Ghanavati and Ayorajadilepa

106

33 Distribution and Result of patients by Incidence of distribution of lesions in

Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

107

34 Distribution and Result of patients by Incidence of clinical type of disease in


109

35 Distribution of patients by Ahara Nidana in Switra Kakodumbaradi Ghanavati

and Ayorajadilepa

110

36 Distribution of patients by Vihara Nidana in Switra Kakodumbaradi Ghanavati 111


3

and Ayorajadilepa

37 Assessment of Subjective parameters in Switra 113

38 Assessment of Objective parameters in Switra 113

39 Results in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa 114

40 Subjective parameter Statistical analysis in Switra with Kakodumbaradi


115

41 Objective parameter Statistical analysis in Switra with Kakodumbaradi


116

42 Distributional (Head & Neck) Statistical analysis in Switra with Kakodumbaradi


116

43 Distributional (Trunk) Statistical analysis in Switra with Kakodumbaradi


117

44 Distributional (Upper Extremities) Statistical analysis in Switra with


117

45 Distributional (Lower Extremities) Statistical analysis in Switra with


118


4

Figures of



AYORAJADILEPA (EXTERNAL) IN THE MANAGEMENT OF SWITRA”

By


SNo Topic Page

1 Components of the integumentary system 25

2 Structure of Melanocyte 35

3 Schematic Representation of Samprapti 43

4 Autoimmune theory of vitiligo showing both cell-mediated and humoral

autoimmune

51

5 Showing pituitary – MSH – Melanocytes axis 54

6 Causes of Tyrosinase Tyrosine DOPA melanin 55

7 Ingredients of Kakodumbaradi Ghanavati and Ayorajadilepa 66

8 Estimating the Degree of Depigmentation for the VASI 88

9 Distribution of patients by Age- gender in Switra with Kakodumbaradi

Ghanavati & Ayorajadilepa

92

10 Distribution and Result of patients by Gender in Switra with Kakodumbaradi


94

11 Distribution & Results of patients by Religion in Switra with Kakodumbaradi


95

12 Distribution of patients by Occupation in trail 96

13 Result of patients by occupation in Switra with Kakodumbaradi Ghanavati and

Ayorajadilepa

97

14 Distribution of patients by Economic status in Switra with


98

15 Distribution of patients by diet in Kakodumbaradi Ghanavati and Ayorajadilepa

in Switra

99


5

16 Distribution of patients by presenting complaints in Kakodumbaradi Ghanavati

and Ayorajadilepa in Switra

102

17 Distribution and Result of patients by Mode of onset in Switra with


103

18 Distribution and Result of patients by Family history in Switra with


104

19 Distribution and Result of patients by Chronicity in Switra with


105

20 Distribution and Result of patients by Incidence of initial site of onset in Switra

with Kakodumbaradi Ghanavati and Ayorajadilepa

107

21 Distribution and Result of patients by Incidence of distribution of lesions in


108

22 Distribution and Result of patients by Incidence of clinical type of disease in


109

23 Distribution of patients by Ahara Nidana in Switra Kakodumbaradi Ghanavati

and Ayorajadilepa

111

24 Distribution of patients by Vihara Nidana in Switra Kakodumbaradi Ghanavati

and Ayorajadilepa

112

25 Results in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa 114

26 Improvement of the patients with Kakodumbaradi Ghanavati and Ayorajadilepa 119


6

Chapter - 1 Introduction

How many of the sun-lovers who crowd the beaches on a warm day ever stop to

consider the contributions and sacrifices made by their skin? This remarkable structure

absorbs ultraviolet radiation, prevents dehydration, preserves normal body temperature, and

tolerates the chafing and abrasion of the sand. Although few of us think of it in these terms,

the skin is an organ—the largest organ of the body 1.

Skin is the index of the health. We spend much time to look better always. But some

times either because of our internal environment or atmospheric effects change subjects us to

many more skin problems. The developed countries are affected more with skin problems

than that of the other organic diseases. It is true that the discoloration of the skin indexes

individual subjected for social stigma. The black, white, yellowish cream or any Asian

colours differentiate individual and small changes in it cause much mental agony.

Acharyas of Ayurveda well recognised the effects of such skin changes towards the

mental attitudes and included many diseases in the classifications of mental tortuous physical

deformities. Thus it is told by the faculty of Yoga, to practice “Surya Namaskara” i.e. Sun

salutations every day in the morning, which prevents the individual from skin problems.

Vitiligo is such a common chronic and progressive skin disease characterised by the

lack of melanin pigments producing skin patches with sharp and often hyper pigmented

edges. This disease affects approximately 1% of the world-wide population 2.

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra – Introduction

1

The aetio-pathogenesis of Vitiligo is still unknown to date, even though the multi-

factorial character of its clinical expression is quite clear. There are three classical pathogenic

theories 3:

1. Immunologic theory

2. Neurologic theory and

3. Self-destruction hypothesis

Possible hereditary factors and psychosomatic issues should undoubtedly be taken

into account as well. The clinical expression of the disease also varies between individual

patients, according to personal characteristics, and between patches, according to the partial

or total lack of pigments. The prognosis of this skin disease is thoroughly benign, even

though the psychological and social implications following up the aesthetic modifications

due to the appearance of patches may be very serious and disabling.

Since the etiological cause of Vitiligo may not be removed, medicine may only act on

symptoms by means of therapies aimed at restoring the lost colour uniformity. However it is

not always easy to suggest to a patient a treatment being effective, long lasting and free of

side effects at the same time. The most widely used therapy in the last thirty years was the

PUVA therapy (UVA + trimethylpsoralen), with results ranging from 25% to 50%. This

therapy requires a careful assessment of the patient's general conditions and clinical picture,

as well as the identification of the correct drug dose to be administered and patient

monitoring throughout the treatment period.

As a border organ, the skin is crucial for the body's homeostasis, to which it

contributes through a number of particles specialized in receiving stimuli and forwarding

them to the central organs of the nervous system. Along with these, there is a special family


2

of receptors, the melanocytes, whose task is to react to the light stimulus by synthesizing a

special protein, melanin, constituting the most important skin-protection factor. Evaluation of

the role of immunogenetic factors and trace elements (copper) in pathogenesis of Vitiligo

provided the basis for the improvement of its photochemotherapy by using Cupir and T-

activin. This yielded an opportunity for a better management of this dermatosis. Results of

the one study suggests that the indications for the use of T-activin (immunomodulator) and

Cupir (copper-containing product) in the treatment of Vitiligo 4.

As Vitiligo is a relatively common skin disorder, in which white spots or patches

appear on the skin. These spots are caused by destruction or weakening of the pigment cells

in those areas, resulting in the Melanin pigments being destroyed or no longer produced.

Melanin is a dark brown pigment of skin and hair in animals. It is synthesized by special cells

called Melanocytes, which store the melanin. In most cases, Vitiligo is believed to be an

autoimmune-related disorder. In Vitiligo, only the colour of the skin is affected but texture

and other skin qualities remain normal.

Vitiligo is not contagious. If it were, many more people in the world, including

doctors who treat Vitiligo and family members of those with Vitiligo, would have the

condition.

Most patients with Vitiligo undergo emotional trauma related to their looks and social

image, especially the young. They should be reassured and supported well. The treatment in

most cases is effective and should be continued till the desired results are obtained.

Most people with Vitiligo have neither parents, nor children, nor siblings with

Vitiligo. Many have no other relatives with Vitiligo. Vitiligo does appear to be hereditary,

that is, it can run in families. No questions of Children whose parents have the disorder are


3

more likely to develop Vitiligo. However, most children will not get Vitiligo even if a parent

has it, and most people with Vitiligo do not have a family history of the disorder.

People who develop Vitiligo usually first notice white patches or spots (de-

pigmentation) on their skin. The skin remains of normal texture, and there are usually no

itching or other symptoms. These patches are more obvious in sun-exposed areas, including

the hands, feet, arms, legs face, and lips. Other common areas for white patches to appear are

the armpits and groin and around the mouth, eyes, nostrils, navel, and genitals. Vitiligo

generally appears in one of three patterns. In one pattern (focal pattern), the de-pigmentation

is limited to one or only a few areas. Some people develop de-pigmented patches on only one

side of their bodies (segmental Vitiligo). But for most people who have Vitiligo, de-

pigmentation occurs on different parts of the body (generalized Vitiligo), often similar on

each side of the body. In addition to white patches on the skin, some people with Vitiligo

may experience white hair growing in on the scalp, eyelashes, eyebrows, and beard. In

extremely rare cases, Vitiligo can affect eye colour or the pigment of the retina 5.

If a doctor suspects that a person has Vitiligo, he or she usually begins by asking the

person about his or her medical history. Important factors in a person's medical history are a

family history of Vitiligo; a rash, sunburn, or other skin trauma at the site of Vitiligo 2 to 3

months before de-pigmentation started; stress or physical illness; and premature greying of

the hair (before age 35). In addition, the doctor will need to know whether the patient or

anyone in the patient's family has had any autoimmune disorders and whether the patient is

very sensitive to the sun 6.

The doctor will then examine the patient to rule out other medical problems. The

doctor may take a small sample (biopsy) of the affected skin. He or she may also take a blood


4

sample to check the blood-cell count and thyroid function. Most certainly, the doctor will

examine your skin with a special black light called a Woods Light, which illuminates areas of

Vitiligo. This also helps the doctor rule out other conditions. For some patients, the doctor

may recommend an eye examination to check for uveitis (inflammation of part of the eye). A

blood test to look for the presence of antinuclear antibodies (a type of autoantibody) may also

be done. This test helps determine if the patient has any other autoimmune conditions.

Today, there is more research and more treatments options available than ever before.

In addition to the traditional therapies such as the PUVA system and steroid creams, new

technologies have been developed, including narrow-band UVB, Pseudocatalase cream,

excimer lasers, skin grafting and pigment transplantation, topical psoralens, and potentially,

the use of immunomodulators.

There is no one treatment that works for everyone. Different therapies work better for

different people. While one person may respond extremely well to PUVA, another may

respond better to narrow band UVB or immunomodulators. For this reason, many Vitiligo

experts will try different therapies on a patient until they find what works best for that

person.

There is no definite method by which Vitiligo can be prevented. However, some

measures may be taken to minimise its effects. People with or without the condition should

always use sunscreen lotions or sun-blocks with a sun protection factor (SPF) of 15 or more

to protect the skin against the harmful effects of UV rays. This should especially be the case

after participating in outdoor sports like swimming 7.

Since condition is cosmetic one, the social effects of Vitiligo may cause more

hardships than the physical limitation. Indian society place great emphasis physical


5

appearance especially, on white discoloration of skin. In Vedic period person suffering from

the Switra and their progeny are disqualified for the wedlock 8.

Need for the study:

‘Switra’ is a disease pertaining to Twak 9 which turns the normal colour of the skin to

white. It can be equated to that of Vitiligo in contemporary medicine which is an achromatic

macular de-pigment condition, resulting from loss of ‘melanin’ pigment 10. This condition

affects about 1-2% of the world’s population 11 and 3-4% in India. All the races and both sexes

are equally affected.

The cardinal symptoms of Switra are the appearance of ‘Aparisravi shweta varna

mandalas, on the skin that is depigmented patches or macules. These patches are more

common in sun-exposed areas including the hands, Feet, arms, face and lips 12. Switra

(Vitiligo) is a cosmetic problem. The change in appearance caused by this condition can affect

a person’s emotional and psychological well being. The person with this condition feels

ashamed and depressed.

Though the contemporary medical science tries to treat this condition with different

types of re-pigmentation therapies, they fail to offer satisfactory results. Ayurvedic treatment in

this concern through holistic approach, can improves the patient’s appearance and restore the

normal pigmentation of the skin.

The tendency of many doctors to trivialize and its consequences was one of the most

difficult problems encountered by patients. Though Vitiligo is cosmetic problem, it may have

profound effect on a patients self esteem and social relationships. So Vitiligo must not be

ignored by the physician.


6

Of the various treatment approaches offered by conventional medicine, from the good

old PUVA therapy, to using corticosteroids, to epidermal grafts or cell culture techniques none

is completely effective in all presentation of Vitiligo.

Further some of conventional approaches have unacceptable side effects or either

unaffordable or not easily accessible in all parts of the country. Since Vitiligo affects

irrespective of poor and rich and as well as children and adults, A clinical study was planned to

access the efficacy of an indigenous preparations based on the Ayurvedic principles.

Thus the ‘Kakodumbaradi Ghanavati and Ayorajadilepa mentioned in Sahasrayoga

and Yogaratnakara are selected for internal and external application respectively, as the

contents of these drugs are easily available, economic and good result oriented. So the present

study “Evaluation of the efficacy of ‘Kakodumbaradi ghanvati’ and ‘Ayourajadi lepa” are

undertaken, which are with Switraghna and Varnaya properties.

Previous work done on Switra:

Recent research works taken place regarding Switra are as follows 13;

1. Ameen A.M. Switra vimarsh (Bhallataka sidha ghrita yoga), 1967, Jamnagar:

2. Dahiya J .Studies on the Switra and its management,1983, Jamnagar:

3. Patil A K Survey of Switra in Jamanagar and vicinity in reference to its

nidan and chikitsa.,1984, Jamnagar:

4. Sardar C L. A clinical study of Switra (Leucoderma), and its management with

Kakodumbar, and manishiladi lepa1993. Jamnagar:

5. Thakore S R Kakodumbara Prayoga in Switra 1989, Amadabad

6. Ansari ZA Efficacy of certain Ayurvedic drugs in the managements of Vitiligo

(Switra), 1985, Banaras Hindu University, Varanasi

7. Upadhya RK. Therapeutic assessment of some Ayurvedic drugs in the treatment of

Vitiligo 1988, Banaras Hindu University, Varanasi


7

8. Prithivraj .The concept of Switra and its management in Ayurveda, Banaras Hindu

University, Varanasi

9. Sharma ( Smt ) M. – Switra Roga par Aylagujadi Gutika ( Bhaya Prayogarth )Evam

Khadira ( Abhyantara Prayoga ) karmukata Ka Adhyana, Jaipur

10. Sheelaratna M.V -- Switra Roga and its management, Mysore: Govt College of

Indian Medicine

11. Shrikantbabu – Evaluation of Kakumbadaradi Yoga in the management of Switra,

Mysore : Govt College of Indian Medicine

12. Mishra .S – A clinical trial of some indigenous drugs on Switra (Vitiligo), Gopa

Bandu Ayurvedic Mahavidyalaya, Puri

13. Burman S – A clinical study on the therapeutic effect of Tuthyadi Lepa on Switra

(Vitiligo), Gopa Bandu Ayurveda Mahavidyalaya, Puri

14. Lahari .P.K – Clinical studies and management of Switra kushtha ( Leucodermia )

with Ayurveda, Gopa Bandu Ayurvedic Mahavidyalaya, Puri

15. Tiwari SK, Evaluation of the efficacy of Dhatryadi Yoga (internal) and Avalgukadi

lepa (External) along with and with out Shodhana (Vamana) in Switra (W.S.R. to

Vitiligo), 2001, DGM AMC, RGUHS, Bangalore.


8

Chapter – 2 Objectives

The present study is intended to focus on the disease evolution that is Switra-vis-

à-vis Vitiligo and the management with Kakodumbaradi Ghanavati internally and

Ayorajadilepa externally application. 30 patients from OPD of Postgraduate studies and

Research centre of DGM Ayurvedic Medical College and Hospital, where scrutinized and

undertaken for the study.

Kakodumbaradi kwatha mentioned in Shashrayoga with switraghna and Varnya

properties as a reference to the management of Switra is prepared in the form of tablet for

the convenience of distribution. In further Vati is easy to consume and convenient to

preserve the drug for longer duration.

Ayorajadilepa mentioned in Yogaratnakara is selected as the external application

and prepared in the form of Varti (5 mg). The compound of lepa has photosensitizing

property in association with sunlight and there by local action facilitates the rapid local

pigmentation. In this regard the objectives proposed in the study are discussed as under.

To evaluate the efficacy of Kakodumbaradi Ghanavati (internal) and Ayorajadilepa

(external) in the management of Switra

Vitiligo affects 1 to 2% of the population. It may be triggered by any kind of

damage to the skin (Koebner Phenomenon). It takes the form of skin white spots with a

sharp margin and a milk white color. The normal texture and sensation of the skin are

preserved. No scaling occurs. Vitiligo spots need to be differentiated from other skin

discolorations, including Tinea Alba and versi color caused by fungus. Vitiligo may

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra – Objectives

9


10

either remain static for years or progress gradually, sometimes extending rapidly over a

period of several months.

Vitiligo is believed to be an autoimmune disorder with a genetic basis. An

autoimmune disorder is any condition in which a person's immune system reacts against

the body's own tissues or organs attacking them. In the case of Vitiligo, the immune

system attacks and damages or destroys melanocytes. Melanocytes are specialized skin

cells that produce melanin. Melanin is the pigment that gives the skin its natural color.

Treatment is based both on a large body of information that supports the

autoimmune theory associated to a genetic defect that makes the melanocytes susceptible

to injury. Current knowledge about how the skin pigmentation process occurs is also

helping to design better Vitiligo treatments.

Treatment may have different targets 14:

1. Limiting or stopping the autoimmune reaction against melanocytes (ex.

corticosteroids).

2. Protecting melanocytes from a group of harmful products called "free radicals",

which are the results of the autoimmune reaction that causes de-pigmentation (ex.

vitamins, pseudo-catalase).

3. Stimulating melanocytes to regenerate and/or produce melanin (ex. UVA, UVB,

PUVA, controlled sunlight exposure).

4. Replacing melanocytes (a modality of surgical treatment) by transplanting grafts

from uninvolved skin into the affected areas.

5. A combination of several of the above mechanisms.


11

Thus the Switra is a condition, which affects the skin with “Aparisravi

swethavarna mandala” i.e. non exudative white circular patches with out changing the

morphology of skin. Switra may have its managements through various methods, such as

Sramsamana, Bhahiparimarjana, Kushtaghna and Varnya etc, mentioned in classics. Out

of all Ayorajadilepa, which is used here as external application and Kakodumbaradi

Ghanavati internally helps to understand the different mechanisms put forth for pacifying

the disease. The present study under takes the treatment under the following headings of

hypothesis.

1. Role of Dosha and its pacification in Switra by Kakodumbaradi Ghanavati

internally and Ayorajadilepa externally

Switra is a Tridoshaja Vyadhi. By indulgence and practice of aetiological factors

vitiation of tridosha takes place. They occupy Rakta, Mamsa and Medo Dhatu to produce

disease in situ. As the Dosha- Dooshya sammurchana of these manifests the Switra, it is

essential to combat the disease based on the ground of Dosha pacification. Hence, the

ingredients of Kakodumbaradi Ghanavati ingredients are scrutinized for want of

pacification of the involved Dosha, i.e. Dosha pratyaneeka Chikitsa is under taken.

The ingredients consist of katu Rasa, rooksha and laghu guna, ushna veerya along

with katu vipaka, by which they act as Kapha hara. The herb with Tikta and kashaya

Rasa, sheeta veerya pacifies the Pitta. The ushna veerya of the drug acts on Vata to

pacify.

The topical application locally acts to relieve the obstructions of the normal

situation maintenance and regulates the Dosha concern such as Bhrajakapitta.


12

2. Protecting skin from "free radicals" vis-à-vis Ama by Kakodumbaradi Ghanavati

internally and Ayourajadi lepa externally

Ayurveda suggests of regular cleansing of the body i.e. purification of the body,

through the day to day activities. Deranged digestion is rectified as the first step of the

treatment, which is possible through Kakodumbaradi Ghanavati inducing free defecation,

considered as the Nitya Shodhana or other wise Koshta Shuddi. The free radicals are the

effective disease producing chemical agents which are produced at the end of the

reactions occurring as a part of metabolism in the body. The Ama according to Ayurveda

mimics the above theory is also cared about in the study. Ayurveda suggests that

regulating the Agni is the treatment. Thus at this juncture the Deepana and Pachana

qualities embedded in the Kakodumbaradi Ghanavati regulates the free radical inflow i.e.

Ama and enhances the effect of the trail drug.

3. Stimulating melanocytes to enrich re-pigmentation by Kakodumbaradi Ghanavati

internally and Ayorajadilepa externally

Switra is a disease of hypo-pigmentation. Thus the enhancing melanin production

becomes a task at the study. For such development the Ayorajadilepa local action is more

beneficial. The internal Kakodumbaradi Ghanavati as it acts to regulate Dosha and the

disease producing factors locally Ayorajadilepa implants counter irritation and regulation

of the Bhrajakapitta. So far it is known that Bakuchi is the only drug that has a dual

action i.e. Action on both Rouget's cells and the melanoblastic cells of the skin. In

leucoderma the malanoblastic cells are not functioning properly and their stimulation by

the oil leads them to form and exude pigment which gradually diffuses into the

decolorized area (chopra).


13

4. Producing long term tissue building effect in the Body through Rasayana effect of

Kakodumbaradi Ghanavati internally and Ayorajadilepa externally

Rasayana is a unique method of protective and nourishing the tissues against the

natural calamities and time bound degeneration. The Ayurvedic medicines will have an

embedded effect of Rasayana in them. The Kakodumbaradi Ghanavati consists of the

Bakuchi, which is said to be a best Twak Rasayana. Switra on the other hand of

contemporary medical specialists is an autoimmune disorder and the management has to

be suppression of free radicals and enhancing immuno-modulation, other wise inducting

Rasayana.

Kakodumbaradi Ghanavati cumulative effect is Rasayana, Brumhana and Balya.

Thus the above said trial drug will repair the tissues deranged and long term tissue

building effect. Rasayana effect could be estimated in four ways viz.-

1) Cell maintenance and nourishment

2) Enhancing the cell growth

3) Expelling the free radicals and

4) Inducting immuno-modulation effect.

The topical preparation i.e. Ayorajadilepa is Twachya (skin promoter) and

Keshya (Hair promoter). So these compounds certainly enhance the tissue

building and pacify the hypo-pigmented patches of Switra.

Chapter – 3 Literary Review

Switra i.e. Vitiligo is an important skin disease having major impact on quality of life

of patients, many of whom feel distressed and stigmatized by their condition. Society greets

Vitiligo patients in much the same way as it does any one else who appears to be different.

They are started at or subjected to whispered comments, antagonism, insult or isolation. The

chronic nature of disease, long term treatment, lack of uniform effective therapy and

unpredictable course of disease is usually very demoralizing for patients suffering from

Vitiligo. It is important to recognize and deal with psychological components of this disease

to improve their quality of life and to obtain a better treatment response 15.

In India and perhaps elsewhere also men, women and children with Vitiligo face

severe psychological and social problems. It is more acute in the case of young women and

children. The first prime minister of India, Pt Jawaharlal Nehru ranked Vitiligo as one of

three major medical problems of India the other two being leprosy and malaria. In India

Vitiligo commonly known as leucoderma is unfortunately associated with some religious

beliefs 16.

In some Indian religious texts where reincarnation is believed, it is said that a person

who did "Guru Droha" in his previous life suffers from Vitiligo in this life. Thus people

suffering from Vitiligo in India have more social problems than in other countries. This is

seriously felt among young unmarried women. This is so because of arranged marriages.

Thus a young woman with Vitiligo has little chance of getting married. A married women

developing Vitiligo after marriage shall have marital problems perhaps ending in divorce.

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –Literary Review

14

Since ancient times patients with Vitiligo suffered the same mental abuses as lepers.

In actual fact Vitiligo was referred as Sweta Kustha meaning "White leprosy". Vitiligo is

disfiguring in all races but particularly more so in dark skinned people because of strong

contrast. Many Vitiligo patients feel distressed and stigmatized by their condition. They

attract undue attention from the general public some times whispered comments, antagonism

and ostrisisam. The self image of the Vitiligo patients drops considerably and may lead to

depression. These patients often develop negative feeling about it, which are reinforced by

their experiences over a number of years. Most patients of Vitiligo report feelings of

embarrassment, which can lead to a low self-esteem and social isolation 17.

Vitiligo lesions over face may be particularly embarrassing and the frustration of

resistant lesions over exposed part of hands and feet can lead to anger and disillusionment

particularly in teenagers, mood disturbances including irritability and depression are

common. Patients with Vitiligo are very sensitive to the way other perceives them and they

will often withdraw, because they anticipate being rejected. Sometimes, strangers and even

close friends can make extremely hurtful and humiliating comments. The impact of such

factors is profound subjecting them to emotional distress, interference with their

employment, or use tension-lessoning, producing substances such as alcohol 18.

