Madhumeha#dg01 gdg

Evaluation of efficacy of Avartaki in Madhumeha (NIDDM)

By

Shashikala. B. Bani

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment of the degree of

Ayurveda Vachaspati M.D. In

Dravya Guna Under the Guidance of

Dr. G.V. Mulagund

M.D. (Ayu) and Co- Guidance of

Dr. Kuber Sankh M.D. (Ayu)

Department of Dravya Guna Post Graduate Studies & Research Centre

D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG

2002-2005

Ayurmitra

Draft

Declaration by the candidate

I here by declare that this dissertation / thesis entitled

“Evaluation of efficacy of Avartaki in Madhumeha (NIDDM)” is a

bonafide and genuine research work carried out by me under the

guidance of Dr. G. V. Mulagund M.D.(Ayu) Professor and Dr. Kuber

Sankh, M.D.(Ayu), Lecturer in Dravya Guna, DGMAMC, PGS&RC,

Gadag.

Date :

Place : Gadag

( SHASHIKALA . B. BANI )

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTRE

GADAG, 582 103

This is to certify that the dissertation entitled “Evaluation of efficacy Avartaki of in

Madhumeha (NIDDM)” a bonafide research work done by Shashikala. B. Bani in partial

fulfillment of the requirement for the post graduation degree of “Ayurveda Vachaspati M.D.

(Dravya Guna)” Under Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka.

Dr. G.V. MULAGUND M.D. (Ayu)

Guide

Professor & HOD

Dept. of Dravya Guna

DGMAMC, PGS&RC, GADAG

Date:

Place: Gadag

Dr. KUBER SANKH M.D. (Ayu)

Co- Guide

Lecturer in Dravya Guna

DGMAMC, PGS&RC, GADAG

Date:

Place: Gadag

J.S.V.V. SAMSTHE’S

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTRE

GADAG, 582 103

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

This is to certify that the dissertation entitled “Evaluation of efficacy of

Avartaki in Madhumeha (NIDDM)” is a bonafide research work done by

Shashikala. B. Bani under the guidance of Dr. G. V. MULAGUND, M.D. (Ayu),

Professor & HOD and Dr. KUBER SANKH, M.D. (Ayu), in partial fulfillment of the

requirement for the post graduation degree of “Ayurveda Vachaspati M.D. (Dravya

Guna)” Under Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka.

.

(Dr. G. B. Patil) Principal,

DGM Ayurvedic Medical College, Gadag

Date: Place: Gadag

(Dr. G. V. Mulagund) Professor & HOD

Dept. of Dravya Guna PGS&RC

Date: Place: Gadag

© 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 : Gadag

( SHASHIKALA . B. BANI )

© Rajiv Gandhi University of Health Sciences, Karnataka

ACKNOWLEDGEMENT

I am very much grateful to my guide, Dr. G.V. Mulagund M.D(Ayu) , Professor

& HOD Post Graduation Research & studies Dept. of Dravya Guna Shri D. G. M.

Ayurvedic Medical College , Gadag. for his valuable suggestions and guidance in

completion of this research successfully .

I am expressing my sincere thanks to my co-guide Dr. Kuber . Sankh M.D(Ayu)

Lecture, Post Graduation Research & studies Dept. of Dravya Guna Shri D. G. M.

Ayurvedic Medical College , Gadag. for his valuable suggestion ,guidelines & kind

co-operation at every moment of the preparations of dissertation .

I offer my sincere thanks to Dr. G.B. Patil Principal, Shri D. G. M. Ayurvedic

Medical College , Gadag. for facilitating the requirements needed during the work.

I am very much thankful to Dr. G. S. Hiremath. HOD Dept of Dravya guna ,

Shri D. G. M. Ayurvedic Medical College, Gadag for his valuable suggestions and

constant encouragement. I also thank Dr. Shashikant . B. N. for his kind co-operation.

I am very thankful to all my teachers of Shri D. G. M. Ayurvedic Medical

College, Gadag .who have given a foundation for this nobler profession.

I am thankful to all my friends for their kind co-operation in completing this

work.

I am highly indebted to my beloved parents, who framed a proper path for my

carrier. I remain ever great full to them.