Severe depression has been known to lead to suicide attempts 19. Last decade has

witnessed an increasing interest in psychological effects of various skin diseases and quality

of life in patients suffering from these diseases 20. A healthy normal skin is essential for a

person's physical and mental well being. It is an important aspect of their sexual

attractiveness, a sense of well being and a sense of self confidence 21. The skin is the largest

and most visible organ of the human body 22. Hence any blemish on the skin visibly affects


15

the onlooker and thus the person affected profoundly 23. Vitiligo is an acquired de-

pigmentation disorder of great concern affecting 1–4% of the world population 24.

Vitiligo is an important skin disease having major impact on the quality of life of

patients suffering from Vitiligo. Appearance of skin condition is an individual self-image,

and any pathological alteration can have psychological consequences 25. Vitiligo has a

profound effect on the quality of life of patients and so the patients go to any extent in getting

it treated although it is not life threatening. The dermatologists should treat it as serious

disease with the various treatment modes now available and not dismiss simply because of

not having a completely successful treatment. Improving the physician's interpersonal skills

with the Vitiligo patients increases patient's satisfaction and consequently may have a

positive effect on adherence to treatment protocol and better out come of treatments.

For such an attempt a through knowledge of the Switra in terms of its etiology,

progression of disease and methods of managements are studied. The study should have

comparison of the ancient told literature to compare and study under the limelight of the

contemporary medical parlance.

HISTORICAL REVIEW

It is the past that has created the present. The study of the past history gives us the

picture of origin of diseases, our ancestor’s knowledge about them and their contribution

towards combating the diseases. Many historical facts are available regarding the disease

Switra since Vedic period. For the sake of convenience the knowledge of Ayurveda can be

divided as follows.


16

Vedic Period (2500BC – 1000BC)

The Vedas establish many subtle links with the hymns and charms. The literature of

many epochs serves as valuable sources of information in understanding the disease Switra.

Rigveda, Yajurveda, Samaveda and Atharvaveda are four Vedas. References regarding

Ayurveda are found in Rigveda and Atharvaveda.

In Rigveda 26 relevant reference regarding Switra is found. A story is narrated where

Shweta Kushta is mentioned. Ghosha, the daughter of Kakshavati was refused by her

husband when Shweta Kushta inflicted her. Ashwini kumaras the pioneers in medical

profession treated and cured her disease, which made to regain her marital status. In Rigveda

Kilasa is the name used to describe the spotted deer, which has striking resemblance with the

disease Switra where the hypo pigmentary patches are diffused over the body without ulcers.

In Athrvaveda the term Switra is not directly described. But the terms like Kilasa,

Palita are used in place of Switra 27. In Koushika Sutra of Atharvaveda Rama, Krishna,

Asikni are the medicinal herbs described as the remedy for the malady Kilasa. Darila, a

commentator says Bringaraja, Indravaruni and Neeli are the drugs described as the drugs

Rama, Krishna and Asikni respectively. The fourth drug appreciated in maintenance of the

colour is Rajani or turmeric 28.

In Yajurveda there is a reference mentioning that Chandra or moon is affected with

the disease Switra 29. According to Taittariya Brahmana, the students suffering from the

following diseases were not acceptable by the guru. ‘ Switri chaiva galatkushti netra rogi cha

vamane kunakha shyavadantavascha’ - Persons suffering from Switra and their progeny are

disqualified for wedlock as per the direction of Manu 30.

In Panini Vyakarana Sutras also references regarding Switra roga are found 31.


17

Samhita Period : (1000 BC – 100AD)

Samhita period is considered as golden era of Ayurveda as maximum contribution is

given in this period.

Charaka describes Switra roga with Kushta chikitsa, specified its dhatugatatwa up to

medodhatu and also mentioned about its specific nidanas 32.

Sushruta also mentioned about Switra roga in Kushta rogadhyaya and dealt its types

as vataja, pitta and kaphaja Switra 33.

Bhela has also described Switra in brief 34.

Kashyapa Samhita has also dealt about Switra in Kushta chapter itself and defined its

cardinal symptom as twacha Shwetata.35

In Ashtanga Sangraha 36 and Ashtanga Hridaya 37, the description of Nidana, Bheda,

samprapti and Chikitsa is available. He has stated that Switra more bheebhatsa than that of

Kushata. So the prognosis of Switra defends on early diagnosis and prompt treatment.

Madyamakala (800 AD – 1700 AD)

Important treatise of this period is Madhava Nidana 38, Bhava Prakasha 39,

Sharangadhara Samhita 40. These books compiled and reproduced the scattered information

of Samhitas in an order. All acharyas of this period follows opinion of Bhritries, very

specifically of Acharya vagbhata. Acharya Sharangadhara has given numerical data and

prescriptions for Switra.

Adhunika Kala : (1700AD onwards)

This started after the entrance of the foreigners. Here especially during recent decades

there has been tremendous and marvellous development in the field of medicines. Becker and

Obermayor reported Vitiligo cases in 1937 and Buckley and Lobitz in 1953. Afterwards


18

A.B.Lerner (1959), Fitz Patric (1974), Parish J.A.(1976), P.N. Behl(1980) and Roxburghii

(1980) have done in depth studies on Vitiligo 41.

NIRUKTI :

Switra:

The term Switra belongs to feminine gender. It is derived from the verb root ‘Swith’

i.e. Shweta varna, meaning white color. When the suffix ‘ rik’ is added to the verb root

‘Swith’ by the rule ‘It Sansnya’ the letter ‘ka’ is deleted, ultimately it becomes the word

‘Switra’ 42.

Swith + Ra = Switra

Vitiligo:

The origin of the term Vitiligo is obscure like the disease itself. Some believe that it is

derived from the Latin word ‘vitelius’ meaning vale i.e., pale pink flesh of a calf, while

others originated from the word ‘vitium’ meaning blemish 43.

Stedman’s dictionary 44 defines Vitiligo as - The appearance on otherwise normal

skin of non-pigmented white patches of varied sizes, often symmetrically distributed and

usually bordered by hyper pigmented areas; hair in the affected areas is usually, but not

always, white.

Epidermal melanocytes are completely lost in depigmented areas by an autoimmune

process. Synonyms of Vitiligo are acquired leukoderma, acquired leukopathia and

leukasmus. Leukoderma is defined as - An absence of pigment, partial or total, in the skin.

PARIBHASHA:

Ayurvedic authors have defined Switra in different ways but all definitions carry the

“Shwetate iti Switram” same meaning.


19

In Amarkosha 45 Gurabala prabhohini the term Switra defined as “Swetate

twaganena Switram” means by which the colour of skin turns to white

. In Shabdhakalpadruma 46 as –“ Shwetate ithi”

In Kashyapa Samhita 47, as ‘ Shwetabhavamichchanti Switram ’.

All above references from the various texts and classics of Ayurveda support the

meaning of the Switra as white discolouration of the skin. The cardinal symptom of the

Vitiligo is milky white macules on the skin. All the above-mentioned definition gives support

to Vitiligo and its cordinal symptom perfectly.

Vitiligo is progressive, chronic pigment anomaly of the skin manifested by

hypo pigmented white patches that may be surrounded by a hyper-pigment border.

PARYAYA

The synonyms of Switra present a typical picture in relation to its symptoms.

Switram 48: ‘Swetate iti Switram’ – that which produces morbid whiteness.

Kilasa 49: ‘Kila varnam yasyati ksheeyati vikruti karoti iti yat ’ – that which

gives vikruta varna to the skin.

Shweta kushtam 50: Shwetate anena iti shweta kushtam’ means the skin

disease which causes whiteness of the skin.

Charuna 51: Reddish brown, tiny, the color of the morning opposed to the

darkness, i.e., the dawn.

Daruna 52: If disease is untreated became Asadya

Synonyms:

Achromoderma, Hypomelanosis, Leukopathia and Leukopathy are the synonyms of

Vitiligo.


20

Role of skin in the Switra

It is very much essential to know and understand the role of skin in the Switra

pathogenesis with its physiological and anatomical considerations.

The skin is the body's largest organ. Knowing its function and how it is related to the

nervous system helps understand how stress can trigger or worsen Vitiligo. It is also

important to know the close relation between the nervous system and the system of defense

i.e. immune system.

Skin functions in general 53

1. It is a barrier to protect the body against the entry of toxic environmental chemicals.

2. It prevents loss of essential body fluids and dehydration.

3. The skin protects the body against invasion by micro-organisms.

4. The skin contributes to the body's supply of vitamin D. Vitamin D3 (cholecalciferol)

is produced in the skin by the action of ultraviolet light on dehydrocholesterol.

5. Melanin, the natural pigment of the skin protects against damage from excessive

ultraviolet radiation.

6. The skin is a part of the body's temperature regulation system, protecting us against

hypothermia (excessive cold) and hyperthermia (excessive heat).

7. The skin is also a huge sensory organ with receptors for heat, cold, pain, touch,

pressure, and tickle.

The skin and the nervous system originate from the same structure during early fetal

development. This is one of the reasons why emotional life may affect the skin either

positively or negatively. The skin has great psychological importance at all ages. It is an


21

organ of emotional expression and a site for the discharge of anxiety. For example, caressing

favors emotional development, learning and growth of newborn infants.

Skin (Twak) in Ayurveda

The term "TWAK" derives from the root "twacha - samvarne" (which cover). It can

be defined as substance of the body, which covers the internal tissues like Rakta, Mamsa etc.

Synonymous of Twak:

1. Twak

2. Charma

3. Sparsanedriya

Skin formation:

The layer of Twak forms in the stages garbhavstha as layer of scum-formation on the

surface of boiling milk 54.Later in the stage of dhatu parinam, Twak forms as an upadhatu

from prasada paka of Mamsa Dhatu. Twak is the mridu bhava of garbha, which can be

considered as Matruja Bhava (Maternal factor) 55. According to Vagbhata Twak is formed

in sixth month of gestation 56.

Layers of the skin:

According to Susruta 57 Twak is composed of seven layers and six layers by

"Charaka". Susruta described the thickness of each layer taking one "vreehi" as standard for

total skin, where as Charaka does not mention the thickness of layers. The above Acharyas

have described the diseases that manifest in each layer. But they have got difference in

opinion of layer, in which the "Switra" occurs. Charaka considered it as third, while Susruta

in the fourth layer. Regarding the number of layers of skin there are some difference of

opinion between the ancient authors; for instance - Charaka 58 described six layers of skin but


22

while elaborating one these layers he has named only two layers the rest four layers have

been described in terms of the diseases. Susruta has described seven layers of skin along with

the specific names. He has also mentioned the thickness of each layer along with the

diseases, which are prone to that layer.

The comparative tabular form of skin layers are depicted as under.

Table – 1

Skin layers according to Charaka, Susruta and Vagbhata

S.No Charaka Disease according to Charaka

Susruta Thickness according to Susruta

Disease according to Susruta

Vagbhata

1 Udakadar - Avabhasini 1/18 vreehi (0.05-0.06mm)

Sidma, padakantaka

Udakadhara

2 Raktadar - Lohita 1/16 vreehi

(0,06-0.07mm)

Tilakalaka, nyacha.

Asrukdhara

3 Triteeya Sidhma, kilasa

Sweta 1/12 vreehi (0.08-0.09mm)

Vyanga, ajagalika, mashaka.

Third layer

4 Chaurth Dadru, kushta

Tamra 1/8 vreehi (0.12-0.15)

Kilasa, Fourth layer

5 Pachama Alaji, vidradi

Vedini 1/5 vreehi (0.2-0.3mm)

Kusta, visara. Fifth layer

6 sashta Arasha, baganhara

Rohini 1 vreehi (1-1.1mm)

Granti, apachi, arbuda, galaganda.

Pranadhara

7 Mamsadhara 2 vreehi (2-2.1mm)

Bhagandara, arsha, vidradi.

Not told

Vagbhata 59 has described seven layers of skin similar to Susruta. He has not given

any description. Sharangdhara 60 has also mentioned seven layers of skin along with the

probable onset of diseases. The names of first six layers are same as Susruta but seventh

layers are named as “Sthula” which is the site of Vidradhi.


23

Dr. Ghanekar has written commentary on Susruta Shareera. He has correlated the

layers of skin mentioned by Susruta with the latest anatomy of skin as under 61.

Table – 2

Skin layers comparison according to Dr. Ghanekar

S.No Ayurvedic nomenclature Contemporary nomenclature

1 Avabhasini Stratum corneum

2 Lohita Stratum Lucidum

3 Sweta Stratum Granulosum

4 Tamra Malpighian Layer

5 Vedini Papillary Layer

6 Rohini Reticular Layer

7 Mamsader Subcutaneous tissue and muscular layer

Surface Anatomy of skin 62:

Chakrapani commenting on Charaka Chikitsa, 15th chapter stated that before

proceeding to the study of vikruti one should have the complete knowledge of its prakruti.

Switra is a hypo pigment disorder affecting the Twak, the most exposed part of the body. A

description regarding anatomy and physiology of skin is necessary to understand completely

the cause, nature and the treatment of this disease.

Within this area the basic studies of the materials that make up the skin and its cells,

how they are assembled into the structure that we see under the light and electron

microscope. In further skin cells interact with one anther via cell to cell signalling and

attachment how the skin protects itself from the external environment has to be studied in


24

detail. And how that protection can breach in a controlled manner to apply drugs to treat skin

and systemic diseases, we have to study skin elaborately.

Figure -1

Components of the integumentary system

St

us

th

ep

sy

wh

ructure of Epidermis: The epidermis is formed of nonvascular stratified epithelium. Its

ual thickness is in between 0.07mm and 0.12 mm. But in certain parts like the soles of

e feet and the palms of the hands it is very thick ranging from 0.8 mm to 1.4 mm. The

idermis is mainly divided into two main systems namely keratinizing or malpighian

stem (keratinocytes) which forms the bulk and the pigmentary system (melanocytes)

ich produces the pigments. Melanin is transferred to the keratinocytes through the

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –Literary Review 25

dendrites of melanocytes. The following are the main layers of the epidermis from above

downwards.

1. Stratum Corneum – This is the most superficial layer, the outer surface of which is

exposed to the atmosphere. It consists of many layers of non-nucleated, flattened

cornified cells. This layer is thickest on the palms of the hands and soles of the feet.

But thinnest on the outer aspects of the lips and the glans penis and the eyes.

2. Stratum Lucidum – This is below the Stratum Corneum and is the pale wavy looking

layer. It is formed by many layers of flattened and closely packed cells whose outline

have become quite indistinct and the nuclei have disappeared. This layer contains

refractile droplets of eleidin.

3. Stratum Granulosum – This layer is composed of flat fusiform cells, which are one to

three layers thick. These cells contain irregular granules of keratohyalin.

4. Stratum Malpighi or the prickle cells layer – This layer is composed of several layers

of polyhydral cells connected to each other by intercellular bridges. Surface of this

layer is covered with minute spines known as prickle cells. As the cells move towards

the surface keratin is synthesized with in them. Melanin pigment is more distinct in

this layer.

5. Stratum Germinativum – This is the deepest portion of the epidermis and is composed

of columnar cells placed perpendicular to the skin surface. The whole of the

epidermis germinates from the stratum hence the name stratum germinativum. The

basal layer contains many mitotic figures signifying the occurrence of cellular

multiplication. More and more cells are formed and pushed of to the superficial

layers. Some of the cells of the stratum germinativum contain granules of pigments


26

called melanin. Besides melanoblasts or melanocytes are found in this layer. These

have branching processes ramifying between other layers. These appear non-

pigmented.

Structure of Dermis: This layer consists of bundles of collagen and elastic fibers arranged

in the reticular fashion. It is profusely supplied with blood vessels. Superficially the

dermis is condensed into a dense fibrous network, the basement membrane to which are

attached the epidermal cells. Its deeper parts merge imperceptibly into the hypodermis.

Beneath the basement membrane are distributed many blood vessels forming a capillary

network, which sends up, loops into the dermal papillae. Thickness of dermis varies from

1 to 3 mm. Other structures found in the dermis include blood vessels, lymphatics,

nerves, nerve endings and receptors, Dartose muscle in the scrotum, appendageal glands

and their accessories, eg. Erector pilli muscles.

Shareera Kriya of Twak:

In Switra the cardinal symptom is accepted as depigmentation. Thus the study

regarding the factors responsible for 'varna' (pigment) as per Ayurveda is essential apart from

the other functions narrated by the Ayurvedic authors’ viz. Sparsnedriya stana, Bhrajakapitta

stana, Sweda gati stana, Absorption area for abhyanga, parisaka and alepa etc.

VARNA OF TWAK:

"Tejobhuta" is the main factor in formation of Twak varna and among the Dosha,

"Pitta" is said to be responsible for the normal as well as abnormal coloration of the skin. The

specific "Bhrajakapitta" is located in Twak. During the garbhavasta, with the predominance

of tejobhuta the colour formation in foetal skin is accepted as below.

• Tejas + Ap -> Goura


27

• Tejas + Prithvi -> Krishna

• Tejas + Akasha -> krishna-shyama

• Tejas + Ap + Akasha -> Shyama.

"Charaka" described 63 prakrita varnas are four in number, those are krisna, krisna

syama, syamavadata and avadata. Beside these are atikrisna and atigoura who are "ninditas"

mentioned in Charaka Samhita Sutra Sthana. Factors responsible for normal skin colour

according to Vagbhata 64 are –

Table – 3

Skin colour according to Vagbhata

S.N colour Sukra varna Garbhini ahara & vihar

Mahambhuta samyoga

Desa kala anuruti

1 Goura Shukla/Ghritabha varna

Ksheeradi madhur

Teja+jala+akash

2 krishna Taila Tiladi vidhahi annasevana

Teja+prithvi+vayu

3 Shyava Madhu Mishara ahara Sarva bhuta sanyoga

Chaya and prabha:

These are the factors, which are having close relation with skin colour. Chaya masks

the varna, while prabha brightens the varna chaya can be appreciated from close vision, while

prabha is visible from distance 65.

Tejobhuta is the basic of all types of prabha. The prabha is classified into seven, viz.

rakta, peeta, sita, syava, harita, pandu and asita 66.

Varna in normal is permanent from birth to death, chaya may alter due to "rishta"

(asanna mrityu lakshana), while prabha changes according to the temporary state of health.

The normal colour of the body is the outcome of these three only.


28

Table -4

Chaya nirupana - Panchabhuta sambandha 67

Type Lakshnas

1 Nabhasi Nirmala, neelavarna, snehayukta, saprabha

2 Vayavi Ruksha, syavavarna, hatahprabha

3 Agneya Visudharakta, deeptabha, darsanapriya

4 Apya Shudha, vaiduryavimala, susnigdha

5 Parthiva Sthira, snigdha, ghana, syama, sweta

Bhrajaka Pitta and skin colour

Bhrajakapitta is stated to be located in the skin and to impart to this structure its

characteristic colour and luster. It has also been stated that it governs the normal and

abnormal temperature of the body.

'Charaka' has not described this Pitta as a separate entity but he has included the

functions attributed to it among those of Pitta in general. He has stated that the production of

normal and abnormal temperature of the body, as well as the normal and abnormal colour of

the skin due to Pitta 68.

Chakrapani, in his commentary on the above, has stated that the regulation or

otherwise of the body heat and variations in the colour of the body are the functions of

Bhrajakapitta which is located in the skin. Susruta 69, Bhela and Vagbhata have, on the other

hand, made separate and mention this Pitta, including the functions ascribed to it.

Bhrajakapitta, which is located in the skin is spoken of as Bhrajakagni, in as much as,

it enables the digestion (utilization) of substances used for "Abhyanga", "parisheka",

"avagaha", "lepana" etc. it irradiates the glow of one's natural complexion. Commenting on


29

above "dashana" observes by Twak is understood the bahya twak, known as avabhasini, by

Abhyanga etc. is meant the dravyas employed for the kriya (preparation) and karma (action)

etc.

"Bhela":

Bhrajaka Pitta is that which is responsible for the manifestation of the specific

characteristic of body, it emphasises its importance, creates different prabhas (hues) of the

head, hands, feet, sides back, abdomen, thighs, face, nails, eyes and hair. It also brightens

them.

"Vagbhata" observes:

Bhrajaka is located in the skin. It is so called because it imparts lustre to the skin and

makes it radiate. Commenting on the above 70,

"Arunadutta" observes:

It is known as Bhrajaka because it performs dipana and pachana of (substances used

for) abhyanga, lepa, parisheka etc.

It will be seen from the citations above that,

Bhrajaka belongs to a larger species of substances described in Ayurveda as Pitta.

It is located in the bahya twak, in its layer known as avabhasini (Dalhana)

Its functions are state to be

The production of normal and abnormal heat of the body (Charaka)

The production of normal and abnormal colour of the skin, as whole , and parts

and structures of the body viz. Hands, feet, sides, back etc., (Bhela)

The absorption and digestion of substances used together with oils, decoctions

used for sprinkling over the body etc.(Dalhana & Arunadutta)


30

It may be stated, in general, that Bhrajaka Pitta may represent the factor or factors present in

the body, which is or are responsible for the colour of the skin and other structures.

Rakta and skin colour:

The color and the functioning of the sparshanendriya depend on the quality of Rakta

Dhatu 71. Further this can be substantiated by the reference that the skin of the Raktasara

person possesses good kanti.

Relation with Dosha:

Vagbhata and Susruta have stated that the seat of Vata is Twak. While describing the

function of Pranavata Vagbhata states it as ‘indriya chitta drik’, that is to say, it keeps all the

indriyas alert and helps them to perform their functions normally. The color of the Twak is

dependent on the functioning of Udanavata. In classics it has been stated that the Udanavata

which is situated mainly in urah stana while circulating in its own channels does the

functions like vakpravrutti, bala, smruti and varnakara 72.

Vyanavata helps in the expulsion of sweda from antahmarga to bahya. The same

Vyanavata helps for the absorption of snehadi dravys that are applied externally.73

Like Vata Twak also is the seat of Pitta. The Pitta, which is located in the skin,

designated as bhrajakagni is responsible for the digestion and absorption of the substances

used for abhyanga, parisheka, avagaha, lepana etc. It is responsible for the glow of one’s

complexion in the normal state. This Bhrajakapitta located in the Twak manifests the color in

Avabhasini layer 74.

Relation with Dhatu:

Twak is considered as the upadhatu of Mamsa Dhatu 75. Twak is nourished by Rasa

Dhatu. The nutrition to it is supplied by innumerable rasavahinis. If there is any vikruti in the


31

Rasa Dhatu, it certainly affects the Twak as the preceding is being nourished by it. Further in

rasasara person it has been mentioned that their Twak will be snigdha, shlakshna etc. By

these references the saying that the Twak is nourished by Rasa can be confirmed 76.

Relation with Mala:

Twak expels Kleda i.e. vidhruti 77 Sweda is an eliminative material from sweda vaha

Srotas which is a mala of medo Dhatu.

Pigmentation of the Skin according to contemporary medical science 78:

Color of the human skin is derived from a variety of chemical and physical properties

associated with the skin structure. Normal skin color is dependent on hemoglobin, both in

oxygenated and reduced state, carotinoids and melanin pigment. Five pigments are known to

influence the skin color. They are -

1. Melanin, is a pigment found more in stratum malpighi. Melanin contributes

color and quality to the skin and protects the organism (human) from the

ultraviolet rays. It is in the form of granules, which vary from light brown to

black in color. Melanin is formed from the amino acid tyrosine by the action

of the enzyme tyrosinase and copper protein complex. Hence it is clear that

copper ions are essential for normal pigmentation of the skin.

2. ‘Melanoid’ is supposed to be a degradation product of melanin and is diffused

through out the epidermis. Melanoid has a different absorption band of visible

light.

3. ‘Carotene’ is yellow orange pigment present in lipid rich areas like stratum

corneum, subcutaneous fat etc. This adds yellow color to the skin of women

that men.


32

4. ‘Oxy hemoglobin’ imparts reddish hue to the skin color and it is evident in

areas where there is rich arterial supply like face, neck, palm, soles and

nipples.

5. ‘Reduced hemoglobin’ contributes bluish or purple character to skin color and

is more evident in lower areas of the trunk.

Two types of melanin pigmentation occur in man. The first ‘constructive’ skin color,

that is the amount of melanin pigmentation, which is genetically determined in the absence of

sun exposure and other influences. The other ‘facultative’ or inducible skin color or ‘tan’

which results from sun exposure.

Variation in the thickness of the skin may modify the skin color. Subjects with thin

epidermis have a ruddier color complexion and with a thicker epidermis look yellower.

Thicker epidermis is less transparent than the thin one. As the transparent stratum corneum

scatters light slightly, the deeper layer appears blue.

The skin remains light when the pigment is appeared in the center of the

melanophores and dark when it is dispersed to their periphery.

Three different mechanisms may be involved in the control of color change. Firstly,

the pigment cell may act as an independent effect or respond directly to the stimulus of light.

There is evidence that this can occur in some fish and amphibians and the tanning of human

skin both immediate and delayed can be considered as analogous process. Secondly, the

movement of pigment with the melanophore may be under the nervous control. Thirdly, the

activity of pigment cells or melanocytes may be under hormonal influence. Pituitary

hormone causes expansion of melanophores or promotes the formation of melanin in

epidermal melanocytes. Diagrammatically it is expressed as -


33

tyrocinase Dopa oxydase

Tyrosine ------------------------ DOPA -------------------------- melanin

+ Copper

Reduced melanin ---------------------------------------- Oxidised melanin

Structure of Melanocytes 79:

Melanocytes form a network of dendritic cells in the basal layer of epidermis. They

are also found in the external hair root sheaths and in the bulbs of the hair follicles. It is these

secretory melanocytes which behave as unicellular glands producing melanosomes which are

transferred to the surrounding epidermal keratinocytes, a cytocrine activity.

The transfer of melanocytes involves the insertion of a tip of the dendrite of the

melanocyte that becomes embedded in the cytoplasm of the keratinocyte. The end becomes

pinched off and a package of melanosomes is transferred to the keratinocyte that acts as a

phagocyte. The melanosomes are packaged according to size, the larger ones as single units,

and the smaller ones as complexes of two or more.

Melanocytes are distinguishable from the karatinocytes by the lack of desmosomes

and tonofibrils and by a more lucent cytoplasm. The characteristic feature of the cell is the

presence of special cytoplasmic organelles, the melanosomes on which melanin is formed by

the action of the enzyme tyrocinase. The developing melanosomes show varying degree of

electron density, the more fully melanized being very dense.


34

Figure – 2

Structure of Melanocyte

F

Ka

our stages of melanosomal antagony are recognized.

• Stage one is a membrane bounded spherical vesicle may show tyrocinase

activity. According to classical theory, tyrocinase is produced on

membrane bound ribosome and transferred via the endoplasmic reticulam

to the golgi where it accumulates in vesicles that are derived from the

golgi.

• In Stage two melanosomes are oval in shape and show numerous melano

filaments with and without cross-linking.

• In stage three the internal structure of the melanosomes is partially

obscured by the deposition of melanin.

• In Stage four, the mature melanosome appear electron dense.

kodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –Literary Review 35

Panchalakshana Nidana

A) Nidana of Switra

Nidana plays an important role in the manifestation of a disease. In classics Nidana is

defined as the factors which lead to the disease by deranging the equilibrium of the doshas in

the body 80. The knowledge of Nidana is essential for the understanding of Samprapti and to

determine the sadhyasadhyata and Chikitsa. In Ayurveda, Nidana have been given utmost

importance because the first line of treatment is Nidana parivarjana.

Coming to the subject proper, i.e., dealing with the aetiological factors of Switra let

us proceed to their study according to the different classical texts. Etiological factors for

Switra are described only by Charaka. It has been regarded as a type of Kushta in Susruta

Samhita 81. Further Vagbhata also states that the etiological factors, which are held

responsible for the causation of Kushta, hold good for Switra also.

Hence it is better to know the etiological factors of Kushta initially under samanya

Nidana before going to the specific etiological factors of Switra. They are discussed under

the headings of 1) Ahara, 2) Vihara and 3) Achara

1) Ahara Hetu :

Ayurveda offers more importance to Ahara, as samyak yojita ahara leads to indriya

prasadana and varna prasada. But asamyak yojita ahara may lead to several diseases.

Hence Twagindriya is also influenced by aharaja Nidana 82.

I) Viruddhahara: It is considered as major nidana for Kushta. Commentator Dalhana

mentions that viruddhahara is the vyadhi hetu for Kushta 83. Charaka opines that the


36

consumption of viruddhahara continuously causes nindita Vyadhi 84. Vagbhata has

compared Viruddha Ahara with Visha and has also given the symptoms occurring due

to Viruddha Ahara in the body. According to Vagbhata Viruddha Ahara can

sometimes become fatal just like the poison & in some case it may become Gara

Visha in long run 85. The different factors related to Viruddha Ahara may be

summarized in two major groups viz. 1) Gunatah Viruddha and 2) Samyoga

Viruddha. The tabular forms of Ahara Nidana told by different authors are as follows.

Table 5 Classification of Viruddha Ahara by different authors

Viruddha Ahara CS SS AS AH BS HS MN BP

(A)Gunatah Viruddha

Intake of Mulaka, Lashuna etc. with milk

+ - - - - - - -

Gramya,Anupa,

Audaka, Mamsa with milk

+ + - - - - - -

Intake of Chilchim fish with milk + - - - - - - -

Milk with Nimb - - - - - - - -

(B) Samyoga Viruddha

- Intake of food mostly containing Hayanka, Yavaka, Chinaka, Uddalaka along with Ksheer , Dadhi, Takra, Kola, Kulattha, Masha, Atasi, Kusumbha, Sneha

+ - - - - - - -

Pippali, Kakamachi, Lakucha with Dadhi and Ghee

- - - - + - - -

Mulaka with Guda - - - - + - - -

Excessive Alcohol and green vegetables with milk.

- - - - + - - -

Articles having sour taste or meat of deer with milk

- - - - - - - -

Honey and meat after taking hot diet and vice versa

- - - - + - - -

Use of fish, Nimba and milk together.

- - - - + - - -


37

II) Mithya Ahara:

Mithya Ahara means improper diet. According to Vijayrakshita, the diet

opposite to ‘Ashta Ahara Vidhi Visheshayatanani’ is designated as ‘Mithya Ahara’.

Charaka has described eight factors determining the quality of food they are called as

‘Aharvidhi Visheshayatanani’. They are Prakruti, Karan, Samyoga, Rashi, Desha,

Kala, Upyoga Samstha and Upayokta 86.

Table: 6 Mithya Ahara Hetu for Kushtha

Mithya Ahara CS

SS

AS

AH

BS

HS

MN

BP

Adhyashana + + - - - + + +

Vishamashana + + - - - - - -

Atyashana + + - - - - - -

Asatmya Ahara - + - - - - - -

Intake of food during indigestion + + - - - - + +

Continuous and excessive use of Madhu, Phanita, Matshya, Lakucha, Mulaka, Kaakmachi and intake of above substances while having Ajirna

+ - - - - - - -

Excessive Snehana + - - - - - - -

Vidahi Ahara without emesis of undigested food

+ - - - + + - -

Dravyataha

Excessive intake of Gramya, Anupa, Audaka Mamsa

- - - + - - -

Navanna, Dadhi, Masa, Matshya, Mulaka, Tila, Pishtanna,Kshira, Guda,

+ - - - - - + +

Dushivisha - + - - - - - -

Polluted water - - - - - + - -

Gunatah

Excessive Drava, Snigdha Ahara + - - - - + + +

Guru Ahara + + - - - - + +

Rasatah

Excessive Amla & Lavana Rasa + - - - - - + +


38

These eight factors give rise to beneficial or harmful effects. Habitual intake of things in

proper way may more useful but in improper way they are always harmful. So they should be

avoided. Types of Mithya Ahara which are known to be responsible in the manifestation of

Switra are illustrated in the above Table.

2) Vihara Hetu :

All kinds of activities done physically, vocally or mentally are considered as Vihara.

Mithya Vihara means improper activities. The activities opposite to ‘Svasthavrita’ is the

‘Mithya Vihara’. The Mithya Vihara is the chief causative factor of many diseases but it has

been considered as main cause for the Kushtha. The factors related to Mithya Vihara by

various Acharyas have been tabulated in table 7.

Table 7 Mithya Vihara Hetu for Kushtha

Mithya Vihara CS SS AS AH BS HS MN BP

Shitoshna Vyatyasa Sevana and Anupurvya

Sevana

+ - - - + - - +

Use of Santarpana and Apatarpana diet

without sequence

+ - - - - - - +

Sudden diving in cold water or drinking

cold water after fear, exhaustion & coming

from sunlight

+ + - - - - + +

Practice of physical exercise & sunbath

after heavy meals.

+ - - - - - + +

Mithya Samsarga - - - - + - - -

Sex indulgence in Ajirna + - - - + - + +

Suppression of Chhardi, Mutra, Purisha

like Vegas

+ + - - + - + +

Kupathya in Panchakarma + + - - - - + -

Divasvapna after lunch + - - - + - - -


39

3) Achara Hetu :

Those diseases, in which no clinical improvement is obtained even after the best

treatment, are considered as Papa Karmaja Vyadhi. Both Charaka 87 and Susruta 88 have

described a Kushta as Papa Karma Vyadhi. Achara hetu by various authors have been

tabulated in table 8.

Table 8

Achara Hetu for Kushtha

Achara Hetu CS SS AS AH BS HS MN BP

Papa Karma + + + + + + + +

Vipra Guru Tiraskara + - - - - - + -

Sadhu Ninda - - + + - - - -

Use of money & material acquired by

unfair means

- - + + - - - -

Killing the virtuous persons. - - + + - - - -

Vishishta Nidana of Switra

Bhaluki considers Switra as Sahaja vyadhi. Specific causative factors for Switra are

mentioned only in Charaka Samhita. Acharya Charaka stresses more on papakarma,

kritaghnabhava, guru gharshana, poorvakrita karma and viruddha Ahara 89.

Viruddha ahara or incompatible diet is mentioned as the prime cause of Kushta in

general and Switra roga in particular. Charaka has described 18 types of incompatible diets.

On consuming such foods a person is susceptible for nindita vyadhi. Chakrapani commenting

on nindita vyadhi considers Kushta and Switra both as nindita vyadhis 90. This vitiates pitta

pradhana tridoshas, which in turn cause rakta dushti and causes Kushta and Switra. Also


40

Charaka mentions Switra as one of the viruddhahara janya Vyadhi 91. Acharya Sushruta is of

the opinion that the viruddha bhojana causes indriya dourbalya, which can be considered as

incompatibility of indriya and its adhishtana 92.

One of the veerya viruddha foods explained as nidana for Kushta is Matsya with

payasa. Bhadrakapya opines that especially Chilachima variety of fish with milk vitiates the

tridosha and cause shonita diseases 93. Vrana is mentioned as one of the causative factor for

Switra. It is also told that mithyopachara of vrana causes Switra 94.

Para samskara, which is interpreted as para samsparshadi means coming into contact

with an affected person of Switra through touch and other intimacies is also a cause for

Switra 95. If ‘Douhrida apachara’ is done during the state of pregnancy, i.e., intake of

excessive kaphakara ahara, then the Switra is said to appear in the baby as a complication 96.

When Jaloukavacharana is done by poisonous jalouka, Switra occurs at the site of the bite.

This is a special contribution by Astanga Sangraha 97.

2) Switra Samprapti

Samprapti is essential for the proper knowledge of a disease entity. This factor is

having more importance than the others as this is a process involving all the other four

factors in producing the disease in particular. This process begins from the time of

consumption of nidanas till the end stage of the disease 98. The reason for this factor to gain

importance is that the treatment procedure is mainly targeted on the Samprapti vighatana.

The initiation of pathogenesis occurs only after consuming the etiological factors. Thus after

considering the nidanas primarily it is necessary to give a detail description on the

pathogenesis.


41

The Samprapti of Switra is not mentioned separately in the classics. Vagbhata

considers both Kushta and Switra are having same causative factors and treatment 99 and

even Susruta 100 opines that the Switra is a type of Kushta, it can be said that the Samprapti of

Kushta holds good for both.

A foresaid Nidana cause vitiation of the Pitta pradhana tridoshas and also cause

Agnimandya. Then the same doshas move in tiryakgata siras and lodged in tamra layer of

twacha and cause sanga or obstruction to the local rasavaha and raktavaha srotas. The reason

behind dosha-dushya sammurchana in tamra layer of twacha is due to the presence of

khavaigunya in the respective areas of twacha. This leads to the Kshaya of local

Bhrajakapitta and causes Twak shwetata.

Further the Samprapti continues and the deeper dhatus like mamsa and medas are also

involved. The involvement of each Dhatu exhibits specific discoloration on the lesion.

Doshas settled in Rakta Dhatu produces Rakta varna, Mamsa dhatu produses Tamra varna

and Shweta varna when settled in medo Dhatu 101.

Though all the three doshas are involved mainly vitiated Udanavata and Bhrajakapitta

are held responsible because these two maintain the color of Twak. The functioning of

Vyanavata can not be neglected as it is the main motivating force behind the movement of

dushta Dosha along with Rasa.

Samprapti Ghataka of Switra:

Dosha – Pitta pradhana tridosha

Dushya – Rasa, Rakta, mamas, Medas

Agni – Jataragni

Ama – Jataragni mandya janya


42

Udbhava Sthana – Amapakvashaya

Sanchara Sthana – Tiryakgata siras

Srotas – Rasavaha, Raktavaha / Mamsavaha / Medovaha (sthanika)

Srotodushti prakara – Sanga

Adhishtana – Tamra layer of Twak

Vyakta Sthana – Twak

Rogamarga – Bahya

Vyadhi Swabhava - Chirakari.

Figure – 3

Schematic Representation of Samprapti

Abhyantara Nidana Sevana Vrana janya Vitiation of doshas Agnimandya

Formation of Ama

Dushta dosha sanchara in tiryakgata siras

Srotosanga

Sthanika Bhrajakapitta kshaya

Sweta Twak


43

3) Poorvaroopa

Poorvaroopa are the premonitory symptoms that occur before the actual disease

manifestation 102. The knowledge of premonitory symptom is essential in assessing the

prognosis of the disease, in differential diagnosis and in the treatment. Also they provide a

clue to the ensuing disease. In classics there is no reference regarding separate poorvaroopa

of Switra. Considering the Acharya Vagbhata’s statement ‘Kushtaika sambhavam Switram’

poorvaroopa of Kushta can be considered for Switra also. Poorvaroopa explained in the

classics are as shown in the Table.

Table – 9 Poorvaroopa according to different authors

Sl No Poorvaroopa CS 103 SS 104 AS 105

1 2 3 4 5 6 7 8 9 10 11

12 13 14 15 16 17 18 19 20 21 22 23 24 25

Aswedana Atiswedana Kandu Lomaharsha Suptata Atishlakshnata Kharatwa Kotha Nistoda Paridaha Pakwa,dagdha,dashta,bhagna,kshatopaskalita ativedana Shrama Vaivarnya vrananam dushtirasamrohanam Pariharsha Parushya Visarpa gamana Gourava Kayachidreshu upadeha Klama Kshudravraneshu dushti Shwayathu Ushmayana Asrija krishnata Rookshata

+ + + + + + + + + + + + + + + + + + + + + + + _ _

+ + + + + _ _ _ _ _ _ _ _ _ + + + _ _ _ _ _ _ + _

+ + + + + + + + + + + + + + _ _ _ _ _ _ _ _ _ _ +


44

4) Lakshana (Roopam) of Switra

It is the stage of a disease where the signs and symptoms of a manifested disease

exposed clearly. In Switra the general symptom is the appearance of swetha varna mandalas

that is depigmented patches or macules. The lakshanas mentioned in various texts, according

to Dosha involved.

Table -10

Depicting lakshana according to Dosha

Text Dosha Lakshana

Vata Mandala, aruna, parusa, paridwamsi

Pitta Padmapatra varna, daha

S.S

Kapha Swetha, snigdha, bahala, kandu

A.S Vata Rooksha, aruna

A.H B.P Pitta Tamravarna, daha, romadwamsi

M.N Kapha Swetha, ghana, guru, kandu

(S.S - Sushruta samhita, A.H - Ashtaga hridaya, A.S - Astanga sangraha,

B.P- Bhava prakasha, M.N - Madhava nidana)

Charaka does not differentiate the particular Dosha lodged in each Dhatu, even

though variability in degree of vitiation is mentioned. In Hareeta Samhita rupa of Switra

explained according to Sadhaya and Asadhya bhedas of Switra. Lakshana mentioned based

on the Dhatus in which Dosha are lodged 106.

Rakta dhatu - rakta varna

Mamsa dhatu - tamra varna

Medo dhatu - sweta varna


45

Asadhya lakshana - Eeshad rakta panduta, sarvanga chira, snigdha.

Sadhya lakshana - peetachavi, pandu, ruksha

Table - 11

Clinical features according to various texts

S.No Lakshana C.S S.S A.H B.P M.N H.S

1 Sweta varna + + + + + +

2 Rakta varna + + + + + +

3 Tamra varna + + + + + -

4 Rookshata - + + + + +

5 Parusha - + - - - -

6 Daha - + + + + -

7 Kandu - + + + + -

8 Romadwamsi - + + + + -

9 Ghanam - + + + + -

10 Bahalam - + - - - -

(C.S - Charaka Samhita, S.S - Susrutha Samhita,A.H - Ashtanga Hridaya

B.P - Bhava Prakasha, M.N - Madhava Nidana, H.S - Harita Samhita)

Classification of Switra

Vitiligo is an organ specific autoimmune disease of the skin characterized by the

development of well-circumscribed white macules associated with local melanocyte loss 107.

Most of the authors in Ayurveda mentioned the Switra varieties as three only. All the

authors of Brihatrayee and Laghutrayee mentioned three types of Switra. But according to

Kasyapa it is of five types. Bhoja described two types, doshaja and vranaja.


46

Classification by Charaka is based on the colour that in turn is depending on the

Dhatugata – Dosha 108. Charaka opines that daruna, Aruna and Switra are the synonyms of

Switra and also are three types it self, tri-discordance in origin.

Table – 12

Colouration of skin as Dosha dislodged in Dhatu

When Dosha dislodged in Rakta Rakta varna Daaruna

When Dosha dislodged in Rakta

Mamsa

Tamra varna Aruna

When Dosha dislodged in Rakta

Medas

Sweta Switra

Vagbhata classified the Switra with direct relation of Doshas with Dhatu 109. Susruta

110 followed the classification of Charaka with Tridosha predominance. Bhoja 111 describes

as Dohsaja and vranaja groups of classification, in which Doshaja has been further classified

into Atmaja - vitiation of the Vatadi Dosha as a result of the indulgences of the person

himself and paraja - by the contact with others in whom the entity already exists. Varanaja

refers to the discoloration that is introduced in to the normal skin as a result of a scar tissue

due to the healing of a wound or as a result of burns - cicatrix.

Since long time researching several medicinal plants and their active principles I

picked-up those that could help in the toxins elimination, but also those that could achieve

balance in the function of organs that are responsible for metabolism and excretion of these

toxins.


47

Table – 13

Switra bhedas - various authors

S.no Text Verities Names

1 Charaka Samhita 3 Daruna Aruna Switra

2 Susruta Samhita 3 Vataja Pittaja Kaphaja

3 Astanga Hridaya 3 Vataja Pittaja Kaphaja

4 Harita Samhita 2 Sadhya Asadya

5 Kashyapa Samhita 5

6 Madhava Nidana 2 Doshaja Vranaja

7 Bhava Prakasha 3 Vataja Pittaja Kaphaja

8 Sarngadhara

Samhita

3 Vataja Pittaja Kaphaja

Switra according to Bhoja

Doshaja Vranaja

Paraja Atmaja


48

5) Vyavachedaka Nidana of Switra

Though the Nidana are same for the disease Switra and Kushta 112, the lakshanas

differ, and hence they are given in a tabular form.

Table – 14

Switra and Kushta lakshana sadharmya and vaidharmyata

Switra Kushta

1 Usually one dosha predominates All the three doshas are involved

2 Only three dhatus(rakta,mamsa,and

medo)are affected

All the dhatus may affected

3 Confines to the skin only (tamra-4th layer) Confines to the fifth layer of the

skin(vedhini)

4 It is of krimirahita Krimisahitam (may be)

5 It is non-infectious and non-contagious It is contagious on prolong contact

6 No destruction of dhatus occurs Destruction of dhatus may occurs

7 No loss of sensation in the lesion There may be loss of sensation in

8 No secretion occurs Often secretion is present

9 It is non-hereditary Found occasionally hereditary

SADYASADYATA

The disease Switra is told as krichrasadhya roga in most of the texts and as asadhya in

only the text "Kashyapa Samhita". The krichratva becomes more and more in Raktagata,

Mamsagata and medogata respectively 113.

In early stages, where the hairs on the patches are not extensive and not turned into

white colour. Not compound and not caused by burns are told as 'sadhya'. Patches opposite

to these conditions and which are appeared in genital area, palms, soles and lips, even if they

are not short duration or of long duration are mentioned as "Asadhya".


49

Vitiligo Modern view

There are several diseases marked by a lack of pigment in the skin that are grossly

referred to as leukoderma; some are caused by an inability of melancocytes to produce

melanin, while others are caused by melanocytes either not being present or being destroyed.

The latter are the pathology of the disease Vitiligo.

Vitiligo is a progressive disease in which the melanocytes are gradually destroyed

causing depigmentation of the skin. The exact etiology of Vitiligo is unknown, but four main

theories exist to explain it. These are -

1). autoimmune hypothesis,

2). neural hypothesis,

3). self-destruct hypothesis, and

4). growth factor defect hypothesis.

It is believed that Vitiligo is a polygenic trait and that a convergence theory,

combining elements of different theories across a spectrum of expression is the most accurate

aetiology.

Autoimmune Theory:

There is great anecdotal evidence that an autoimmune disorder causes the destruction

of melanocytes, and this theory is now generally accepted as the common cause of Vitiligo. It

is known Vitiligo appears in conjunction with several other autoimmune disorders, such as

juvenile diabetes mellitus, Addison's disease, and pernicious anemia, and additionally organ-

specific antibodies can often be seen in patients with Vitiligo. If the immune system raises


50

antibodies or cytotoxic T cells to damage melanocytes, the mode of action the cells take

against the melanocytes could be apoptosis induction directly against melanocytes or Ig

induced complement-both are demonstrated in figure-4 114.

Proving this theory, there is histological evidence in Vitiligo patients that apoptosis is

occurring in the un-pigmented skin lesions: there is damage to the melanocytes and

keratinocytes in these areas, and the melanocytes exhibit nuclear shrinking, vacuolization,

loss of dendrites, and detachment. If antibodies do cause Vitiligo, some research suggests the

Ig’s may bind to tyrosinase related proteins 1 and 2, which are important for melanogenesis,

instead of Ig's targeting the melanocytes directly (Huang et al. 2002) responses.

Figure 4

Autoimmune theory of Vitiligo showing both cell-mediated and humoral autoimmune

.
Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –Literary Review 51

Neural Theory:

There is also evidence that peripheral nerve endings may secrete a substance that is

cytotoxic to melanocytes and causes their destruction. This is supported by the segmental

variety of Vitiligo, which occurs in specific dermatomes, indicating the skin is possibly only

being affected by the nerves of that specific dermatome. Additionally, Vitiligo appears with

certain neurological disorders such as encephalitis, and trauma that causes peripheral nerve

damage. Nerve endings in depigmented areas were seen to produce abnormal neuropeptides

and nerve growth factors, and displayed axonal degeneration-these abnormal chemicals may

be toxic to melanocytes. Additionally, depigmented areas showed some abnormal autonomic

function, such as increased adrenergic tone, increased norepinephrine, and an increased

concentration of catecholamines. These data then suggest that neurotransmitter release could,

directly or indirectly, have an affect on melanocyte destruction and depigmentation.

Self-Destruct Theory:

It is known that some of the intracellular pre-melanogenesis metabolites are toxic to

melanocytes, such as dopa and dopachrome. Normally melanocytes possess cellular

measures to counteract these toxic substances, but it is believed that cells may lose the ability

to counteract these toxic metabolites and are destroyed by leakage of metabolites into the

cytoplasm and eventually cell lyses. There is evidence that points to this in that certain

hydroquinone derivatives that are similar to these intra-cellular metabolites causeVitiligo

experimentally.

Growth Factor Defect Hypothesis:

A study in the 1980's found that melanocytes in lesions from Vitiligo patients

contained melanocytes, but that these cells exhibited "defective growth and passage


52

capacities." The researchers then noted that the growth defects of the melanocytes were

partially corrected by adding a growth factor to their culture, additionally suggesting that

growth defects may be part of the pathology of Vitiligo. In depigmented areas, cellular

analysis showed that there were melanocytes but that they grew poorly. These data suggest

that, whether a primary or secondary cause, growth defects appear to play a role in

leukoderma and Vitiligo 115.

Genetic Influences:

A positive family history has been reported in about 20% of patients and it has been

found in monozygotic twins. Studies have shown that Vitiligo does not progress via a simple

Mendelian pattern, but more likely is coded polygenically and can be expressed across a

spectrum. There has been some evidence both proving and disproving the involvement of the

HLA system in the occurrence of Vitiligo. So, it is believed that genetic factors probably play

a key role in the pathogenesis of Vitiligo, but the exact cause is unknown.