I express my heartfelt gratitude to my brother, Prashant for constant help and

encouragement to move ahead.

My deepest gratitude to my husband , Dr. Rajendrakumar. Angadi for

enormous love & moral support.

I would like thank all my family members who have given love and care ,

during my studies.

It would not enough without remembering my lovely, sweet, little daughter,

Sanjana whose entry become turning point of life and brings cheerfulness throughout.

Finally I am thankful to all those persons who so helped directly or indirectly

for the completion of this work.

Date:

Place: Gadag Shashikala.B.Bani

LIST OF ABBREVIATION USED

A.H -Astanga hridayam

A.S - Astanga sangraha

C.S - Charaka samhita

D. Ni - Dhanwantari nighantu

DM - Diabetes mellitus

FBS -Fasting blood sugar

IDDM - Insulin dependent diabetes mellitus

K.Ni - Kaiyadeva nighantu

M. N - Madhava nidana

M. Ni -Madanapala nighantu

M.D.G - Madhava dravya guna

Ni. R - Nighantu ratnakara

Ni.A - Nighantu adarsha

NIDDM - Non-insulin dependent diabetes mellitus

OHA - Oral hypoglycemic agents

PPBS -Post partial blood sugar

R.Ni - Raja nighantu

S.K.D - Shabda kalpa druma

S.S - Sushruta samhita

US - Urine sugar

ABSTRACT

Background

Madhumeha which has been correlated with DM is a chronic metabolic disorder,

described more than 2000 years has become an epidemic with a world wide incidence

of 5% in the general population. The patients experiences significant morbidity and

mortality from microvascular, macrovascular complication .The drug from

contemporary science shows adverse effect and declines in their action after prolong

administration .Since immemorial time medicinal plants are used in such condition

and Avartaki (Cassia Auriculata ) is one among them, described as antidiabetic in

most of nighantu.

Objectives:

Evaluation of efficacy of Avartaki beeja and pushpa in the management of

Madhumeha and to evaluate the comparative hypoglycemic effect of Avartaki beeja

and Pushpa.

Methods:

In this prospective Comparative clinical study, 30 Patients of Madhumeha are selected

and randomly grouped as Group A and B receiving Avartaki beeja churna and

Avartaki Pushpa Churna respectively, for a duration of 30 days with dose of 2gms per

day. Efficacy was assessed by difference between baseline and assessment data.

Results:

A significant reduction in all the parameters was noted in both group. Individually

both groups are highly significant ( p< 0.001). But the comparison is non significant

except for 2 parameters trishna and ashaktata ( p <0.05 ) . Comparison of ‘t’ values

shows avartaki pushpa is more efficacious than beeja.

Interpretation :

The result shows both Avartaki beeja and pushpa are efficacious in the management

of madhumeha. The mean net effect of FBS is more in Group B .The mean effect of

trishna is same in both the groups

Conclusion:

The hypoglycemic effect of Avartaki pushpa and beeja is highly significant after

30days therapy and comparatively Avartaki pushpa is extremely effective in

management of madhumeha.

KEY WORDS

Avartaki beeja; Avartaki pushpa; Cassia auriculata; Madhumeha; Diabetes mellitus;

Antidiabetic; Hypoglycemic; FBS;

TABLE OF CONTENT

1. Introduction Page No.- 01

2. Objectives Page No.- 03

3. Review of Literature

• Drug review- Avartaki (Cassia auriculata) Page No.- 04

• Disease review- ►Madhumeha Page No.- 29

►Diabetes Mellitus (NIDDM) Page No.- 45

4. Methodology Page No.- 62

5. Result Page No.-75

6. Discussion Page No.- 119

7. Conclusion Page No.-123

8. Summary Page No.- 125

9. Bibliography Page No.- 127

10. Annexures Page No.- 141

List of Tables

SL No Tables Page No.