Convergence Theory:

Following genetic studies, researchers have begun to lean towards a multi-faceted

etiology for Vitiligo that combines components of the aforementioned theories and genetics.

This theory states that genetic influences have a role in causing Vitiligo in addition to other

elements, such as stress, accumulation of toxic compounds, infection, autoimmunity,

mutations, and impaired melanocyte proliferation.

Other Causative Factors:

1) Nutritional deficiency

• . The diet poor in Proteins particularly the essential amino acid L-

phenylalanine can contribute to the causation of Vitiligo.


53

• Deficiency of B- complex factors especially Thiamine, Riboflavin,

Pyridoxine, Pantothenic acid, Folic acid and Biotin is usually related with

Vitiligo.

2).Achlorhydria

There are stray reports that indicating stomach malfunction, with partial or

complete lack of hydrochloric acid and pepsin production to be cause Vitiligo.

3) Amoebiosis

Amoebiosis and intestinal parasites are said to be responsible for Vitiligo by

interfering with the absorption of nutrients and by producing toxin.

4) Endocrinal cause

• Amongst endocrinal factors, anterior pituitary is possibly the most important.

Intermediate lobe of pituitary secretes melanocyte-stimulating hormone.

(M.S.H.) stimulates melanin formation and melanin dispersal.

• ACTH and MSH have some structural similarity and slight functional

overlapping.

Figure – 5 - Showing pituitary – MSH – Melanocytes axis

Anterior Pituitary

Pancreas Thyroid MSH Adrenal Gonads Para Cortex Thyroids

Melanocytes


54

• Oestrogen increases melanin synthesis and the quantity of free melanin.

Progesterone is supposed to potentate pigmentary action of Oestrogen.

5) Trauma

Many Vitiligo patients develop color loss at local sites of skin-damaging

injury or trauma.

6) Drugs and chemicals

Drugs and chemicals, like quinines, qunofuracin, amylphenol, chlothizide,

broad-spectrum anbiotics, and chlroquin may initiate vitiligo.

7) Miscellaneous factors

Constant rubber friction, pressure, and trauma tight clothing can precipitate

the lesions of Vitiligo.

These various factors are enumerated and discussed in order of their sequence

in the pathogenesis are as follows.

a. Deficiency of MSH

b. Other hormonal factors

c. Heredity d. Copper deficiency

Figure – 6 Causes of Tyrosinase Tyrosine DOPA melanin

a. Nutritional deficiency b. B – Complex deficiencyc. Amoebiasis d. Liver function

deficiency

Neural concept melatonin

Tyrosinase Tyrosine DOPA

melanin

Self destruction of melanocytes

♦ Rubber friction ♦ Chemicals

Autoimmune


55

Table – 15

Causes of localized hypo pigmentation

Disorders Distinguishing features Vitiligo Destruction of melanocytes, common, acquired, multiple sharply

defined non-pigmented patches anywhere. Pityrias isverscicolor Superficial fungus infection leading to disturbance in pigment

production, common, multiple pale scaling patches on trunk. Pityriasisalba Mild patchy eczema of the face in children causing a disturbance in

pigment reductions. Leprosy One or several paler macules on trunk or limbs that are hypoaesthetic. Albinism Congenital stationary disorder, distribution may complete or partial.

Hairs and eyes may be affected. White macules of tuberous sclerosis

Uncommon development of anomaly affecting CNS connective tissue and skin, several maple leaf shaped hypo pigmented macules.

Post inflammatory After inflammatory skin disease (often eczema) or trauma to the skin, irregular in shape and in depth of pallor.

Naevus anaemicus Rare developmental solitary white patch usually on trunk thought to have a vascular basis.

Chemical toxicity May took very like Vitiligo, seen in workers in the rubber industry exposed to paratertiary benzyltoluene.

PATHOLOGY:

a) A defect in enzyme tyrosinase is held responsible for Vitiligo. According to some,

"melatonin" a substance secreted at nerve endings inhibits tyrosinase, thus interfering

in pigment formation.

b) The Vitiligo appears to be due to an immunological attack on the melanocytes. This

would suggest that Vitiligo is an autoimmune disorder.

Clinical forms of Vitiligo

a) Focal

b) Segmental

c) Acrofacial

d) Generalized


56

Common lesions seen on the body are -

a) scalp

b) retro-auricular folds

c) upper eye lids

d) lips

e) finger tips, palms

f) nipple

g) waist

h) scrotum, glands

i) legs

j) Toe tips and soles.

Often the depigmented patches are symmetrical, especially when the disorder is

distributed over the peripheral parts of the limbs and the face.

CLINICAL FEATURES: APPEARANCE

Completely depigmented macules and patches of varying sizes and shapes

characterize it. Besides loss of colours, there is no other structural change. The depigmented

areas are paling white or slightly pink and ill defined at the start of the disorder. In doubtful

cases, the pigmentation can be made to appear more distinct by pressing the patch with a

glass side. This pressure momentarily obliterates the blood supply and hence the

depigmentation stands out more prominently. In early doubtful cases examination under

"woods lamp" is also helpful.

Often the depigmented patches are symmetrical, especially when the disorder is

distributed over the peripheral parts of the limbs and the face.


57

The border: A rim of hyper pigmentation generally lines the border of the depigmented

patch. It looks as the pigment is removed from the patch and is thrown at the periphery.

Hair on the patch: Hair may or may not become depigmented in vitilliginous areas. Presence

of depigmented hairs (leucotrichia) or a patch is a strong point in favour of the diagnosis of

Vitiligo.

Distribution - lesions: Distribution of the lesions is determined by the supply and demand

behaviors of the pigment commodity. Whenever there is scarcity of any commodity two

diagonally opposite areas suffer most thus;

1) Peripherally situated, badly supplies areas, which are even normal at a critical

level of supply with little or no stored material, suffer commonly. Hence

mucocutaneous junctions. Finger tips, palms, soles and toe lips are commonly

involved in any extensive Vitiligo.

2) Areas where the consumption rate is normally very high suffer most in any

scarcity or pigment commodity. Pigmented like nipples, scrotal skin, scalp

(because of hair) and moles are also commonly involved in any extensive

Vitiligo.

Classification of Vitiligo:

Vitiligo has been divided into three stages

A) Localized Vitiligo:

1) Focal: One or more macules in one area, but not clearly in a segmental or

Zosteriform distribution.

2) Segmental: One or more macules involving a unilateral segment of the

body that is fault of the face, fault of the trunk, and extremity.


58

3) Mucosal: Vitiligo of the mouth and mucus membrane and the genital.

B) Generalized Vitiligo

1) Acrofacial : Distal parts of the extremities and face .

2) Vulgaris: Scattered macules.

3) Mixed : Accrofacial and Vulgaris or segmental and accrofacial and / or

Vulgaris

C) Universal Vitiligo

Complete or nearly complete depigmentation

Second Classification 116 considering the aspects of progression of disease, prognosis

and treatment.

a) Segmental (Unilateral)

b) Non-segmental. (Bilateral)

I) Focal

II) Mucosa

III) Accrofacial

IV) Vulagaris and

V) Universal

c) Mixed , Segmental and Non –Segmental


59

Table -16

Clinical criteria for classification of Vitiligo

Stages of Vitiligo Clinical feature

Active stage 1 New lesions developing

2 Lesions increasing in size

3 Border ill - defined

Quiscent stage 1 No new lesions developing

2 Lesion stationary in size

3 Border hyperpigmented and well defined

Improving stage 1 Lesions decreasing in size.

2 No new lesions developing

3 Border defined and signs of repigmentation

(follicular and peripheral)

Zosteriform Vitiligo 1 Unilateral distribution of lesions, preferably

along the course of nerves.

Clinical associations - Vitiligo:

1. Cutaneous

a) premature graying of hair

b) halo naevi

c) alopecia areata

2. Systemic

a) thyroid disorders

b) Diabetes mellitus.

c) Addisons disease

d) Pernicious anemia

e) Multi endocrinopathy syndrome

f) Oculo and auditory abnormalities


60

Differential diagnosis of Vitiligo

Causes for localized de pigmentation of skin: In many countries the fear of leprosy

makes differential diagnosis of a "white patch" an urgent and vitally important issue.

Examination of the skin in long wave UVR helps distinguish whether these is total de

pigmentation (as in Vitiligo) or not. It may also detect areas of depigmentation not easily

seen in ordinary daylight as well as detecting a lemon-yellow fluorescence seen in some

cases of pityriasis versicolor.

Zosteriform Vitiligo –

Lesions develop along the distribution of a peripheral nerve. Halo neavus (sutton's

nevus) - a related disorder in which the depigmentation begins around one or a few

compound naevi.

Occupational Vitiligo (Oliver):

It is seen on the dorsum of the hands of tannery workers caused by the use of rubber

gloves containing agerite Alba. Monobenzyl ether of hydroquinone (MBEH), The chemical

gets dissolved by sweat and acts on the melanocytes in such away as to interfere with the

formation of malanin. In early cases, depigmentation may disappear spontaneously.


61

Switra

Chikitsa The description and various treatments for Switra mentioned in almost all the

Ayurvedic texts along with kushtas. Same general principles of treatment for Kushta and

Switra are similar. But the number of special preparations only for Switra is available in

many texts.

Switra is more complicated disorder than all types of kushtas, which becomes

incurable within small period of duration. The Chikitsa is advised as soon as possible in this

disorder, which is compared with a - "Burning building" which needs a fast management.

Switra is a dosha-karmaja vyadhi. With this fact the treatment methods for switra can

be adopted under three headings - Daivavyapasraya, Yuktivyapasraya, and Satvavajaya

Chikitsa.

Daivavyapashraya Chikitsa

In Vagbhata along with other Chikitsa karmas daivavyapasraya Chikitsa (which

relieves the effect of papakarmas) mentioned for good prognosis. The mentioned

diavavyapasraya Chikitsa for Kushta and Switra are - practice of vrata-dana-yama,

tyagasheelata, friendship and mercy to all kinds of beings, worship of brahmins-devas-guru,

shiva and bhaskara aradhana etc, which cure the effect of papakarmas 117.

Satwavajaya Chikitsa:

Controlling of the manas from ahita indriyarthas i.e., from causative aharas and

viharas for Switra. It is also named as Nidana parivarjana, which also plays a key role in

Chikitsa.


62

Yuktivyapasraya Chikitsa 118

The person is made to undergo all types of shodhanas. Then once again is made to

drink malapurasa with guda to his capacity, which is preceded by oleation and then made to

expose to sunrays (suryapada santapam) as long as he can. This drink will have a purging

action. The procedure is repeated for three consecutive days.

The blisters so formed should be punctured with badara kantaka and the fluid allowed

oozing out completely. When undergoing this line of treatment he must be given to drink the

decoction prepared out of bark of malapu, asana, priyangu and satapushpa taken in equal

quantities, or palasa kshara along with phanita taken according to his capacity.

Whatever else non-curative of Kusta in general is beneficial if taken with

khadirodaka. Internal usage of only khadirodaka is like wise beneficial 119. The patient

should expose to sunrays and when a blister forms he advised to take food with takra

(nirlavana). Vagbhata also tells internal administration of gomutrarista 120.

Bahiparimarjana Chikitsa

There are so many topical lepas prescribed in various texts. Some of them are as

below -

1. manahsiladilepa - manahsila, vidanga, kasisa, rochana, kanakapushpi and

saindavam.

2. Kadalikshara+burnt bone of donkey in cow’s blood.

3. Nilotpala, Kusta and saindavam in elephant urine.

4. Mulaka beeja and bakuchi-paste.

5. Kakodumbara, bakuchi seeds and chitraka in cow’s urine.

6. Manahsila in peacock bile.


63

7. Udayadityarasa.

8. Putikaranjadilepa.

9. Bakuchi with one fourth of talaka in cow’s urine.

10. Bringaraja, haridra, doorva, ajaji, vidanga, tila, chitraka, harichandana in cows

urine.

11. Bakuchi, karanja, jyothishmati taila in equal quantities.

12. Bakuchi seeds, laksha, cow-bile, anjanadwaya, long piper and kalaloharajah.

Shastrapranidhana Chikitsa

In Vagbhata the raktamokshana is mentioned as a part in treatment of Switra. The

above mentioned shonitamokshana supports the Switra as Rakta dushti janyaroga 121.

Even though vamanarechanadi shodhanas, shonitamokshana, virukshana and intake

of saktu are done carefully, swithra can become sadhya only to those persons whose effect of

papakarmas are cured completely with vrata, dana, dharmadi karmas.

PATHYA & APATHYA IN SWITRA

As the Nidana factors mentioned it for both the Kushta and Switra in almost all

Ayurvedic texts. Hence the pathya apathyas for both disorders may appear similar (almost)

with each other 122.

Apathya in Kushta

a) Ahara : Atilavana - atiamla padartha sevana, dadhi, ksheera, guda, anupamamasa, tila,

masha, vasa, kulutha, nishpava, lkshu, pistavikara, virudha - adhayasana, ajeerna, vidaha

- abisyandahara etc.,

b) Vihara : Diwaswapna and vyavayam


64

Above mentioned dravyas and causative factors mentioned for Switra are said to be

apathyas in kishta as well as in Switra.

Pathyas in Kushta:

The following are indicated as usual ahara, achara - vibhaga for are who suffers from

Kusta.

♦ Ahara: Shashtika shali, koradushaka, uddalak, mudga, adaki, peya, tiktasaka, jangala

mamasa, saktu sevana, pachagavya sataa sevana.

♦ Ausadha: Avalguja, nimba, arushkara, aragwada, chakramarda, palasakshara, atarusha,

mandukaparni and khadira - their various preparations.

♦ Vihara: Vrata, dwija-sura-gurupuja, bhaskararadhana, ravivaravrata, dana dharma,

tyagasheelata, goseva and satyadharmata etc.

COURSE AND PROGNOSIS

Variable and some what unpredictable, may remain static, spread or re-pigment. But

usually the condition is gradually progressive, sometimes extending rapidly over a period of

several months and then remaining quiescent for many years. Spontaneous re-pigmentation is

noted in about 10-20% of patients. 1) Factors indicating good prognosis for regimentation

are: Recent onset < 6 months, in a young individual on the facial area. 2) Conversely factors

which indicate an unfavorable prognosis are: Late onset in life, long-standing persistent

lesions, located on the extremities and on the lips. 3) Re-pigmentation begins within the

affected area from the hair follicles where there may be residual melanocytes; or else they

occur from the normal pigmented skin immediately adjacent to the vitiliginous area. Once re-

pigmentation begins it tends to continue, albeit slowly and sometimes trivial.


65

Figure - 7

Drug Review

In the present study the drug for study choose is - Kakodumbaradi Ghanavati

internally and Ayorajadilepa externally possess the following proportions in it.

1) The combination and proportion of Kakodumbaradi Ghanavati is as follows.

S.No Drug & Botanical Name Proportion

1 KAKODUMBAR TWAK (Ficus hispida) 123 One part

2 VIDANGA (Emblia ribes) 124 One part

3 BAKUCHI BEEJA (Psoralia corylifolia) 125 One part

2) The combination and proportion of Ayorajadilepa is as follows

S.No Drug & Botanical Name Proportion

1 AYORAJA (Ferrum) 126 One part

2 KRISHNATILA (Sesamum indicum) 127 One part

3 RASANJANA (beriberi extract) 128 One part

4 BAKUCHI BEEJA (Psoralia corylifolia) One part

5 AMALAKI (Emblica officinalis) 129 One part

6 BHRINGARAJA (Eclipta alba) 130 One part


66

All the drugs are well identified and collected from local areas. Good manufacturing

practice will be followed for the preparation of Yogas. The Kakodumbaradi kwatha which is

mentioned in kwatha kalpana is taken in the form of Ghanavati because of its palatability

form. The individual drugs are discussed as under.


67

1) KAKODUMBAR TWAK (Ficus hispida) 131

Description

It is 5 meter tall tree grown all over India.

Useful part:

Bark, root bark, latex, Fruit

Chemical constituents

β-Sitosterol, Hispidin, Phenanthraindolizidine alkaloid, Bergapten, Psoralen.

A new norisoprenoid, ficustriol (1), and the known phenanthroindolizidine alkaloid

O-methyltylophorinidine (2), were isolated from a CHCl3 extract of the leaves and twigs of

Ficus hispida. O-Methyltylophorinidine showed potent cytotoxic activity when tested against

a small panel of human cancer cells, while ficustriol was inactive. The structure and

stereochemistry of 1 were determined using chemical and spectral methods 132.

Action and uses

Kapha Pitta hara, Sukrala, Grahi, Brumhana, Switra hara, Vrana hara, kamala hara,

Pandughna, Arshoghna and Atisara hara.

2) VIDANGA (Emblia ribes - Myrsinaceae) 133

Description

These climbing herbs are found in India, Central and lower Himalayas, Sri Lanka and

Singapore

Useful part

Berries (fruit), leaves, root bark


Embelin, Christembine, Homoembelin, Homorapanone, Vilangine, Quercitol, etc.


68

Action and uses

Vidanga is used to destroy parasites, intestinal peristalsis and flora, and for blood and

liver detoxification. This herb is pungent and has decongestant, carminative, anti-helminthes,

antibacterial, diuretic, stimulant, alterative, and anti-inflammatory properties 134.

Vidanga is one of the most effective treatments for expelling tape worms. It is used as

a laxative and is helpful in reducing flatulence. This herb can also be used to treat E. coli,

dyspepsia, piles, toothache, fungus, pneumonia, and sore throat. Vidanga can also be applied

to the chest area for lung diseases, and rubbed onto the head for headache relief, and it can be

used on children who are experiencing habitual constipation and acute capillary bronchitis.

When combined with ginger, it can be used topically for the treatment of ring worm and

internally for parasitic infections.

Alternative, anti-helminthes, carminative, stimulant, abdominal disorders

constipation, fungus, gas, indigestion, headache, heart disease, hemorrhoids, insanity,

lung disease, mouth ulcers, obesity, pneumonia, sore throat, toothache, worms. Decoction of

the roots given in insanity and heart diseases.

3) BAKUCHI BEEJA (Psoralia corylifolia - Papilionaceae) 135

Description:

This is an Ayurvedic herb. It is found in many parts of India.

Useful part:

Babchi Seeds,

Constituents

The chief active principle of the seeds is an essential oil; and a fixed oil, a resin, and

traces of a substance of alkaloidal nature. The seeds of psoralea coryfolia contains essential


69

oil (in pericarp to the extent of about 0.05 - 0.12%), a fixed oil, a resin, a volatile terpenoid

oil and two crystelline principles psoralen (c11 H6 o3)m.p 162 c. Iso - psoralen m.p 112c. A

crystelline substance called psorolidin (c16 H14 o4)m.p 315c has been isolated from the

pericarp. Psoralin and Iso-psoralen are oil soluble furocoumrins.

Actions and Uses:

This herb is so effective in the treatment of leprosy that it was given the name of

'Kushtanashini'. Seed powder is used to treat leprosy and leucoderma internally. It is also

applied in the form of paste or ointment externally. The unsaponified oil has been used with

success in case of leucoderma and psoriasis.

It was shown to improve the color of skin (including removing white spots), hair, and

nails. For instance, an ointment made by combining one part of an alcoholic extract of the

seeds with two parts of chaulmugra oil and two parts of lanoline has been found to be

effective in treating leucoderma, white leprosy, psoriasis, and other inflammatory skin

diseases and febrile conditions. The oil can be used either internally or as a simple ointment

externally. Gently rub the oil once or twice daily. The proportion of the active ingredients

may be increased if needed. Seeds are also used for scorpion sting, and snake-bite. Bakuchi is

Aromatic, anthelmintic, antibacterial, antifungal, diuretic, diaphoretic, laxative, stimulant,

and aphrodisiac 136.

4) AYORAJA (Ferrum)

Description

Ayoraja is fine powder of kantaloha and it is dark reddish brown in colour

Useful part

Powder of kantaloha


70


Fe3O4 (Magnatite)

Action and uses

Tridoshadhara, rasyana, keshya, and pandu hara pramehahara, gulmahara,

pleharogahara, yakrit rogahara, kandu hara, externally it is used for Alopecia areata 137

5) KRISHNATILA (Sesamum indicum - Pedaliaceae) 138

Description:

It is an annual herb growing up to 1 meter bering white or light pink couloured

flowers. It is mainly cultivated in the temperate regions of India.

Parts used

Seeds

Chemical composition:

It contains protein carbohydrate, minerals, phosphorous; oil contains 70p.c of liquid

fats consisting of the glycerides of oleic and linoleic acid Properties and used

Uses: It is having vatahara, Madhya, pain-relieving property (soola prasaman) Balya

Action and uses

It is a Vata hara, Twachya, Balya, Keshya, Sukralam. It is considered best in

Bahumootra and paste is used in Bhagandhara.

6) RASANJANA (Berberis Aristata (Daruharidra) extract) 139

Description

A genus of shrubs or small trees, distributed in the temperate and sub-tropical parts of

Asia, Europe and America. About 77 species are recorded from India. Commonly known as


71

BARBERRY (Vern.-Kashmal, kinjosa), several species are grown in gardens for their

ornamental leaves and bunches of succulent, acidic, edible barries. They are also planted in

hedges due to their straggling habit. The roots of these species are collected in fairly large

quantities in Chamba district of Himachal Pradesh and in Tehri-Garhwal of Uttar Pradesh

during Aug-Sept and are sold in drug markets of Chamba, Dehra Dun and Hardwar.

Daruharidra is yellowish brown, cylindrical, more or less knotty, hard and tough.

With the bark intact they are cut into pieces of varying length and a maximum diameter of 45

mm. The bark is internally dark brown and soft, breaking away into a powdery mass 140.

Part Used

Extract -

Chemical composition

The roots of Daruharidra were chemically analysed to afford a protoberberine

alkaloid named as karachine which was characterised 141 and the sructure was confirmed by

synthesis 142 taxilamine was also isolated 143.

The berberine content of 2.65% was observed in the dried powder samples analyzed.

The method can be used for the detection, monitoring, and quantification of berberine in B.

aristata 144.

The roots and stembark contain a number of alkaloids of which the chief active

alkaloid is berberine, its concentration being higher in plants growing at lower altitudes.

Berberine (C20H18O4N, m p 145°) forms yellow needles which are soluble in water but are

less soluble in alcohol 145.


72

Alkaloids of the isoquinoline type, Mainly berberine, Berbamine and derivatives,

Berberrubine, Bervulcine, Columbamine, Isotetrandrine, Jatrorrhizine, Magnoflorine,

Oxycanthine and Vulvracine o Miscellaneous, including Chelidonic acid, resin, tannin etc.

Actions and Uses:

Cholagogue, hepatic, anti-emetic, bitter, laxative Diuretic, Antibilious, Refrigerant,

Stomachic, Bitter tonic, Antiperiodic, Alterative, Antipyretic. Used for the treatment as an

Antibiotic, Immune Stimulant, for treating pinkeye, High blood pressure.

For bile and urinary conditions, Pitta detoxification, and congestion of abdomen and

pelvic, cavities; rheumatism, scarlet fever, brain disorders, heat, thirst, nausea; small

amounts- tonic; large doses-purgative; excellent herb for jaundice, during pregnancy, mild

laxative, periodic neuralgia, fevers, skin diseases, vomiting in pregnancy; fruit-mild

laxative/purgative for children, fevers, blood purifier, malaria, gastric and duodenal ulcers;

sores, jaundice, enlarged liver and spleen, and regulates liver functioning, diabetes, and

toxins/.Amla (with twice as much turmeric); destroys toxins, reduces body fat (with

turmeric); renal calculi, abdominal and pelvic congestion; G.I. stimulant, reduces blood

pressure.

7) AMALAKI (Emblica officinalis)

Description:

A small or medium-sized deciduous tree with smooth, greenish grey, exfoliating bark.

Leaves of smaller dimensions, distichous . Branches looking like pinnetely compound leaves.

Flowers greenish yellow in axillary fascicles, unisexual.

Fruits depressed globose, 1-3 cms in diameter, fleshy and obscurely 6-lobed, breaking

into three crustaceous cocci, each containing two trigonous seeds. The tree is common in the


73

mixed deciduous forests of India ascending to 1,500 meter on the hills. It is often cultivated

in gardens and homeyards. A type bearing comparatively larger fruits than the wild plant is

known in cultivation.

Parts used

Dried fuit, the nut or seed, leavesroot, bark and flowers. Ripe fruits used generally fresh

dry also used.

Chemical composition

Chemical investigation of the fruits of Amalaki afforded trigalloylglucose, terchebin,

corilagin and ellagic acid 146 preparation of salts of phyllembic acid and structural studies

were reported 147. Seed fat contained linoleic acid (64.8%) and closely resembled linseed oil

148 ellagic acid and lupeol were reported from roots 149. Fresh fruit pulp contains vitamin C

up to 720 mg./100 g. and press juice contains 921 mg./100 cc. The fruit is a rich source of

pectin 150. Proteolytic and lipolytic enzymes are present in the seeds 151.

Actions and uses –

Fresh fruit is refrigent diuteric and laxative. Green fruit is exceding acid. Fruit is also

carminative and stomachic. Dried fruit is sour and astringent. Flowers are colling and

apreient. Bark is astringent. Rasa all except lavana, kashyam dominates, setha veeryam,

mathura viprakam, tridosha haram, Rasayana, increases sukram. Raktapittam, prameham,

vata-raktam, giddiness, and vertigo. Extrnal use: in method disorders as a paste and tailum to

head. 'Tara-dravam'.

8) BHRINGARAJA (Eclipta alba)

Description:

This herb is found throughout India and the southwestern U.S.


74

Parts Used:

Herb, roots, leaves

Actions and uses:

Alterative, antipyretic, hemostatic, laxative, nervine, rejuvenative, tonic, vulnerary,

Roots and leaves are cholagogues, Root is tonic, alterative, emetic, purgative. Leaf juice is

hepatic tonic and deobstruent aging. The herb maintains and rejuvenates hair, teeth, bones,

memory, sight, and hearing. Cirrhosis, ear aches are relieved. Used as Hair tonic - oil

removes graying, balding, makes the hair darker. Make hair oil by boiling leaf juice in

coconut oil. This is useful to remove gray hair and balding. Remunerative for kidneys, and

liver. It improves complexion and useful in skin disorders.

sleep - oil promotes deep sleep.

Preparation of Kakodumbaradi Ghanavati

Ingredients of Kakodumbaradi 152 Ghanavati identified and collected are undertaken

for preparation by Sharangadhara mentioned Raskriya vidhi. Ghanavati was prepared at

Khajarekar pharmacy of Belagum for purpose of study.

Prescribed quantity of Bakuchi is taken and soaked in to gomootra for purification for

7 days. Everyday fresh gomootra is used. Then the Bakuchi is dried under the shade. Equal

quantity of Vidanga and Kakodumbara Twak were taken and physically purified for

unwanted materials. After words 240 liters of water were added and boiled on constant

regulated heat till it reduces to one forth. This padava shesita kashaya was filtered and

reheated to semisolid form on mild fire. Then 500mg vati is prepared and stored in glass

container.


75

Advantages of vati preparation

They are easy to carry and swallow and patient doesn’t experience unpleasant taste.

Vati do not require any measure cups and is convenient to preserve for long duration.

Preparation of Ayorajadilepa

Prescribed quantities of Bakuchi were taken and soaked into gomootra for 7 days for

purification. Everyday fresh gomootra is used. Prescribed quantity of Kantaloha were taken

and heated to red hot and dipped into Triphala kwatha for sodhana. This was repeated for

seven times then shodita loha made as fine powder. Later equal quantities of purified

Krishnatila, Rasanjana and Amalaki from physical impurities and made into fine powder.

All the above drugs were thoroughly added along with shodita Bakuchi and Kanta

loha and grind with Bhringaraja swarasa. As the paste grinded is soft and with out any hard

particles of additives, Chakrika were prepared and dried under sun shade. The Chakrikas

were kept in Sharawa samputa and subjected to lughu puta in Rasa shala. After cooling the

contents are subjected to Bhavana with Bhringaraja swarasa till it becomes as fine paste. The

paste made as a vatri (Sticks) of 5 mg each and dried under shade. Finally prepared medicine

is packed in tight glass jars and offered for trial patients.

POSOLOGY

Internal Kakodumbaradi Ghanavati

3 gms/day in three divided doses or 50 mg / kg body weight per day in 3 divided

doses

External application

Ayourajadi Lepa -- QS

Table - 17

Pharmacological properties of Kakodumbaradi Ghanavati

S.N Drug Name & Latin Name Rasa Guna Veerya Vipaka Doshaghnata Karma1 KAKODUMBAR TWAK

(Ficus hispida) Tikta

Kashaya Rooksha Laghu

Sheeta Katu Kapha Pittahara

Sthmbhaka, Vrana shodhaka, Kustaghna

2 VIDANGA (Emblia ribes)

Katu LaghuTeekshna

Ushna Katu Kapha Vatahara

Krimighna, Adhmana Vibandha hara

3 BAKUCHI BEEJA(Psoralia corylifolia)

Katu Tikta

Laghu Rooksha


Twachya, Kandughna, Krimighna, Switra hara

Table - 18

Pharmacological properties of Ayourajadi lepa

1 AYORAJA (Ferrum)

Tikta UshnaSnigdha

Sheeta - Tridoshahara Rasayana, Keshya,Twachya,

2 KRISHNATILA(Sesamum indicum)

Madhura Kashaya

Guru, Snigdha

Ushna Madhura Vatahara Twachya, Keshya

3 RASANJANA (beriberi extract)

Katu, Tikta,

Kashaya

Laghu Rooksha


Kandughna, Varnya

4 BAKUCHI BEEJA(Psoralia corylifolia)

Katu Tikta

Laghu Rooksha


Twachya, Kandughna, Krimighna, Switra hara

5 AMALAKI (Emblica officinalis)

Amla, Madhura,

Katu, Tikta,

Kashaya

Laghu Rooksha Sheeta

Sheeta Madhura Tridoshahara Rasayana, Vrushya,Kustaghna

6 BHRINGARAJA(Eclipta alba)

Katu Tikta

Laghu Rooksha


Keshya, Twachya, Krimihara

Kakodumbaradighanavati (internal) and Ayorajadilepa

(external) in Switra –Literary Review 76

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –Methodology

77

Chapter – 4 Methodology

The methods adopted in the study are discussed as under.

A) Source of data:-

a) Patients suffering from Switra are selected from P.G.S.A.R.C. Dept of

Kayachikitsa OPD of D.G.M. Ayurvedic Medical College and Hospital by Preset

Inclusion and exclusion criteria.

b) Literary: - Literary aspects of study are collected from classical Ayurvedic and

contemporary texts and updated with recent Medical Journals.

B) Method of collection of data:-

a. Study Design: Prospective clinical trail.

b. Sample size : A minimum of 30 patients are taken in randomized selection

c. Study duration :60 days – treatment schedule

d. Follow up: 30 days

e. Administration of Drug:

Internally Kakodumbaradi Ghanavati 3 grams / day in divided doses or 2 tabs of

500 mg thrice daily after the food with water

Externally Ayourajadi lepa Q.S. rubbed in water to paste and applied all over the

effected skin for 30 minutes exposed in the sun light

C) Exclusion criteria:-

1. Patients below 10 years irrespective of sex are excluded: because the

children under the age of 10 may not be co-operative and also are not


78

accepted for any trail. Thus the below 10 years of age children are

excluded.

2. Patients above 60 years of age, irrespective of sex are excluded:

because the old age people are of Vata ages and above the age of 60

may not be accepted as they are under the influence of degeneration.

Thus the above 60 years of age people are excluded.

3. Pregnant women and lactating women are excluded: because the drug

may be placental barrier, thus pregnant women and lactating women

are excluded.

4. Patients suffering from other systemic disease are excluded: Because

the other systemic diseases may mask the disease original and the

effect of the trail drug may not elicited perfect. Thus the Patients

suffering from other systemic disease are excluded.

5. Patients with Burnt areas are excluded: Because the burnt area skin

loses permanently melanocytes and scar is formed, which is a

irreversible white patch mimics the Vitiligo. Thus the Patients with

Burnt areas are excluded.

6. The patches over lips and mouth angulations are excluded: The

patches over lips are excluded because the application over the area is

not possible as it is a cornified tissue. Thus the people with such

lesions are excluded.


79

7. The genital area patches are excluded: Because, after the application as

generally asked to expose for the sun light which is not possible. Thus

such cases are excluded in the study.

D) Inclusion criteria:-

1. All the Patients other than that of exclusive criteria are included in the

study.

2. Patients with classical symptoms of Switra as explained in Ayurvedic

classics and diagnosed case of Vitiligo according to the contemporary

diagnostic system are included.

F) Method of Diagnosis:

1. Medical history:

Evaluation and diagnosis of Vitiligo require obtaining the following information:

i. The age of onset of the white spots; Vitiligo rarely begins before the age

of 6 months.

ii. Family history of Vitiligo and early greying of the hair (i.e., significant

loss of hair colour before the age of 30 years)

iii. Inflammation, irritation, or rash preceding the white sports.

iv. Potential precipitating events including emotional stress, physical illness,

sunburn, or other forms of cutaneous forms occurring within 2 to 3 months

prior to the onset of de pigmentation.

v. Personal stress to the patient resulting from the disease

vi. Ocular or auditory dysfunction.


80

vii. Previous forms of therapy, either systemic or topical, how the therapy was

prescribed, and the effects or toxicity of the treatment.

viii. Stability or progression of the disease.

ix. Allergies and personal family history of atopy.

x. Occupational hazards and hobbies to define chemical exposures that might

be responsible for chemically induced Vitiligo.

xi. Personal or family history of associated diseases including thyroid

disorders, premature graying, alopecia areata, diabetes mellitus, collagen

vascular diseases, permicious anaemia, and addision’s disease; personal

history of other disorders aggravated by photo exposure or of

photosensitivity.

2. Physical examination

The diagnosis of Vitiligo is based exclusively on the clinical examination of the

patient. The physical examination includes the following findings; the presence of

acquired asymptomatic depigmented macules or patches, usually without clinical signs of

inflammation. Hypopigmented lesions may coexist with depigmented lesions. Such

trichrome lesions are often observed in individuals with darker skin. Trichrome Vitiligo

is characterized by depigmented, hypopigmented, and normally pigmented skin. About

2% to 5% of patients may exhibit one or more depigmented lesions with dermatitic

/inflamed borders.

Vitiligo lesions may be found in any area of the body. The initial lesions are

frequently found on the hands, forearms feet, face and lips. The borders of the lesions are

usually discrete and well defined.


81

The distribution of skin lesions, the number, and the approximate surface area of the

integument involved by de pigmentation should be determined in order to establish the

baseline extent of the disease. Some investigators classify Vitiligo into two groups —

generalized and segmental. Others subclass generalized Vitiligo into three subcategories;

a) Generalized: Symmetric macules or patches occurring in a random

distribution over much of the body; acral / acrofacial depigmented

macules or patches confined to the extremities and /or face; focal/localized

isolated macules or patches on one or two sites of the body.

b) Segmental: Vitiligo restricted to one portion of the body such as one leg,

one portion of the trunk, or the face. The lesions are rarely if ever

distributed in a dermatomal pattern.

Other important physical findings include acquired depigmented hairs within a

vitiliginous region and poliosis of scalp hair, eyelashes, eyebrows, and/or beard hair.

Areas of hypopigmentation and hyperpigmentation of the choroid and retinal pigment

epithelium may be evident by ophthalmologic examination. The presence or absence of

uveitis also should be determined. This examination is best done by an ophthalmologist.

Referral to an ophthalmologist is of particular importance if the patient has complaints of

photophobia, decreasing visual acuity, or poor night vision.

For patients with fair skin, such as those with skin types I and II, detection of

depigmented or hypopigmented patches of Vitiligo may require the use of a wood’s lamp

to delineate the areas of involvement. In-patients with darker skin, a wood’s lamp

examination also can be helpful to assess the degree of hypopigmentation or

depigmentation in individual lesions.


82

3) Diagnostic tests

In most instances the diagnosis of Vitiligo is based on the history and physical

examination. However, I some instances additional diagnostic tests may be indicated to

differentiate Vitiligo from conditions that may mimic it clinically. These conditions

include piebaldism, nevus depigmentosus, nevus anemicus, postinflammatory

depigmentation hypopigmentation, pityriasis alba, tinea versicolor, discoid lupus

erythematosus, and scleroderma. In addition, certain tests are sometimes helpful to detect

the presence of associated systemic disorders such as thyroid disease, pernicious anemia,

diabetes, or Addison’s disease. Some useful tests include the following.

a) Biopsy from the border stained with fontana Masson technique to differentiate

Vitiligo from some of the aforementioned conditions. Melanocytes are decreased in

the early stages of Vitiligo. As the disease progresses, they are completely absent.

Other changes include basilar vascuolopathy, exocytosis of lymphocytes, spongiosis,

and lymphohistiocytic infiltrates, especially in inflammatory Vitiligo. For most

patients a biopsy is not necessary

b) Baseline blood chemistry may include a complete blood count, a differential with

erythrocyte sedimentation rate, and thyroid function studies including thyroid

stimulating hormone. In addition, tests for antiparietal cell, antithyroid (thyroglobulin

and microsomal), and antinuclear antibodies are frequently indicated. These tests are

more important if signs or symptoms of endocrine disease or collagen vascular

disease are present. Abnormal test values should be followed clinically or by

laboratory examination as indicated.


83

c) If patients are to undergo photo chemotherapy, a baseline ophthalmologic

examination and antinuclear antibody determination are advisable. Some physicians

recommend a repeat of these tests at 6- month intervals. Other at 12 month intervals

while on PUVA therapy.

Inappropriate diagnostic tests include serum alpha-MAS levels, serum ACTH

levels, hair analyses, and trace metal analyses.

G) Assessment of result

Subjective and objective parameters will be assessed for result.

I) Subjective parameter: Signs and symptoms as designed in classical texts.

1. Rukshata: becoming skin dryness at depigmented surface is identified as

different grades are as follows –

Grade 0 – Normal skin dryness

Grade 1 – Mild -

Grade 2 – Moderate –

Grade 3 – Severe -

2. Parushata: becoming skin roughness at depigmented surface is identified as


Grade 0 – Normal skin roughness

Grade 1 – Mild -



3. Paridwamshi: getting dusty skin at depigmented surface is identified as different

grades are as follows –

Grade 0 – Normal dusty skin Grade 1 – Mild - Grade 2 – Moderate – Grade 3 – Severe -


84

4. Daha: getting burning sensation of skin at depigmented surface is identified as


Grade 0 – No Burning sensation

Grade 1 – Mild -



5. Roama Patana: getting hair falling at depigmented surface is identified as


Grade 0 – No hair fall

Grade 1 – Mild -



6. Kandu: getting itching at depigmented surface is identified as different grades are

as follows –

Grade 0 – No itching

Grade 1 – Mild -



7. Kleda: getting moisture skin at depigmented surface is identified as different

grades are as follows –

Grade 0 – Normal skin

Grade 1 – Mild -




85

8. Srava: getting discharge at depigmented surface is identified as different grades

are as follows –

Grade 0 – Normal skin

Grade 1 – Mild -



II) Objective parameter

For the assessment of results the following objective parameter were consider

i) Colour

ii) Margin

iii) Number

iv) VASI score.

To assess the effect number and VASI score were consider as they are without

grading before and after treatment. To assess the improvement in colour and margin the

following grading were given.

1. Colour: The colour of your skin is due to an interaction between –

(1) Pigment composition and concentration and

(2) The dermal blood supply. The grades are as follows –

Grade 0 – Normal skin colour

Grade 1 – Non-unified normal skin

Grade 2 – Pigmentation is more than depigmentation

Grade 3 – Depigmentation equal or more than pigmentation

Grade 4 – Depigmentation more than pigmentation

Grade 5 – Complete Depigmentation


86

2. Margin: margins of the lesions are enumerated as grades are as follows.

Grade 0 – Normal skin colour attributed

Grade 1 – Hyper pigmented thick broad width graduated margin

Grade 2 – Hyper pigmented broad width graduated margin

Grade 3 – Hyper pigmented well defined margin

Grade 4 – Hyper pigmented thin edge margin

Grade 5 – Ill defined margin

3. VASI score:

When patients or physicians try to determine how well a particular treatment

works for Vitiligo, it is often difficult to compare different treatment options. There is no

standardized measure for the amount of Vitiligo someone has and how it responds to

treatment. There is a standard for psoriasis known as the PASI (psoriasis Area and

Severity Index) score, which has been quite helpful in comparing different treatment

options in numerical terms. The PASI has been the basis for the FDA in its evaluation of

the rapid increase in new psoriasis treatments. This is not the case for vitiligo. Presently,

when a patient wants to determine how well Narrow Band UVB (NBUVB) may work for

their Vitiligo they are given the statistic that is often not intuitive.

The first step of the VASI is to divide the patient into various body regions such

as the arms, trunk, legs, hands and feet. Then, using the assumption that a palm of the

hand is equivalent to 1% of the body surface, the physician determines how much of the

skin is affected by Vitiligo. Then the physician determines what percent of the skin is

depigmented by referring back to standardized pictures of various degree of pigmentation

(see attached pictures) 153.

Sum of value of product of palm units X Extent of depigmentation VASI = Total Body surface area II) Over all assessment

Over all assessment of the results are done considering the cumulative effect of

subjective and objective parameters. The disease is not totally manageable with in the

scheduled time, the grades of assessment of results made as under.

1) Cured:

Colour – Normal skin colour

Margin – Normal or No margins

Number –100% reduction

VASI – VASI score is “Zero”

2) Well Responded:

Colour – non unified normal skin colour

Margin – hyper pigmented thick broad width graduated margin

Number – more than 75% reduction

VASI – more than 75% reduction

3) Moderately Responded:

Colour – pigmentation equal to depigmentation

Margin – hyper pigmented broad width graduated margin

Number – more than 50% reduction

VASI – more than 50% reduction

4) Poorly Responded:

Colour – depigmentation is more than pigmentation

Margin – hyper pigmented well defined margin

Number – less than 50% reduction

VASI – less than 50% reduction


87

5) Not responded:

Colour – No pigmentation developed

Margin – No changes in margin

Number – No reduction

VASI – No reduction

Figure - 8 Estimating the Degree of Depigmentation for the VASI

Kako

dumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –Methodology 88

CHAPTER-5

RESULTS

Present study registers 35 patients, out of 40 approached patients. The percentages of

patients undertaken from the scrutinised are 87.5%. Out of the 35 patients of Switra 33

(94.28%) patients were undertaken for the study. Out of 33 patients 3 (9.09%) patients were

discontinued hence their data has not been included in the assessment. The remaining 30

(90.9%) patients of Switra viz. Vitiligo, fulfilling the criteria of diagnosis and inclusive

criteria were included in the study. Vitiligo area scoring index (VASI) is considered as a

specific objective parameter for the assessing patients in the present study.

All the patients were examined before and after the trail, according to the case sheet

format given in the annex. Both the subjective and objective criteria were recorded. The data

recorded are presented under the following headings.

A. Demographic data

B. Evaluating disease Data

C. Result of the Kakodumbaradighanavati & Ayorajadilepa in Switra and

D. Statistical analysis of the subjective (clinical) and objective parameters

A) Demographic data:

The details of Age, Gender, Religion, and Occupation etc. of the 30 patients are as

follows.

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 89


Table – 19

Demographic Data of trail in Switra with Kakodumbaradi Ghanavati & Ayorajadilepa

SN OPD Age Gender Religion Occupation Economical status

Food habits

Result

1 5327 41 M H ACT MID VEG MR 2 5517 16 F H ACT MID VEG PR

3 5524 37 F H ACT MID VEG MR

4 5589 16 F H ACT HMC VEG PR 5 5650 30 F H ACT MID VEG PR 6 16 10 F MU ACT MID MIX WR

7 209 13 F H ACT MID VEG WR

8 272 10 M H ACT POOR MIX WR 9 281 16 M H ACT MID VEG WR

10 485 28 M H ACT MID VEG WR 11 495 11 F H ACT HMC VEG MR 12 496 17 F H ACT MID VEG WR

13 599 43 F H ACT HMC VEG MR 14 145 12 M H ACT MID VEG PR

15 906 40 F H ACT MID VEG CUR

16 1186 28 M H LAB POOR MIX PR

17 1223 45 M H ACT HMC VEG WR

18 1435 38 M H LAB POOR MIX PR

19 2352 18 F H ACT MID VEG WR 20 2370 12 F MU ACT HMC MIX NR 21 2438 24 M H ACT MID VEG MR

22 2439 28 F H ACT MID VEG CUR

23 2485 22 F H ACT MID MIX MR

24 2570 27 M H SED MID MIX MR

25 2628 30 F MU ACT MID MIX MR

26 2653 21 M H ACT MID VEG WR

27 2744 19 M H ACT MID VEG PR

28 2804 13 F H ACT HMC VEG WR

29 2892 15 M H ACT MID VEG MR

30 2898 18 M MU LAB POOR MIX PR

M =Male, F = Female, H = Hindu, Mu = Muslim, ACT = Active, SED = sedentary, LAB = Labour, POOR = poor, MID = Middle class, HMC = Higher Middle Class,

VEG = Vegetarian, MIX = Mixed diet, CUR = cured, WR = Well Responded, MR = Moderately Responded, PR = Poorly Responded, NR = Nor Responded


A) Demographic data:

The details of Age, Gender, Religion, and Occupation etc. of the 30 patients is as

follows.

A1) Distribution of patients by Age – gender

Intervals of 10 have considered from the ages 10 to 50 as discussed in the methods. In

the study it is revealed that skin discoloration is continued from the ages of 10 and even less

ages and as the age advances the samples are settled to have Vitiligo. At the older age group

of 40-50 only 3 (10%) patients are reported. Where in 30-40 age group reported with 3 (10%)

and 5 patients in each group of male and female in total 10 (33.3%) reported from the ages of

20-30. larger sample age group 10-20 reported with the 14 (46.7%) patients with the

symptoms of Switra vis-à-vis Vitiligo. The tabulation is depicted as under.

Table- 20

Distribution of patients by Age- gender in Switra with

Kakodumbaradi Ghanavati & Ayorajadilepa

Male patients Female patients Total patients Age

Number % Number % Number %

10 - 20 6 20 8 26.67 14 46.7

20 – 30 5 16.66 5 16.67 10 33.3

30 - 40 1 3.33 2 6.67 3 10

40 – 50 2 6.67 1 3.33 3 10

Totals 14 46.66 16 53.34 30 100

Here in this study an attempt is made to understand the male female responses to the

management with respect to that of the age groups.

Figure – 9

Distribution of patients by Age- gender in Switra with

Kakodumbaradi Ghanavati & Ayorajadilepa

Kakodumba

Result of p

Age

Tot

al n

o of

10 - 20 15

20 – 30 9

30 - 40 3

40 – 50 3

Total 30

radighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 92

68

55

1

22

1

0 2 4 6 8

20-Oct

20 – 30

30 - 40

40 – 50

DISTRIBUTION OF PATIENTS BY AGE - GENDER

Female 8 5 2 1

Male 6 5 1 2

20-Oct 20 – 30 30 - 40 40 – 50

Table- 21

atients by Age in Switra with Kakodumbaradi Ghanavati & Ayorajadilepa

pati

ents

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

50 0 0 6 20 2 6.66 6 20 1 3.33

30 1 3.33 2 6.66 4 13.3 2 6.66 0 0

10 1 3.33 0 0 2 6.66 0 0 0 0

10 0 0 0 0 3 10 0 0 0 0

100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33


Observations of result in the study are good as the cured (6.66%) and well responded

are 8 (26.6), in total is 33.33% of the patients included in the study. As the observations are

expressed the early age groups are responded well and the late ages are not. Thus the age

impact is observed in the study as this disease of depigmentation is well tackled at the early

ages than that of late ages.

A2) Distribution of patients by Gender

Table- 22

Distribution and Result of patients by Gender in Switra with


Gender

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Male 14 46.6 0 0 4 13.3 6 20 4 13.3 0 0

Female 16 53.4 2 6.66 4 13.3 5 16.7 4 13.3 1 3.33

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

The male female ratio in the study is 7:8 patients. The percentage of the distribution

does not show any gender differentiation to get this skin disease, except a small lean towards

Female population. The observations are 14 Patients i.e. (46.6%) male and 16 patients i.e.

(53.4%) were female. As the results observed, out of 14 (42.86%) males much are distributed

between well to moderate response but no body got cure. Out of 16 female patients, 2 cured

and 9 patients well and moderately responded show that the disease regression with the

present trail is relevant for the female population. The tabulation shown above is pictorially

expressed below.

Figure - 10

Distribution and Result of patients by Gender in Switra with


A3) dist

F

Christia

commun

Muslim

(6.66%)

moderat

group o

commun

Kak

Distribution of patients by Gender in Switra

Male46.67%

Female 53.33%

ribution of patients by Religion

or the convenience of the study, the religion groups are noted as Hindu, Muslim,

n and Others. The maximum number of patients are noticed from the Hindu

ity as the ratio of community at the study area is more i.e. 26 (86.67%) along with

patients 4 (13.33%). At the results observed, out of 26 (86.66%) of Hindu patients, 2

patients cured, 7 (23.33%) patients’ well responded and 10 (33.33%) patients

ely responded. 7 (23.33%) patients poorly responded and no patients are from the

f not responded reported. On the other hand the results observed at Muslim

ity are, out of 4 (13.33%), one patient (3.33%) in each group of well responded,

odumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 94

moderately responded, poorly responded and not responded are observed. The tabulation and

graphical representation is as under.

Table- 23 Distribution & Results of patients by Religion in Switra with Kakodumbaradi Ghanavati and

Ayorajadilepa

Religion

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Hindu 26 86.7 2 6.66 7 23.3 10 33.4 7 33.3 0 0

Muslim 4 13.3 0 0 1 3.33 1 3.33 1 3.33 1 3.33

Christian 0 0 0 0 0 0 0 0 0 0 0 0

Others 0 0 0 0 0 0 0 0 0 0 0 0

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

Figure – 11 Distribution & Results of patients by Religion in Switra with Kakodumbaradi Ghanavati and

Ayorajadilepa

Kak

odumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 95

Graph – 13 Distribution of patients by religion in Switra

Christian 0.00% Hindu

86.67%Muslim13.33%

Others0.00%

A4) Distribution of patients by Occupation

Table- 24

Distribution & Result of patients by occupation in Switra with


Occupation

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Sedentary 1 3.33 0 0 0 0 0 0 1 3.33 0 0

Active 26 86.7 2 6.66 8 26.6 11 36.6 4 13.7 1 3.33

Labour 3 10 0 0 0 0 0 0 3 10 0 0

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

Figure - 12

Distribution of patients by Occupation in trail

Kakodu

PATIENTS BY OCCUPATION

Active86.67%

Sedentary3.33%

Labour10.00%

mbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 96

The distribution of the patients in the occupational groups are enlisted and pictorially

presented above. It clearly expresses that the patients those whoa re more active are prone to

get this skin disease Switra which is said as the anxiety prone. A very high number of 26

(86.7%) of the patients are recorded in this group. As the results are observed, out of 26

(86.7%) of active patients, 2 (6.66%) cured, 8 (26.66%) patients are well responded, 11

(36.66%) patients moderately responded, 4 (13.66%) patients poorly responded and 1

(3.33%) patient not responded to the treatment.

Figure – 13

Result of patients by occupation in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

Kakodu

A5) Distrib

As t

20 (66.66%

(6.66%) cu


ution of patients by economic status

Result of patients by occupation in Switra

0

0

0

1

0

2

8

11

4

1

0

0

0

3

0

0 2 4 6 8 10 1

Cured

WR

MR

PR

NR

2

Labour

Active

Sedentary

he distributions are observed, out of 30 patients a maximum of middle class i.e.

) are witnessed. As the results are encourage in the trail for middle class people 2

red, 6 (20%) well responded, 8 (26.66%) moderately responded, 4 (13.33%)

patients poorly responded and no patient of not responded reported. Out of the 4 poor

patients only one (3.33%) well responded and rest of 3 (10%) poorly responded. From the

higher middle group one each in the well, poor and not responded along with 3 (10%) in

moderately responded. The tabulation and graph are given below.

Table- 25 Distribution and Results of patients by Economic status in Switra with Kakodumbaradi

Ghanavati and Ayorajadilepa Economic

status

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Poor 4 13.3 0 0 1 3.33 0 0 3 10 0 0

Middle 20 66.6 2 6.66 6 20 8 26.6 4 13.3 0 0

Higher Middle

6 20 0 0 1 3.33 3 10 1 3.33 1 3.33

Higher 0 0 0 0 0 0 0 0 0 0 0 0

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

Figure - 14 Distribution of patients by Economic status in Switra with


Kakodumbar

adighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 98

4

20

6

00

5

10

15

20

25

Poor Middle Higher Middle Higher

Patients by economical status

Patients

A6) Distribution of patients by diet in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

Table- 26 Distribution and Result of patients by diet in Switra with Kakodumbaradi Ghanavati and

Ayorajadilepa

Diet consumption

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Vegetarian 21 70 2 6.66 6 20 7 23.3 6 20 0 0

Mixed diet 9 30 0 0 2 6.66 4 13.3 2 6.66 1 3.33

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

Figure –15

Distribution of patients by diet in Kakodumbaradi Ghanavati and Ayorajadilepa in Switra

Kakodumba

The die

Out of 21 (70%

6 (20%) patien

(3.33%) not res

well responded

PATIENTS BY DIET CONSUMPTION

Vegetarian 70.00%

Mixed diet30.00%


t variances in the Switra with distributions and results observed are as under.

) of vegetarian patients, all most all are responded to the management except

ts who are poorly responded. On the other hand mixed diet consumers 1

ponded, 2 (6.66%) poorly responded and no one cured apart from 2 (6.66%)

and 4 (13.33%) patients moderately responded, is as described above in table.


B) Data related to the disease.

B1) Presenting complaints

Table-27 - Data of patients by presenting complaints in study SN

OPD

Tw

ak

Shw

etat

a

Rom

a V

ivar

nata

Ruk

shat

a

Par

usha

ta

Par

idw

ams

hi

Dah

a

Roa

ma

Pat

ana

Kan

du

Kle

da

Sra

va

1 5327 + + 2 5517 +

3 5524 +

4 5589 + 5 5650 + + + + 6 16 + +

7 209 +

8 272 + 9 281 + + + +

10 485 + 11 495 + + 12 496 +

13 599 + 14 145 +

15 906 +

16 1186 + +

17 1223 +

18 1435 + +

19 2352 + 20 2370 + + + 21 2438 +

22 2439 +

23 2485 +

24 2570 +

25 2628 +

26 2653 + +

27 2744 + + +

28 2804 +

29 2892 +

30 2898 + +


Table -28

Distribution of patients by presenting complaints in Switra

Presenting complaints Patients Before Percentage

Twak Shwetata 30 100

Roma Vivarnata 3 10

Rukshata 5 16.66

Parushata 2 6.66

Paridwamshi 0 0

Daha 2 6.66

Roama Patana 0 0

Kandu 5 16.66

Kleda 0 0

Srava 0 0

Guruta 2 6.66

As the above table explains about the different symptoms evaluated at the study under

the heading of Switra vis-à-vis Vitiligo with the presenting complaints put forth here. The

first and fore most complaint is hypo-pigmentation i.e. Twak Swetata (100%) patients in the

study is reported. The next most common complaint is Roma Vaivarnyata i.e. hair

discoloration with 3 patients (10%) reported. The third complaint is kandu – itching with the

Rookshata – dryness is found in each 5 (16.66%) patients. Daha and Parushyata found only

in 2 (6.66%) patients each in the study. The graphical representation is as under.

Figure – 16

Distribution of patients by presenting complaints in Kakodumbaradi Ghanavati and

Ayorajadilepa in Switra

B2) Mode

Mode o

Onset

Gradual

Sudden

Total

Kakod

Distribution by Presenting Complaints in Asthigata Vata

Kleda, 0

Srava, 0

Kandu, 5

Daha, 2

Roama Patana, 0Paridwamshi, 0

Roma Vivarnata, 3

Rukshata, 5Twak Shwetata, 30

Parushata, 2

0

5

10

15

20

25

30

35

of Onset

Table- 29

Distribution and Result of patients by Mode of onset in Switra with


f

Tot

al n

o of

pa

tien

ts

% C

ured

% Wel

l R

espo

nded

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

28 93.3 1 3.33 8 26.6 11 36.7 7 23.3 1 3.33

2 6.67 1 3.33 0 0 0 0 1 3.33 0 0

30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

umbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 102

Figure –17

Distribution and Result of patients by Mode of onset in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

The m

only 2 patient

in the pathoge

one patient h

responded to

B3) Family h

The fa

history and o

hereditary fac

of categories

Only one pati

are gradually

Kakodum

Mode of Onset

Gradual 93.33%

Sudden6.67%

ode of onset is studied here is observed as more (28) patients of gradual and

s of sudden in nature, suggests the gradual mode of onset with causative factors

nesis of Switra. Each one of sudden and gradual onset got cured in total. Only

ad poor response in the gradual group. All other patients are gradually

the treatment depicted in the above table and graph.

istory

mily history is studied here is observed as more (25) patients of no family

nly 5 patients of family history in nature, suggests the disease may not be with

tors related but the dietetic causative factors in the pathogenesis of Switra. Each

has the poor responses, but non family history patients show cure in the study.

ent of no response is in the non family history patient group. All other patients

responded to the treatment depicted in the below table and graph.

baradighanavati (internal) and Ayorajadilepa (external) in Switra –– Results 103

Table- 30

Distribution and Result of patients by Family history in Switra with


Family

history

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Present 5 16.6 0 0 3 10 0 0 2 6.66 0 0

Absent 25 83.3 2 6.66 5 16.6 11 36.6 6 20 1 3.33

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

Figure –18

Distribution and Result of patients by Family history in Switra with


Kakodumba

Family history

Present16.67%

Absent83.33%


B4) Chronicity

Table- 31

Distribution and Result of patients by Chronicity in Switra with


Chronicity in

years

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

< 1 year 10 33.3 2 6.66 5 16.6 2 6.66 1 3.33 0 0

1 to 2 years 12 40 0 0 3 10 4 13.3 5 16.6 0 0

3 to 4 years 5 16.6 0 0 0 0 4 13.3 1 3.33 0 0

5 & above 3 10 0 0 0 0 1 3.33 1 3.33 1 3.33

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

Figure –18

Distribution and Result of patients by Chronicity in Switra with


Kakodumba


Chronicity

3 to 4 years16.67%

< 1 year33.33%

1 to 2 years40.00%

5 & above 10.00%


The chronicity history is studied here is observed as more (10+12) patients are of less

than 2 years of history and only 8 patients are of longer duration, suggests the disease may

be with long non curative. Each of categories has the poor responses, but more than 5 years

of history (one) patient show no response in the study. The cured patients are of from less

than 1 year duration. All other patients are gradually responded to the treatment depicted in

the below table and graph.

B5) Incidence of initial site of onset

Table- 32 Distribution and Result of patients by Incidence of initial site of onset in Switra with


Incidence of initial site of

onset

Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Head & Neck 7 23.3 1 3.33 2 6.66 3 10 1 3.33 0 0

Trunk 6 20 0 0 1 3.33 3 10 2 6.66 0 0

Upper Extremities

13 43.3 1 3.33 4 13.3 3 10 4 13.3 1 3.33

Lower Extremities

4 13.3 0 0 1 3.33 2 6.66 1 3.33 0 0

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

The Incidence of initial site of onset history is studied here is observed as more

(7+13) patients are of either to head neck or upper extremities history and only 6 patients are

of trunk exposure along with 4 patients on lower extremities, suggests the disease may be

with much on exposed parts. Each of categories has the poor responses, but one patient

shows no response in the study had lesions on upper extremities. The cured patients are one

each of from head & neck and upper extremities groups. All other patients are gradually

responded to the treatment depicted in the above table and below graph.

Figure –19

Distribution and Result of patients by Incidence of initial site of onset in Switra with


B6) Incidence o

Distribution

distribution of lesions

Symmetrical

Asymmetrical Total

Kakodumba

Incidence of initial site of onset

Upper Extremities

43.33%

Head & Neck23.33%

Trunk20.00%

Lower Extremities

13.33%

f distribution of lesions

Table- 33 and Result of patients by Incidence of distribution of lesions in Switra with


Tot

al n

o of

pa

tien

ts

% C

ured

% W

ell

Res

pond

ed

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

22 73.3 1 3.33 4 13.3 9 30 7 23.3 1 3.33

8 26.6 1 3.33 4 13.3 2 6.66 1 3.33 0 0

30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33


The Incidence of distribution of lesions history is studied here is observed as more

patients (22) are observed that symmetrical, and the rest (8) are asymmetrical in nature. The

symmetrical distributaries patients show 1 (3.33%) cure, 4 (13.33%) well response, 9 (30%)

moderate response, 7 (23.33%) patients of Poor response along with one patient of no

response. From the other category 1 (3.33%) cure, 4 (13.33%) well response, 2 (6.66%)

moderate response and 1 patient of poor response is observed. All other patients are

gradually responded to the treatment depicted in the above table and below graph.

Figure –20

Distribution and Result of patients by Incidence of distribution of lesions in Switra with


Incidence of distribution of lesions

Asymmetrical, 8Symmetrical , 22

0 5 10 15 20 25

B7) Incidence of clinical type of disease

The Incidence of clinical type of disease with lesions history is studied here is

observed as more patients (23) are observed that generalized, and the rest (7) are localised in

nature. The localized distributaries patients show 2 (6.66%) cure, 2 (6.66%) well response, 2


(6.66%) moderate response, 1 (3.33%) patients of Poor response along with no patient of any

response. From the other category of generalized no cure, 6 (20%) well response, 9 (30%)

moderate response and 7 (23.33%) patients of poor response is observed. One patient of this

category is not responded to the treatment. The data is depicted in the below table and graph.

Table- 34 Distribution and Result of patients by Incidence of clinical type of disease in Switra with


clinical type of disease

Tot

al n

o of

pa

tien

ts

% C

ured

% Wel

l R

espo

nded

%

Mod

erat

e R

espo

nded

%

Poo

r R

espo

nded

% Not

R

espo

nded

%

Localized 7 23.3 2 6.66 2 6.66 2 6.66 1 3.33 0 0

Generalized 23 76.6 0 0 6 20 9 30 7 23.3 1 3.33

Universal 0 0 0 0 0 0 0 0 0 0 0 0

Total 30 100 2 6.66 8 26.6 11 36.7 8 26.6 1 3.33

Figure –21 Distribution and Result of patients by Incidence of clinical type of disease in Switra with


Kakodumba

Incidence of clinical type of disease

23

0

7

0 5 10 15 20 25

Localized

Generalized

Universal



B8) Distribution of patients by according to Ahara Nidana in Kakodumbaradi Ghanavati and

Ayorajadilepa in Switra

Table- 35

Distribution of patients by Ahara Nidana in Switra Kakodumbaradi Ghanavati and Ayorajadilepa

Ahara Nidana Total no of patients

%

Anashana 4 13.33

Adhyassana 13 43.33

Ajeernadhyasana 2 6.66

Atilavana 3 10

Ati amla 2 6.66

Kulatha 0 0

Masha 0 0

Dadhi 5 16.66

Ati drava 5 16.66

Navanna 0 0

Ati snigdha 0 0

Ati guru 4 13.33

Taila 6 20

Viruddha Ahara 30 100

Mamsa 9 30

The Nidana observed in the Switra are as above. Out of 30 patients maximum of

Nidana observed is viruddha Ahara (100%) along with 13 (43.33%) patients of Adhyasana.

No patients are reported with Kulutha, Masha, Moolaka, Navanna and Atisnigdha Ahara. The

table shown above and graph below as here.

Figure – 22

Distribution of patients by Ahara Nidana in Switra Kakodumbaradi Ghanavati and

Ayorajadilepa

B9) Distributio

Ghanavati and A

Distributio

Vihara N

Vegadh

Diwasw

Ativyavaya &

Sheeta jal

Atapa se

Kakodumba

Patients by Ahara Nidana

Atilavana, 3Ati amla, 2

Kulatha, 0Masha, 0

Dadhi, 5

Ati guru, 4

Viruddha Ahara, 30

Mamsa, 9

Anashana , 4

Adhyassana, 13

Ati drava, 5

Navanna, 0Atisnigdha, 0

Taila, 6

Ajeernadhyasana, 2

n of patients by according to Vihara Nidana in Switra Kakodumbaradi

yorajadilepa

Table- 36 n of patients by Vihara Nidana in Switra Kakodumbaradi Ghanavati and

Ayorajadilepa

idana Total no of patients

%

arana 4 13.33

apna 5 16.66

Papa Karma 0 0

a snana 3 10

vana 0 0


Figure – 23

Distribution of patients by Vihara Nidana in Switra Kakodumbaradi Ghanavati and

Ayorajadilepa

The vih

of Nidana obse

(13.33%) patien

table and graph

Kakodumba

Patients by Vihara Nidana

Sheeta jala snana, 3

Vegadharana, 4

Diwaswapna, 5

Ativyavaya & Papa Karma,

0

Atapa sevana, 0

0

1

2

3

4

5

6

ara Nidana observed in the switra are as above. Out of 30 patients maximum

rved is of 5 patients’ diwaswapna (16.66%) along with 4 Vegasandharana

ts and 3 (10%) of sheeta jala snana after undergoing shrama and bhaya. The

are shown above.



C) Result in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

C1) Assessment of Subjective parameters in Switra

Table- 37

Subjective parameters Patients Before

Patients After

Patients Changed

Changed %

Rookshata 5 1 4 80

Parusha 2 1 1 50

Daha 2 1 1 50

Kandu 4 2 2 50

Guruta 1 0 1 100

C2) Assessment of Objective parameters in Switra

Table -38

Objective parameters Mean Before Mean After Mean Difference Colour 4.06 1.866 2.0194

Margin 4.133 1.866 2.266

Number 13.76 9.76 3.99

VASI 1.174 0.579 0.595

Serum Copper 160.37 167.26 6.93

The subjective parameters which are considered here show marked response with

good percentage of relief. At the objective parameters all has shown the variances on the

positive declination in the study.

C3) Results in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

Table-39 Results in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa Result Number of patients Percentage

Cured 2 6.67

Well Responded 8 26.66

Moderately Responded 11 36.67

Poor Responded 8 26.66

Not Responded 1 3.34

Total 30 100

Figure – 24

Results in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

Kakodu

The

criteria cons

Results in Switra with Kakodumbaradi Ghanavati and Ayorajadilepa

Poor Responded26.67%

Well Responded26.67%

Cured6.67%

Moderately Responded

36.67%

Not Responded3.33%


results of the study are based upon the assessment of the subjective and objective

idered in the study. Mainly the objective parameters are considered to show the


evidences of the relief in the study. The result encourages the Ayurvedic fraternity even

though the cure is only 6.67% (2 Patients) in the time bound study. Many patients are at

virtue of getting relief is grouped as well responded listed as 26.66% (8) patients along with

the 37.66% of moderately responded patients. In the study many causes made hindrances of

the melanin re-pigmentation and 8 i.e. 26.66% patients fall under poor response. Only one

patient i.e. 3.34% noticed as the no response patient in the entire study. The tabulations and

graphical expressions are shown as above.

D) Statistical analysis of the clinical and objective parameters

D1) Subjective parameter Statistical analysis in Switra with Kakodumbaradi Ghanavati and

Ayorajadilepa

Table -40

Subjective parameters Mean SD SE t-Value p-Value

sign

ific

ance

Rookshata 0.266 0.52 0.095 2.804 >0.05 NS

Parusha 0.066 0.365 0.066 1.0 >0.05 NS

Daha 0.1 0.402 0.073 1.36 >0.05 NS

Kandu 0.3 0.65 0.118 2.523 >0.05 NS

Guruta 0.13 0.434 0.079 1.68 >0.05 NS

HS = Highly Significant, ID = Insufficient Data


D2) Objective parameter Statistical analysis in Switra with Kakodumbaradi Ghanavati and

Ayorajadilepa

Table -41

Objective parameters Mean SD SE t-Value p-Value

Sig

nifi

canc

e

Colour 2.2 0.961 0.175 12.53 <0.001 HS

Margin 2.26 1.04 0.191 11.84 <0.001 HS

Number 4.06 5.686 1.03 3.94 <0.001 HS

VASI 0.296 0.435 0.079 3.72 <0.001 HS

Serum Copper 33.2 19.36 3.535 9.39 <0.001 HS

HS = Highly Significant

D3) Distributional (Head & Neck) Statistical analysis in Switra with Kakodumbaradi


Table -42

Head and Neck Mean SD SE t-Value p-Value

Sig

nifi

canc

e Colour 2.58 0.792 0.228 11.28 <0.001 HS

Margin 2.33 0.778 0.224 10.38 <0.001 HS

Number 2.66 3.66 0.971 2.74 <0.02 HS

VASI 0.081 0.138 0.039 2.085 > 0.05 NS

HS = Highly Significant, NS = Not Significant


D4) Distributional (Trunk) Statistical analysis in Switra with Kakodumbaradi Ghanavati and

Ayorajadilepa

Table -43

Trunk Mean SD SE t-Value p-Value

Sig

nifi

canc

e

Colour 1.72 0.786 0.237 7.28 <0.001 HS

Margin 0.19 0.943 0.284 6.708 <0.001 HS

Number 1.9 3.11 0.938 2.03 >0.05 NS

VASI 0.1662 0.249 0.075 2.216 > 0.05 NS


D5) Distributional (Upper Extremities) Statistical analysis in Switra with Kakodumbaradi


Table -44

Upper Extremities Mean SD SE t-Value p-Value

Sig

nifi

canc

e Colour 1.77 0.83 0.27 6.4 <0.001 HS

Margin 2.11 0.781 0.26 8.1 <0.001 HS

Number 1.66 1.93 0.645 2.58 <0.05 HS

VASI 0.194 0.296 0.098 1.97 > 0.05 NS



D6) Distributional (Lower Extremities) Statistical analysis in Switra with Kakodumbaradi


Table -45

Lower Extremities Mean SD SE t-Value p-Value

Sig

nifi

canc

e

Colour 2.05 1.08 0.26 7.8 <0.001 HS

Margin 1.88 1.11 0.269 6.98 <0.001 HS

Number 2.94 3.69 0.89 3.27 <0.01 HS

VASI 0.263 0.305 0.07 3.55 <0.01 HS


Individually all the objective parameters show high significance by comparing p

value. The parameter colour, margin, S. Copper show high significance than the other

parameters (By comparing t value). The parameter S. Copper show more net mean effect,

with more variations, where as VASI show less mean effect with less variation (by

comparing mean and SD). In the head and neck the parameters colour and margin show high

significance than the number. Where as VASI show non significance (by comparing p & t

values). In the trunk region the parameters colour and margin shows high significance, but

the parameters number and VASI are not significant (by comparing p & t values). In upper

limb the parameters margin and colour show high significance than number. The parameter

VASI is not significant in upper extremities (by comparing p & t values). In the lower

extremities the parameters colour and margin show high significance but the parameters

number and VASI show moderate high significance (by comparing p & t values).

CHAPTER-6

Discussion

The skin is the largest and most visual organ of the human body. Hence any blemish

on the skin visible effects onlooker and the person affected profoundly. Switra is most

blemishing disease compared to other dermatological problems.

It is being told that Vitiligo only a cosmetic problem. Unfortunately poor fellow

suffering from not scared by the disease but also the social stigma and scorn of the society

make their life miserable. In India Switra has been medico-social problem since the time

immemorial. The first prime minister of India Pandirt Jawahar Lal Nehru ranked Vitiligo

(Switra) as one of the three major medical problems of India, other being leprosy and

Malaria.

Switra is characterised by Aparisravi swetha varna mandala i.e. non exudative skin

lesions. It can be equated that of Vitiligo in contemporary science which is hypo-pigmentary

disease. It affects about 1-2% of world population. All the races and both genders are

equally affected by the disease.

In India and perhaps elsewhere also men, women and children with Vitiligo face

severe psychological and social problem. It is the most acute in the case of young women

and children.

Vitiligo lesions over face, particularly embracing and cause frustration. The lesions

over exposed parts such as hands feet and can lead to anger and disillusion, particularly in

teenage. Patients with Vitiligo are very sensitive to the way other pursue them and they will

often withdraw, because they anticipate being rejected. The impact of such factors is

profound subjecting them to emotional distress. Such severe depression been known to lead

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Discussion

119

suicide attempts. Last decade has witnessed an increasing interest in psychological affect of

the various skin diseases, and quality of life in patients suffering from disease.

Keeping the above facts in view it was decided to go through knowledge of Switra of

its aetiology progression of the disease and methods of managements are studied according

to Ayurvedic literature.

Acharyas suggested good remedies like kushtagna and varnya drugs to cure the

disease. Thus Kakodumbaradi Ghanavati internal and ayorajadi lepa external were selected

for conducting clinical observation as switragna oushadhi in single group. All patients

advised to exposure to sunlight after the local application. Such an effect is likely to give

some useful information for the perfect treatment of Switra.

Discussion on demographic data

The efficacy of any drug can not be proved unless it is subjected to clinical trial and

analyzed statistically. The trial drug Kakodumbaradi Ghanavati internal and Ayourajadi lepa

external are considered for the evaluation in Switra. The clinical study was undertaken on 30

patients in a single group. In the foregone pages observation were made systematically

presented.

Relevancy of age

Vitiligo may appear any time from shortly after birth to senescence although on

onset between 5 and 30 years of age is most common. In the present study, it is found as the

age group below 30 years age more than 80% (10-20 age group -50% and 20-30 age group -

30%) the rest of the age group are 20% (30-40 and 40-50 age group) perhaps the cosmetic

values commenced in the Vitiligo might be dragged more youth than that of aged people.


120

Disease long term association and incurability would have disappointed the elder groups not

to attend the treatment schedule.

Gender

The percentage of distribution of gender does not shows any differentiation to get the

Switra (Vitiligo), except small lean towards female population is 53.4% and 46.6% male.

According to the literature prevalence is equal in between males and females.

Religion

Religion does not play any major role in the causation of the disease though in the

present study the percentage of Hindu patients are more.

Occupation

This is done under three categories. It seems that active patients have high incidence

of Vitiligo. This is mainly because active people are over exerted and excited. The

psychological intervention can not be ruled out, as it is a psychosomatic disorder.

Economical status

In the present study highest numbers of patients reported were from lower middle

class, probably they undergo insecurity feeling or crave for the higher status. For the above

the reason they strain and stress themselves and get captured into the clenches of Vitiligo.

Diet

Viruddha Ahara is explained as prime causative factor for the Switra. In present

study salt, pickles, milk, mixed with food is more practiced in this area may be the causative

factor for the disease.


121

Discussion on disease Switra

Nidana

Ayurveda emphasized diet as an important etiological factor. Because samyak yojita

Ahara leads to indriya prasadana and varna prasadana. But asamyak yojita Ahara leads to

several diseases. Hence Twak is also influenced by aharaja Nidana, recent studies have been

shown significant role of food as possible etiological factor in cause the disease.

Viruddha Ahara i.e., incompatible diet is mentioned as the prime causative factor of

Kushta in general and Switra in particular. These incompatible foods are responsible for the

formation of Ama (exogenous antigen source). Ama may interfere with absorption nutrients

which accepted as one of the etiological factor for Vitiligo. Ama can also be generated

within the body by virtue of excessively vitiated doshas (auto immune antibody production,

free radicals mediated tissue injury) those are postulated as the etiological factors of the

Vitiligo. (Dr. R.H singh)

Charaka also opines that the papakarma, guruninda, unlawful acts, are also causes

Switra. There is no logic which can be put forth regarding involvement of these Nidana. But

these may induce stress in the patients and become vyanjaka hetu triggering of further

depigmentation.

Vrana including agnidagdha or injury like cuts crapes can be destroy pigment cell

resulting in Vitiligo Lesions to develop in trauma prone areas, a Koebner’s reaction is

observed. In present study salt, wheat, floor, curd and milk mixed with foods which are

more practiced in this area may common causative factor of this disease.

Poorvaroopa


122

A wide range of poorvaroopa for Kushta has been listed in the classics though none

of mentioned especially for Switra. No poorva roopa could be elicited in the present study.

Roopa

Samanya lakshana of Switra are aparisravi sweta varna mandala found in almost all

patients. Rookshata, parushata, paridwashi, roma patina, daha, roma vivarnata, and srava are

told as samanya lakshana of Switra. But srava, romavidweshi are not found in any of the

patient. Kandu and rookshata were found in five patients and daha and guruta found in two

patients. In classics specific colours are described to denote the Dhatu gatatwa of Switra.

But colours could not be differentiated in patients’ skin. Also specific symptoms of doshaja

verities were not found in any of the patients. In the present clinical study except aparisravi

sweta mandala other lakshanas were not observed in much of the patients. As this trial is

limited all can only be observed more in large samples.

Samprapti

Switra is a Pitta pradhana tridoshaja Vyadhi. Bhrajakapitta is responsible for the

normal pigmentation of skin. Pitta and Rakta got asrayaasrayee sambandha i.e., the

pathogenecity of Rakta means pathogenecity of Pitta. Involvement of Pitta is inevitable in

Switra which is said to be Rakta pradoshaja Vyadhi. But along with these factors Agni, Rasa

and Mamsa also influence the mechanism of pigmentation. This is so because food that the

individual consumes is first digested by Agni and converted into Ahara Rasa. This Ahara

Rasa is for the metabolized by the succeeding dhatwagni’s to produce respective dhatus. The

skin receives the nourishment by Rasa, Rakta and Mamsa Dhatu. So hypo function of

Jataragni and dhatvagni affects the pigmentation of the skin. Pachakapitta is said to be


123

nourish the rest of the Pitta like Bhrajakapitta and Ranjakapitta etc., hence Pachakapitta

dushti may also lead to dushti of other Pitta.

Viruddha Ahara, mithya Ahara and papakarama has been explained to great detail in

causation of Kushta. This etiological factors cause the vitiation of tridosha and production of

Ama. But do not propel out of the body. So these Dosha undergo sthana samshraya in Twak

and results in hypo pigmentation of the skin.

Treatment principle

Chakrapani commenting on Switra Chikitsa opines that treatment of Kushta holds

good even for the Switra. Switra is Dosha karmaja Vyadhi. With this fact the treatment of

Switra can be adopted in three headings.

1. Daivavyapasraya Chikitsa

2. Yuktivyapasraya Chikitsa and

3. Satvavyajaya Chikitsa

Daivavyapasraya Chikitsa

Switra roga has been discussed as a separate entity in Ayurvedic classics. Switra

roga pigmented macular plaque seen in skin and mucus membrane. Actual etiological factor

has not been identified by the modern medicine. The pathophysiology has been proposed by

certain hypothesis. Autoimmune phenomenon has been considered as the prime pathology

facilitated into destruction of melanocytes. The main cause behind the triggering of

autoimmune phenomena is not known. In western modern medicine this is called as an

idiopathic state, meaning that the cause is unidentified. One of the causes described for

Switra roga by Ayurvedic classics is Poorvajanmakrutapapam (sinful acts of past life). The

system of Ayurveda accepted the theory of birth and rebirth cycle. It also states that many


124

things are unperceived to sensory organs; such are infinite in number. We attribute these

factors under the word daivam. Daivam is etymologically defined as 'Daivam adrushtam

evam purvajanmakruta karmam'. The factors, which are unidentified and unperceivable, are

called idiopathic and can be rationally explained under papakarmas. That is the reason why

daivavyapasraya Chikitsa has become the first and the foremost therapeutic module in many

diseases like Switra. Though the principles remain unchanged, the perception has been

changed. The western medicine calls it as idiopathic and Ayurveda considers it as

purvajanmakruta karma, which makes no significant difference 154.

Yukti vyapashra Chikitsa

In this treatment Charaka specially mentioned person to make to undergo all types

Shodhana. Then once again is made to drink malapurasa with guda to his capacity and then

may to exposure to sunrays as long as he can. And same has been followed in western

system of medicine in the topic of tanning.

It is astonishing fact the ancestor had good awareness about the pigmentory action of

sunlight. The bhaskara dhana surya namaskara ravivara vrata etc., daiva vyapashraya

Chikitsa are directly related to exposure to sunlight, also explained in the management of

Switra.

Satwavajaya Chikitsa:

Controlling of the manas from ahita indriyarthas i.e., from causative aharas and

viharas for Switra. It is also named as Nidana parivarjana, which also plays a key role in

Chikitsa.


125

Discussion on Results:

The hypothesis on the action of Kakodumbaradi Ghanavati (internal) and Ayourajadi

lepa is verified by this observational study. Both treated and untreated cases of Switra were

taken for the study and the treatment was administered on OPD basis. Observations were

made before, during and after the treatment in two follow ups. To assess the effect of

treatment decrease in the color, number of mandalas, VASI Score, hyper-pigmentation of

margin and increase in serum copper level were considered.

Serum copper:

The tyrosinase is a copper containing enzyme responsible for synthesis of melanin.

In literature it has been mentioned that lesser percentage of serum copper causes Vitiligo.

But in present study total 35 patients (included and excluded) were subjected for lab

investigation not a single case shown lesser percentage of serum copper. Majority of patients

expressed normal level of serum coppers viz. 100-200 micro grams per dl. There it can be

consider that serum copper have no specific role in the manifestation of Vitiligo.

The major improvement was observed in colour and maragin of the mandala. The

cure rate was observed 6.66% in all the parameter. Well response was found in 33.33% of

patients in the colour, 46.66% in the margin, 26.66% VASI score and 0% in the number of

mandala. Moderate response was noticed in 36.66%of the patients in the colour.16.66% in

the margin and 36.66% in the number and 23.33% in VASI score of mandala. Poor response

was observed in 16.66% in the colour, 26.66% in both margin and number and 40% of

patients in VASI score of the mandala.


126

Probable mode of action:

For any disease to manifest Dhosha-Dosha Samurchana is must, that is nothing but

what we say as Samprapti. This having maximum attention as Samprapti vighatan itself is

the basic thought of treatment in any disease. So to understand probable mode of action of

yoga we have to think how the quality of individual drugs of the yoga will act against the

Samprapti ghatakas.

Dosha and its pacification:

As already explained Switra is a Tridosha Vyadhi. The ingredients of

Kakodumbaradi Ghanavati act over tridoshas and pacify them.

Kakodumbara: By its tikta, kashaya rasa acts as kapha-pitta shamaka,

kushtaghna and kandughna.

Vidanga: By its ushna veerya acts as vata shamaka. By katu rasa and katu

vipaka acts as kapha shamaka, and srotoshodhaka.

Bakuchi: By its katu, tikta rasa, laghu-rooksha guna, and ushna veerya acts as

srotoshodhaka, kapha-pitta shamaka and krimighna.

Ayourajadi lepa having ushana,teekshana and srotoshodaka properties the veerya

of lepa reaches the siramuka of swedava srotash and reach the deeper layer twak and it act

locally to relive the sanga. By this the samapurana of Bhrajaka pitta takes place and hence

normal function is noticed.

Action on Agnimandya and Ama:

Agnimandya is the prime causative factor in manifestation of any disease. This is

well appreciated in Switra also. Here Dosha involved is Pitta mainly i.e. in terms of Kshaya

of Bhrajaka and Ranjaka. These are dependent over Pachakapitta. Each drug of this yoga are


127

said to be Deepan, which is estimated to regulate Pachakapitta indirectly influencing

Bhrajakapitta and Ranjakapitta.

Ama is inevitable factor in causation of Kushta in general and Switra in particular.

The regulation of Agni is the treatment thus at this juncture Deepana and Pachana properties

embedded in the Kakodumbaradi Ghanavati helps in reliving the Ama.

Role of Rasayana:

Twak is indicator of status of Rasa Dhatu. This Rasa Dhatu if not properly formed

then there will be vikruti in terms of its appearance, colour, and luster etc, because Rasa

Dhatu nourishes the Twak. So treatment should also target for the correction of Rasadhatu.

The Kakodumbaradi Ghanavati possesses the properties of deepana, pachana, Bruhana,

Balya and Vrushya properties which help in increasing the quality of Rasa and succeeding

Dhatus later. According to modern science Vitiligo is an autoimmune disorder, the drugs

used in this study being Rasayana etc. specific gunas play an effective role in protecting or

correcting or toning the immune system of the body and thus may result in curing the

Vitiligo. Psoralens are the active principles of Bakuchi. When ingested the seeds are

believed to facilitate amino acid transport across the intestinal mucosa and induce

pigmentation (Chakraborty D.P. et al). Seeds are having anti fungal, anti protozoan activity

and are also used in intestinal amoebasis (Gogate V.M, D.C.P). The pharmacological

action of this compound drug is mainly seen as Kushtagna, krimighna, varnya. The

Kushtaghna and Switraghna prabhava of this compound is responsible for relieving the

lesions of the skin. Thus the drugs act by relieving the toxins or checking the absorption of

toxic substances from the gut and facilitate the amino acid transport across the intestinal

mucosa and induce pigmentation.


128

Stimulation of melanocytes to enrich re pigmentation

Vitiligo is a condition in which only active (melanin-producing) melanocytes

destroyed and the inactive melanocytes in the (ORS) outer root sheath of normal hair

follicles are preserved and serve as the only source for the re pigmentation Recovery of

Vitiligo is initiated by the proliferation of these inactive melanocytes, followed by the

upward migration of inactive melanocytes to the nearby epidermis to form peri-follicular

pigment islands 155. Regimentation also begins with shrinking of patches from periphery to

the center. But these inactive melanocytes dose not synthesis melanin under normal

circumstances. They need stimulation to synthesis melanin. In such condition topical

application Ayourajadi lepa stimulate inactive melanocytes. Thus stimulated melanocytes

release melanin which gradually diffuse into de pigmented area and results in re

pigmentation

Topical preparation Ayourajadi lepa consist Bakuchi, Ayoraja, Krishn tila, Rasanjana,

Amalaki and Bhringaraja. The essential oil of Bakuchi is able to permeate through the

epidermis to the prickle cells of the lymphocytes and so it finds it way to sub capillary area,

which is dilated so that plasma is increased in that area. The skin becomes erythemic and

melanocytes are stimulated (Chopra 1958). This is also well supported by the rest of the

ingredients of the preparation like Ayoraja, Krishn tila, Rasanjana, Amalaki and Bhringaraja

because of their ushna teekshna lekhana and kshareeya guna. Amalaki which is known for

its anti oxidant property may help in the rejuvenation of the melanocytes. Bringaraja etc

which are otherwise known to have keshya effect, here this property may be thought to

strengthen the hair root which is said to be the reservoir of inactive melanocytes would

regularize the synthesis.


129

The Bakuchi and Kakodumbara contain active principle psoralin, when

Kakodumbaradi Ghanavati is administered internally this psoralin gets absorbed into the

systemic circulation and reaches the inactive melanocytes getting concentrated into the

cytoplasm which then increases the photosensitivity of the inactive melanocytes. Further this

helps in synthesis of melanin pigment which is deficient in Vitiligo.

Exposure to Sunlight:

In the present clinical study exposure to sunlight was advised to follow after the local

application early in the mornings to patients. Both the Psoralens and sunlight stimulate

tyrosinase enzyme which is responsible for the merlanin synthesis. The sunlight being

radiant energy it may potentiates the action of external application. Thus may results in

perfect permeability of drug through epidermis and which result in perfect stimulation of the

melanocytes for their normal function melanogenesis. This increases the production of

facultative melanin. By reviewing qualities and actions of Kakodumbaradi Ghanavati, and

Ayourajadi lepa, we may conclude that, systematic correction with internal preparation and

the local stimulation by external application may appear effective in this disease.

General Observations:

During the course of the study, it has been observed that some patients developed

visphota and the improvement was found to be fast in these patients. Some other patients

developed erythema and itching where fast improvement was also observed. During re-

pigmentation process, two patterns were observed. First pattern was re-pigmentation of the

lesions from the periphery to centre which showed delay in reduction of size. Second pattern

was peri-folliculor, later configurating into the normal skin colour. During the initial

improvements, the size of the dark spots increases and subsequently coalescence to form


130

large pigmented patches. The smaller patches will disappear and the larger ones will

decrease in size significantly. In some case re- pigmented areas may be hyperpigmented

and thus appear darker than the surrounding normal skin. Lesions on hairy areas respond

better to treatment than when it appears on non-hairy parts like the Palm and foot. In the

recent studies shown that, the lesions on the face had quick resolution when compared to

other areas. No particular observation in any area regarding quick response was found in the

present study.

No increase in the size and number of the mandala was seen in any of the patients

during follow up except in one patient where little increase in the size due to unknown

reasons was noticed.

Limitation of the study

1. The sample size was small

2. Limited to that of one particular geographical area

3. The period of study was limited

4. Longer follow up was not done

Recommendation for future study:

The following recommendations are made on the basis of observations and

conclusions made in the study, as guidelines for the further studies, which are made in future

to over come, the limitations listed.

1) Same study can be repeated by taking a large number of samples and longer duration

2) Comparative study between Shamana Oushadhi and lepa is required to assess the

effect of the individual preparation.

3) The effect lepa along with and without Rasayana can be studied.


131

CHAPTER-7

Conclusion

Based on the discussion of this study it is fairly concluded that -

1. Switra is a Pitta pradhana tridoshaja twak vikara.

2. Switra is a disease which effectively represents Vitiligo.

3. The varna of doshaja varieties of Switra were unable to identify and differentiate in

the patients.

4. Switra is more prevalent between the age group of 10-30 years.

5. Family history of Vitiligo is observed in 16.66% of patients.

6. The mental state of the patient as something that could influence the outcomes. Those

who are able to remain calm and mentally stable are thought to have a good chance of

success, while those who are anxious or depressed and who are not having patience

with the treatment are expected to have a poor chance. Indeed, the latter group of

patients may experience treatment failures due to noncompliance with the regimen, as

much as any psychophysical adverse effects of the mental state on their skin

condition.

7. Some physician emphasizes the topical treatment, others emphasize the internal

treatment, but both appear important to the prompt and complete resolution of Switra.

8. Finally it can be very safely concluded that the above mentioned drug combination

has positive role in the management of Switra.

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Conclusion

132

CHAPTER-8

Summary

The present study was under taken to evaluate the effect of lepa along with

shamanoushadhi in the management of Switra.

Lepa Chikitsa, a cognate therapy is included under bahi parimarjana chikitsa. This

therapy is specially meant for the twakgata vikaras. The lepa Chikitsa also facilitates the

expulsion of the doshas locally. Ayorajadi lepa is selected according to Yogaratnakar

explanation. The lepa contains Bakuchi which is the drug of choice in Switra. Other

ingredients of lepa like Ayoraja, Krshanatila, Rasanjana, Amalaki, and Bhringaraja are

having the properties Twachya, Keshya, and kuthaghna as mentioned in classics.

Kakodumbaradi Ghanavati was selected because of the presence of Bakuchi along

with Kakodumbara and vidanga which are said to be tridosha shamaka and also having

Switra hara prabhava.

The research design was pre-test and post test design with an observation study of 30

patients who were incidentally selected for the study. Patients were diagnosed on the

symptomatolgy explained in classics and with modern description.

The historical review, nirukti, paribhasha, bheda, nidana panchaka, sadhyasadhyata

and chikitsa of Switra according to the classics were reviewed. Detailed available

information about drugs and also latest research on these individual drugs was searched.

The observations were done on the factors like age, sex, religion, marital status, ,

socio economic status, occupation, food habits, family history, , chronicity, type of Vitiligo,

age and sites of first onset, color, margin, number and VASI score of the mandalas.

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Summary

133

Recorded observation were analyzed, it reveled that the most of the patients are from

less than 30 years of age, Hindu, middle class and active.

The complete cure was observed, 6.66% i.e.2 patients, who are having small lesion

and recent onset. The remaining patients were also relieved moderately, from their

symptoms.

Clinical and statistical analysis reveals that the systemic corrections can be done with

internal preparation and the local stimulation by synthesis of melanin through external

application may be effective in the management of Switra vis-à-vis Vitiligo.

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra –– Summary

134

Bibliographic References

1) Kevin Barry, Body works version 6, CD ROM, The learning company Medical Library, 1997, TLC properties Inc., Orem, Utah, 84058

2) Sidarth N shaha. API Text book of medicine, 23rd chapter, 7th edition, 2003, publisher the Association of Physician of India Mumbai, page no 1322.

3) 3 .R G Vallia, IADVL,Text book and Atlas of dermatology, volume 2,1st edition, Bhalani pulishing house, Bombay. Page no 518.

4) Seung-Kyung Hann and James J, Norland, Vitiligo, 1st chapter, 1st edition, 2000, Panthaer publishers’ private limited, Bangalore, page no 3.

5) DoctorNDTV team, Dr. Rishi Parashar, Consultant Dermatologist, Sir Ganga RamHospital, New Delhi http://www.doctorndtv.com/topics/detailtopics.asp?id=302#q61554447

http://www.doctorndtv.com/reg, 05102006 6) Ibid, 7) Ibid 8) R G Madana shastri, Vedome Ayurveda, Manusmriti, 3-7, Mohanlal Ayurvedic trust

Delli, 1956. 9) Ambikadatta Shastri,Susruta Samhita,Nidanastana,5th chapter,17th sloka,15th

edition,2002,Chokamba Sanskrit samstana, Varanasi, page no 249. 10) Seung-Kyung Hann and James J, Norland, Vitiligo, 1st chapter, 1st edition, 2000,

Panthaer publishers’ private limited, Bangalore, page no 3. 11) Ambikadatta Shastri,Susruta Samhita,Nidanastana,5th chapter,17th sloka,15th

edition,2002,Chokamba Sanskrit samstana, Varanasi, page no 29. 12) 12..Http/www.nimas.nih.gov/Index.htm. 13) Dr. M S Bhagel, Research in Ayurveda, 1st edition, Mridu Ayurvedic publication and

sales, India. 14) D/05102006/dermo best, Inc-what is Vitiligo.htm. (http://www.dermabest.com/) 15) Davinder Parsad , Sunil Dogra and Amrinder Jit Kanwar, Department of

Dermatology, Venereology and Leprology, Postgraduate Institute of Medical Education & Research, Chandigarh, India, Quality of life in patients with Vitiligo, Health and Quality of Life Outcomes 2003,1:58 doi:10.1186/1477-7525-1-58 (http://www.hqlo.com/content/1/1/58 Published 23 October 2003 © 2003 Parsad et al; licensee BioMed Central Ltd

16) Fitzpatrick TB: The scourage of vitiligo. Fitzpatrick's J Clin Dermatol 1993, 68-69. (http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B7)]

17) Mattoo SK, Handa S, Kaur I, Gupta N, Malhotra R: Psychiatric morbidity in vitiligo: prevalence and correlates in India. J Eur Acad Dermatol Venereol. 2002, 16:573-578. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B6].

18) Ginsburg IH: The psychological impact of skin diseases: An overview. Clin 1996, 14:473-484. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B9].

19) Cotterill JA, Cunliffe WJ: Suicide in dermatological patients. Br J Dermatol 1997, 137(2):246-250. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B10].

Kakodumbaradighanavati (internal) and Ayorajadilepa (external) in Switra – References 1

http://www.doctorndtv.com/reg

http://www.dermabest.com/

http://www.hqlo.com/content/1/1/58

http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B7




20) Lerner AB: Vitiligo. J Invest Dermatol 1959, 32:285-310. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B1

21) Lerner AB, Nordlund JJ: Vitiligo. What is it? Is it important? JAMA 1978, 239:1183-1187. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B2

22) Bolognia JL, Pawelek JM: Biology of hypopigmentation. J Am Acad Dermatol 1988, 19:217-255. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B3

23) Handa S, Kaur I: Vitiligo: clinical findings in 1436 patients. J Dermatol 1999, 26:653-657. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B4

24) Handa S, Dogra S: Epidemiology of childhood vitiligo: a study of 625 patients from North India. Ped Dermatol 2003, 20:207-210. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B5].

25) Savin J: The hidden face of dermatology. Clin Exp Dermatol 1993, 18:393-395. http://www.hqlo.com/sfx_links.asp?ui=1477-7525-1-58&bibl=B8].

26) R G Madana shastri, Vedome Ayurveda, Rigveda,1-117-7,Mohanlal Ayurvedic trust Delli,1956.

27) R G Madana shastri, Vedome Ayurveda, Atarvaveda, 5-53-1, Mohanlal Ayurvedic trust Delli, 1956.

28) R G Madana shastri, Vedome Ayurveda, Atarvaveda, 1-23-1, Mohanlal Ayurvedic trust Delli, 1956.

29) R G Madana shastri, Vedome Ayurveda, Yesurveda, 30-21, Mohanlal Ayurvedic trust Delli, 1956.

30) R G Madana shastri, Vedome Ayurveda, Manusmriti, 3-7, Mohanlal Ayurvedic trust Delli, 1956.

31) R G Madana shastri, Vedome Ayurveda, Paninivyakarna, 5-2-120, Mohanlal Ayurvedic trust Delli, 1956.

32) Satyanarayana Shastri,Charaka samhita, Chikitsa sthana,7th chapter, sloka 173-177,1st edition,2001,Choukambha bharati Academmy,Varanasi,page no 274-275.

33) Ambikadatta Shastri,Susruta Samhita,Nidanastana,5th chapter,17th sloka,15th edition,2002,Chokamba Sanskrit samstana, Varanasi, page no 249.

34) Girijadayala Shukla,Bhela samhita,Chitsa Sthana,6th chapter, 29th sloka,1st edition,1959,Choukamba vidyabhavana,Varnasi, page no150.

35) Satyapal Bhishagacharya, Kashapa Samhita,Chikitsa stana,chpter,sloka,4th edition,1988, ,Chokamba Sanskrit samstana, Varanasi, page no 115.

36) Shrikanta murthy,Astnga Sangraha,Nidanastana,14th chapter, sloka 39-40,1st edition,1996, Chokamba Orientalia, Varanasi, page no 239-240.

37) 37.Hari Sadashiva shastri Parashara,Astanga Hrudaya, Nidana stana,14th chapter,sloka 37-40,1st edition,2002, , Chokambha Surabharati prakashan, Varanasi, page no 527-528.

38) 38.Yadunandan Upadhyaya, Madavanidana, Madukosha commentary,vol II,49th

chapter,37-40 sloka,26th edition,1996, Chokamba Sanskrit samstana, Varanasi, page no 164-166.

39) Brahamashankar mishra,Bhavaprakasha,Chikitsa prakarna,Kushata rogadhikara,54th chapter,46th sloka,5th edition,1969, Chokamba Sanskrit samstana, Varanasi, page no 2037.







40) Shridara Krishana Parasher,Sharangadara Samhita, Purvakhanda,7th chapter,90th sloka,3rd edition, 1984, Bhaidhyanath Ayurvedia Bhavana Limited, Nagapur, page no 148.

41) 41. Seung-Kyung Hann and James J, Norland, Vitiligo, 3rd chapter, 1st edition, 2000, Panthaer publishers’ private limited, Bangalore, page no 16.

42) Radhakanta deva,Shabdakalpa Dhruma,5th part,3rd edition,1967, Chokamba Sanskrit series office, Varanasi, page no 180.

43) R G Vallia,IADVL,Text book and Atlas of dermatology, volume II,1st edition, Bhalani pulishing house, Bombay. Page no 518.

44) Stedmen’s Stedmins medical dictionary, vol 4, 22nd edition, 1974, Williams Wilkins company Battimore publishing, page no –

45) Viswanath Jha, Amarakosha, 2nd edition, Motilal Bamarasidar, Pune, page no 283. 46) Radhakanta deva,Shabdakalpa Dhruma,5th part,3rd edition,1967, Chokamba Sanskrit

series office, Varanasi, page no 180. 47) Satyapal Bhishagacharya, Kashapa Samhita,Chikitsa stana,chpter,sloka,4th

edition,1988, ,Chokamba Sanskrit samstana, Varanasi, page no 115. 48) Radhakanta deva,Shabdakalpa Dhruma,5th part,3rd edition,1967, Chokamba Sanskrit

series office, Varanasi, page no 180. 49) Radhakanta deva,Shabdakalpa Dhruma,5th part,3rd edition,1967, Chokamba Sanskrit

series office, Varanasi, page no 180. 50) Viswanath Jha, Amarakosha, 2nd edition, Motilal Bamarasidar, Pune, page no 283. 51) Monier-williams, Sanskrit English Dictionary, 1st edition, 2003, Asian Educational

service, New-Delli, page no 393. 52) Veni madhava Shatri Joshi, Ayurvediya shabdakosha, 1st vol,1968, Maharastra

Rajya sahitya and Sanskrit mandala, Mumbai, page no 397. 53) D:\05102006\ Derma Best, Inc -Vitiligo & Skin functions.htm 54) Ambikadatta Shastri,Susruta Samhita,Sharirastana,4th chapter,4th sloka,15th

edition,2002,Chokamba Sanskrit samstana, Varanasi, page no 28 55) Bramanand Tripati, Charaka samhita,Sharira stana, 3th chapter, 6th sloka, 6th edition,

1999, Chokamba Sanskrit surabharati, prakashan, Varanasi, page no 862. 56) Hari Sadashiva shastri Parashara,Astanga Hrudaya,Sharira stana,1th chapter,57th

sloka, 1st edition,2002, , Chokamba hurabharati prakashan, Varanasi, page no 527-528.

57) Ambikadatta Shastri,Susruta Samhita,Sharirastana,4th chapter,4th sloka,15th edition,2002,Chokamba Sanskrit samstana, Varanasi, page no 28-29.

58) Bramanand Tripati, Charaka samhita, Sharira stana, 7th chapter, 4th sloka, 6th edition, 1999, Choukamba Sanskrit surabharati, prakashan, Varanasi, page no919.

59) Shrikanta murthy,Astnga Sangraha,Nidanastana,5th chapter, 7th sloka, 1st edition,1996, Chokamba Orientalia, Varanasi, page no 62.

60) Shridara Krishana Parasher,Sharangadara Samhita, Purvakhanda,5th chapter, sloka 37-40, 3rd edition, 1984, Bhaidhyanath Ayurvedia Bhavana Limited, Nagapur, page no 77.

61) Bhashkar Govinda Ghanekar, Susruta Samhita, Sharirastana, 4th chapter, 4th sloka, 17th edition, 2004, Lakshmandas publications, Newdelli, page no 107.

62) Martion Fundamentals of Anatomy and Physiology, 4th edition, 1998, Prentice Hall Inc (pub) New Jersey, page no 147-162.


63) Bramanand Tripati, Charaka samhita,Indriya stana,1st chapter, 8th sloka, 6th edition, 1999, Chokamba Sanskrit surabharati, prakashan, Varanasi, page no 989.

64) Shrikanta Murthy,Astnga Sangraha,Shrirastana,1st chapter, sloka 39-40,1st edition,1996, Chokamba Orientalia, Varanasi, page no 15.

65) Bramanand Tripati, Charaka samhita,Indriya stana,7th chapter, 16th sloka, 6th edition, 1999, Chokamba Sanskrit surabharati, prakashan, Varanasi, page no 1021-1022.

66) Bramanand Tripati, Charaka samhita,Indriya stana,7th chapter, 14-15 sloka, 6th edition, 1999, Chokamba Sanskrit surabharati, prakashan, Varanasi, page no 1021.

67) Bramanand Tripati, Charaka samhita,Indriya stana,7th chapter, 10-13 sloka, 6th edition, 1999, Chokamba Sanskrit surabharati, prakashan, Varanasi, page no 1021

68) 68. Bramanand Tripati, Charaka samhita,Sutra stana,12th chapter, 11th sloka, 6th edition, 1999, Chokamba Sanskrit surabharati, prakashan, Varanasi, page no 259.

69) Ambikadatta Shastri,Susruta Samhita,Sutraastana,21st chapter,10th sloka,15th edition,2002,Chokamba Sanskrit samstana, Varanasi, page no 89.

70) 70.Hari Sadashiva Shastri Paradakar, Astangahrudaya,Sutrastana, 12th chapter,14th sloka,7th edition, 2002, choukamba surabharati prakashan, Varanasi, page no 194.

71) Bhramananda Tripati, Charaka samhita, Vimana stana, 8th chapter, 104th sloka, 6th edition, 1999, choukamba surabharati prakashan, Varanasi, page no 764.

72) Hari Sadashiva Shastri Paradakar, Astangahrudaya,Sutrastana, 12th chapter,6th sloka,7th edition, 2002, choukamba surabharati prakashan, Varanasi, page no 193.

73) Satyanarayana Shastri, Charaka samhita, Chikitsa stana, 28th chapter, 38th sloka, 1st edition, 1999, choukamba bharati Acadamy, Varanasi, page no 459.


75) Satyanarayana Shastri, Charka samhita, Chikitsa stana, 15th chapter, 17th sloka, 1st edition, 1999, choukamba bharati Acadamy, Varanasi, page no 456



78) Mortin, Fudamenatls of Anatomy and physiology, 4th edition, 1998, Prentice Hall Inc (pub), New Jersey, page no 157.

79) Mortin, Fundamentals of Anatomy and physiology, 4th edition, 1998, Prentice Hall Inc (pub), New Jersey, page no 151.

80) Yadunanda, Upapadya, Madavanidana, Vol 1,1st chapter, 4th sloka, 26th edition, 1996, choukamba Sanskrit samsthan, Varanasi, page no 8.

81) Ambikadatta Shastri,Susharut samhita,Nidanastana, 5th chapter, 17th sloka, 15th edition,2002, choukamba Sanskrit samsthan, Varanasi, page no 249.

82) Satyapal Bhisagacharya, Kasyapa samhta,Khilastana, 5th chapter, 3rd sloka, 4th edition,1988, choukamba Sanskrit samsthan, Varanasi, page no 255.

83) Yadavaji Trikamaji Acharya,Susrita samhita,Dallana commentary, Nidanastana, 5th chapter, 3rd sloka, 8th edition,2005, choukamba Orientalia, Varanasi, page no 283.




86) Bhramananda Tripati, Charaka samhita, Vimana stana, 1st chapter, 21st sloka, 6th edition, 1999, choukamba surabharati prakashan, Varanasi, page no 662-663.

87) Bhramananda Tripati, Charaka samhita, Vimana stana, 25th chapter, 39th sloka, 6th edition, 1999, choukamba surabharati prakashan, Varanasi, page no 662-663.

88) Ambikadatta Shastri,Susharut samhita,Uttaratantra, 40th chapter, 163rd sloka, 15th edition,2002, choukamba Sanskrit samsthan, Varanasi, page no 234.


90) Bhramananda Tripati, Charaka samhita, Vimana stana, 25th chapter, 40th sloka, 6th edition, 1999, choukamba surabharati prakashan, Varanasi, page no 453

91) Bhramananda Tripati, Charaka samhita, Vimana stana, 7th chapter, 103 sloka, 6th edition, 1999, choukamba surabharati prakashan, Varanasi, page no 598-599.

92) Ambikadatta Shastri,Susharut samhita,Sutrastana, 20th chapter, 16th sloka, 15th edition,2002, choukamba Sanskrit samsthan, Varanasi, page no 85.

93) Bhramananda Tripati, Charaka samhita, Vimana stana, 7th chapter, 83 sloka, 6th edition, 1999, choukamba surabharati prakashan, Varanasi, page no 996.



96) Hari Sadashiva Shastri Paradakar, Astangahrudaya,Nidanastana, 14th chapter,37th sloka,7th edition, 2002, choukamba surabharati prakashan, Varanasi, page no 527.

97) Srikantamurty, Astanga-Sangrha, Sutrastana, 35th chapter, 3rd sloka, 1st edition, 1996, choukamba Orientalia, Varanasi, page no 571.

98) Srikantamurty, Astanga-Sangrha, Sutrastana, 22nd chapter, 89th sloka, 1st edition, 1996, choukamba Orientalia, Varanasi, page no 391.




102) Yadunanda, Upapadya, Madavanidana, Vol 1,1st chapter, 5th sloka, 26th edition, 1996, choukamba Sanskrit samsthan, Varanasi, page no 9.



105) Srikantamurty, Astanga-Sangrha, Nidanastana, 14th chapter, 12-13 sloka, 1st edition, 1996, choukamba Orientalia, Varanasi, page no 236.

106) Satyanarayana Shastri, Charaka samhita, Chikitsa stana, 7th chapter, 174th sloka, 1st edition, 1999, choukamba bharati Acadamy, Varanasi, page no 274

107) R G VALLIA,IADVL,Text book and Atlas of dermatology, volume 2,1st edition, Bhalani pulishing house, Bombay. Page no 518.


108) Satyanarayana Shastri, Charaka samhita, Chikitsa stana, 7th chapter, 174th sloka, 1st edition, 1999, choukamba bharati Acadamy, Varanasi, page no 274




112) Yadunandan Upadhyaya, Madavanidana, Madukosha commentary,vol II,49th

chapter,37-40 sloka,26th edition,1996, Chokamba Sanskrit samstana, Varanasi, page no 164-166.


114) http://www-emm.cbcu.cam.ac.uk/01003398h htm. 115) http://www-emm.cbcu.cam.ac.uk/01003398h htm. 116) Seung-Kyung Hann and James J, Norland, Vitiligo, 6th chapter, 1st edition, 2000,

Panther publishers’ private limited, Bangalore, page no 39-43. 117) Hari Sadashiva shastri Parashara,Astanga Hrudaya, Chikitsa stana,20th chapter, 1st

sloka,1st edition,2002, Chokambha Surabharati prakashan, Varanasi, page no 718. 118) Hari Sadashiva shastri Parashara,Astanga Hrudaya, Chikitsa stana,20th chapter,25th

sloka,1st edition,2002, Chokambha Surabharati prakashan, Varanasi, page no 719. 119) Satyanarayana Shastri, Charaka samhita, Chikitsa stana, 7th chapter, 166th sloka,

1st edition, 1999, choukamba bharati Acadamy, Varanasi, page no 273. 120) Hari Sadashiva shastri Parashara,Astanga Hrudaya, Chikitsa stana,20th chapter, 18th

sloka,1st edition,2002, Chokambha Surabharati prakashan, Varanasi, page no 718. 121) Satyanarayana Shastri, Charaka samhita, Chikitsa stana, 7th chapter, 172nd sloka,

1st edition, 1999, choukamba bharati Acadamy, Varanasi, page no 275. 122) Ambikadatta Shastri,Susharut samhita,Chikitsastana, 9th chapter, 45th sloka, 15th

edition,2002, choukamba Sanskrit samsthan, Varanasi, page no 53. 123) K.M Nadakarni, Indian Materia Medica, Vol I, 3rd edition, popular prakashan,

Bombay, 1996, Page 550. 124) K.M Nadakarni, Indian Materia Medica, Vol I, 3rd edition, popular prakashan,


Bombay, 1996, Page 1019. 126) K.M Nadakarni, Indian Materia Medica, Vol II, 3rd edition, popular prakashan,





Bombay, 1996, Page 169.


131) Dr. J L N Shastry,Drayaguna Vijnana, vol II, 1st edition,2004, Choukhambha Orientalia,Varanasi,page no 950-951.

132) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11859479&query_hl=4&itool=pubmed_docsum

133) Dr. J L N Shastry,Drayaguna Vijnana, vol II, 1st edition,2004, Choukhambha Orientalia,Varanasi,page no 318-319.

134) http://shop.store.yahoo.com/herbal-remedies-usa/index.html 135) Dr. J L N Shastry,Drayaguna Vijnana, vol II, 1st edition,2004, Choukhambha

Orientalia,Varanasi,page no184-186. 136) http://www.holistic-online.com/herb_home.htm 137) Gulbaraj Sharama Mishra, Ayurveda prakasha. 3rd chapter, 1999, 218-222 sloka,

Choukhambha Bharati Acodamy, Varanasi,page no 362. 138) Dr. J L N Shastry,Drayaguna Vijnana, vol II, 1st edition,2004, Choukhambha

Orientalia,Varanasi,page. 139) Dr. J L N Shastry,Drayaguna Vijnana, vol II, 1st edition,2004, Choukhambha

Orientalia,Varanasi,page. 140) I.P., 90; Uniyal & Issar, Indian For , 1967, 93 , 107; Gupta, ibid , 1964, 90 , 454;

I.P.C.,40 141) J. Am. Chem. Soc. 1982, 104, 2039 142) Chem. Commun. 1983,1425 143) Heterocycles 1982, 19, 257 144) Indian Drugs, 35(8), 468,1998; Chem Abstr 129:335838 145) Lu, S.H.; Natural Medicines, 52(4), 310, 1998 146) Leather Sci. 1968, 15, 337; Chem. Abstr. 1969, 71, 10285 b 147) Bull. Res. Inst. Univ. Kerala 1959, 6, 21; Chem. Abstr. 1960,54,16746 e 148) J. Oil Technol. Assoc. India 1973, 5, 8; Chem. Abstr. 1973, 78, 156602 a 149) Indian J. Chem. 1977,15B, 291 150) Hlth Bull ., 23, 1951, 38; Nature, 1944, 153, 684; Proc.Indian Acad. Sci., 1949, 29B,

155 151) J. Sci. Industr. Res., 1951, 10B, 88; Annu. Progr. Rep., CDRI, Lucknow , 1951-52 152) Shridara Krishana Parasher,Sharangadara Samhita, Madhyamakhanda,8th chapter,1st

sloka,3rd edition, 1984, Bhaidhyanath Ayurvedia Bhavana Limited, Nagapur, page no 306.

153) Dr Harvey Lui. Reference: Hamzavi I, Jain H, McLean D, Shapiro J, Zeng H, Lui H Parametric Modeling of Narrow Band UVB Phototherapy for Vitiligo with a Novel Quantitative Tool: the VASI Score Archives of Dermatology June: 140; 677-683, Update on Clinical research for Vitiligo: The VASI score, By Iltefat Hamzavi, MD, Clinical Assistant Professor, Department of Dermatology, Wayne State University

154) R G Vallia, IADVL,Text book and Atlas of dermatology, volume I,1st edition, Bhalani pulishing house, Bombay. Page no 52-56.

155) Seung-Kyung Hann and James J, Norland, Vitiligo, 8th chapter, 1st edition, 2000, Panthaer publishers’ private limited, Bangalore, page no 112.


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11859479&query_hl=4&itool=pubmed_docsum

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11859479&query_hl=4&itool=pubmed_docsum

http://shop.store.yahoo.com/herbal-remedies-usa/index.html

http://www.holistic-online.com/herb_home.htm

DEPARTMENT OF POST GRADUATE STUDIES IN KAYACHIKITSASHRI. D.G.M. AYURVEDIC MEDICAL COLLEGE, GADAG.

SPECIAL CASE SHEET FOR SWITRA

Guide : Dr. V. Varadacharyulu Scholar : Venkareddiyavar B. H.

Co-Guide : Dr. R. V. Shetter

01. Name of the Patient :

02. Father’s Name / Husband’s Name :

03. Age : Years

04. Sex :

05. Religion :

06 Educational Status :

07. Economical Status :

08. Marital Status :

09. Occupation :

10. Address :

11. Selection :

12. Result :

13. Consent :I is fully aware of the fact that

am a part of clinical trial. The investigator has explained me in detail about the out-comes of the trail in the language I understand. I voluntary submit myself to the trail andgive my consent to be one of his trial case.

SIGNATURE OF THE SCHOLAR SIGNATURE OF THE PATIENT

M. D. ScholarM. D. (Ayu) (OSM)

M. D. (Ayu)

Sl. No. :OPD No. :IPD No. :SCHEDULEInitiation :Complition :Male Female

Hindu Muslim Christain Other

Poor Middle class Higher class

Married Unmarried

Sedentary Active Labour

-----------------------------------------------

----------------------------------------------------

---------------- Pin. ------------ Ph. (---------------)------------------

Included Excluded

Cured Well resp. Not resp. Discontinued

11111

Moderate resp.

A. PRADHANA VEDANA:

Sl. Complaints Duration Before After

01 Twak Shwetata

02 Roma Vivarnata

03 Rukshata

04 Parushata

05 Paridwamshi

06 Daha

07 Roama Patana

08 Kandu

09 Kleda

10 Srava

B. ANUBANDHI VEDANA :

Sl. Associated Complaints Duration Before After

01 Vruna

02 Pandu

03 Shareera Gauravata

C. VYADHI VRITTANTA :

a. How it was noticed ? Intentional / Accidental. b. Mode of Onset Sudden / Gradual. c. Initial site of lesion d. H/O any physical injury

Burn : (What sort of it?)

Direct heat Thermal Sun Electrical Chemical

Trauma : (What sort of it?)

Accident Abrasion Scratches of itch Post surgery

2

Other factors: Shoes Gloves Bind’s Tight clothing

e. Natural causes

Pregnancy Parturition

f. Psychotic traumas –

i. Cause

ii. After what time patch appear

g. Pt. Suffering form any systemic disease

h. Any skin disorders reported

i. H/O of Heredity

Maternal Paternal.

D. CHIKITSA VRITTANTA:

E. VAYAKTIKA VRITTANTA:

Ahara Vegetarian Mixed

Rasa preferred M A L Kt Tk Ks

Vyasana Tea / Coffee Tobacco Smoking

Nidra Sound Disturbed

Mootra pravritti Normal Polyuria Micturia

Mala pravritti Normal Loose Constipated

Rajaha Regular Irregular Menopause

3

F. SAMANYA PAREEKSHA:

01. Pulse 02. B.P. 03. Temperature

04. Res. Rate 05. Weight 06. Height

07. Dashavidha & Ashtasthana Pariksha

Prakruti V P K VP VK PK VPK

Sara Pravara Avara Madhyama Samhanana Susamhita Asamhita Madhyma samhita Pramana Height in Cms Weight in Kgs Satmya Ekarasa Sarvarasa Ruksha Sneha Satwa Pravara Avara Madhyama Ahara Shakti Abhyavaharana Jarana Vyayam Shakti Pravara Avara Madhyama Vaya Balya Yauvana Vardhakya

Nadi Dosha Pravrutti

Gati Varna

Purnata Gandha

Spandana Kathinya

Mutra

Jihwa Ardra Sushka Sama Nirama Lepa Nirlepa

Mala

Shabda Sparsha Sheeta Ushna

Ast

asth

ana

Drik Akruti G. SPECIAL EXAMINATION OF SKIN:

a. Site of the lesion – Area of lesion in % Sl. Part Right Left

B A 01. Arm 02. Forearm 03. Palm 04. Thigh 05. Leg 06. Foot 07. Trunk front 08. Back 09. Neck 10. Face 11. Cheeks 12. Lips 13. Genitals

4

Distribution – Symmetrical Asymmetrical

Number –

Size – Smaller Small Big Gross

(0.1-1.0cm) (1-5cm) (5-15cm) (>15cm)

Colour – Red Coppery red White

Surface – Dry Moist

Margin – Thin Thick Extending Nondifferencible

Hairs – Krishna Tamra Shweta Alomata

Any system involved –

H. Evaluation of Ayurvedic etiology:

I. Nidana -

A. Ahara sambhi nidana -

Mithya ahara Anashana Adhaysahana Ajeerna adhyashana

Dravyata Navanna Gunata Atidrava Atisnigdha Atiguru Rasa pradhanyata

Atilavana Atiamla

Dhanya Chanaka Masha Yava Kulathya Shaka varga Moolaka Mamsa varga Matsya Taila Tila taila Kusumbha taila Ksheera vikriti Dadhi Takra Virushha ahara Dadhivada Dudgha and

Lavana Dadhi & ghrita /

taila.

B. Vihara sambandhi nidana –

Vega dharana Divaswapna Ativyavaya

Atapasevana Sheeta jalasnana and pana after shrama and Bhaya

C. Manasika samabandhi nidanas – Dharma viruddha Shastra viruddha Nyaya viruddha Guru nindaneeya

5

III. Poorvaroopa

IV. Roopa

Poorvaropa P/A When it was observed

Atisweda

Asweda

Atislakshna

Parusha

Vivarnata

Kandu

Daha

Romaharsha

Rookshata

Krishnata

Sl. Laxana Present / Absent

01. Twak Arunata

02. Tamra varna

03. Shweta varna

04. Rooskhata

05. Parusha

06. Paridwamshi

07. Roma vidhwamshi

08. Paridaha

09. Ghana

10. Guru

11. Kandu

V. Vinischaya

a. Doshaja b. Vranaja

VI. Sadhyasadhyata

VII. Arishta laxana

6

K. Laboratorial investigations

A. Objective criteria Sl. Investigations Before After

01. Serum copper µmole/lit. µmole/lit.

B. Exclusion criteria

Investigations Values

RBS Mg/dl.

TC Cells/cubinmm

DC – Polymorphs

- Lymphocytes

- Monocytes

- Basophils

- Eosnophil

ESR mm /1st Hour

Hb % Gm/dl

VIII. CHIKITSA KARMA:

INTERNAL YOGA – Kakodumbaradighana Vati

Posology – 3 gms per day in divided dosage.

ANUPNA –

EXTERNAL – Ayorajadi lepa (Q.S.):

Sl. Schedule Investigator’s Observations01. Day 1 02. Day 15 03. Day 30 04. Day 45 05. Day 60 06. Day 75 07. Final follow up 90th day

7

IX. ASSESSMENT OF RESULTS:

Sl. Patch area Before After Difference01. Colour 02. Number 03. Margine 04. VASI score

Investigator’s note:

Signature of scholar Signature of supervisor

GRADING CHART Colour – Grade 0 – Normal skin colour

Grade 1 – Non-unified normal skin Grade 2 – Pigmentation is more than depigmentation Grade 3 – Depigmentation equal or more than pigmentation Grade 4 – Depigmentation more than pigmentation Grade 5 – Complete Depigmentation

Margin – Grade 0 – Normal skin colour attributed Grade 1 – Hyper pigmented thick broad width graduated margin Grade 2 – Hyper pigmented broad width graduated margin Grade 3 – Hyper pigmented well defined margin Grade 4 – Hyper pigmented thin edge margin Grade 5 – Ill defined margin

VASI – Area (Palm units) x Extent of de-pigmentation in % Total body surface area

8

Documents

Switra kc032 gdg