Drug review

1. Varga of Avartaki According to different nighantu 06

2. Synonyms according to different nighantu 08

3. Properties according to different nighantu 14

4. Therapeutic actions according to different nighantu 15

5. Therapeutic uses according to different nighantu 16

Disease review

6. Kaphaja Prameha according to Brihatrayess 38

7. Pittaja Prameha according to Brihatrayess 39

8. Vataja Prameha according to Brihatrayess 39

9. Aetiologic classification of Diabetes mellitus 47

10. Showing cells of islet of Langerhan and their relative hormones 50

11. Metabolic actions of insulin 52

12. Showing the symptoms of hyperglycemia 58

13. Showing the complications of DM 59

14. Showing the risk factors for type 2 DM 59

Methodology

15. Showing normal values of objective parameters 69

16. Pipetting scheme for determination of blood sugar 70

17. Observation for urine sugar 71

18. Gradation for subjective parameters to asses the result 73

SL No Tables Page No

Results

19. Demographic data 75

20. Data related to complaints 76

21. Data related to personal history 77

22. Data related to the srotodusti before and after the treatment 78

23. Subjective parameters of group A 79

24. Subjective parameters of group B 79

25. Objective parameters of group A 80

26. Objective parameters of group B 80

27. Showing the age ratio 81

28. Showing the sex ratio 82

29. Showing the incidence of religion 83

30. Showing the nature of occupation 84

31. Showing the socio economic state 85

32. Showing the diet 86

33. Showing the chronicity of madhumeha 87

34. Showing the complaints 88

35. Showing the family history 89

36. Showing the treatment history 90

37. Showing the ratio of involved agni 91

38. Showing the vyasana in relation with disease 92

39. Showing the Prakruti 93

40. Showing the kind of Ahara 94

41. Showing the vihara 95

SL No Tables Page No.

42. Showing the involvement of manasika chinta 96

43. Showing the comparison of udakavaha srotodusti lakshana before

and after the treatment 97

44. Showing comparison of medovaha srotodusti lakshanas before


45. Showing the comparison of mootravaha srotodusti lakshana before


46. Showing the Prabhoota mootrata before treatment in group A and group B 100

47. Showing the Prabhoota mootrata after the treatment in group A and group B 100

48. Showing the Avila mootrata before treatment in group A and group B 102

49. Showing the Avila mootrata after the treatment in group A and group B 102

50. Showing trishna before the treatment in group A and B 104

51. Showing trishna after the treatment in group A and B 104

52. Showing Ashaktata before treatment in group A and B 106

53. Showing Ashaktata After treatment in group A and B 106

54. Data showing the relief from complaint after treatment in both groups 108

55. Showing the result of group A 113

56. Showing the result of group B 114

57. Showing the total result 115

58. Individual study of Group A before and after the treatment 116

59. Individual study of Group B before and after the treatment 116

60. Comparative study of group A and group B after the treatment 117

List of Figures

SL .No Figures Page No

Graphs exhibited in the Results

1. Showing the age ratio 81

2. Showing the sex ratio 82

3. Sowing the incidence of religion 83

4. Showing the nature of occupation 84

5. Showing the socio economic state 85

6. Showing the diet 86

7. Showing the chronicity of madhumeha 87

8. Showing the complaints 88

9. Showing the family history 89

10. Showing the treatment history 90

11. Showing the ratio of involved agni 91

12. Showing the vyasana in relation with disease 92

13. Showing the Prakruti 93

14. Showing the kind of Ahara 94

15. Showing the vihara 95

16. Showing the involvement of manasika chinta 96

17. Comparison of udakavaha srotodusti lakshana before and after the treatment 97

18. Comparison of medovaha srotodusti lakshanas before and after the treatment 98

19. Comparison of mootravaha srotodusti lakshana before and after the treatment 99

20. Comparison of Prabhoota mootrata before and after treatment in group A 101

SL .No Figures Page No

21. Comparison of Prabhoota mootrata before and after treatment in group B 101

22. Comparison of Avila mootrata before and after treatment in group A 103

23. Comparison of Avila mootrata before and after treatment in group B 103

24. Comparison of trishna before and after treatment in group A 105

25. Comparison of trishna before and after treatment in group B 105

26. Comparison of Ashaktata before and after treatment in group A 107

27. Comparison of Ashaktata before and after treatment in group B 107

28. Showing the relief from complaint after treatment in both groups 108

29. Comparison of FBS before and after the treatment in group A 109

30. Comparison of FBS before and after the treatment in group B 109

31. Comparison of PPBS before and after the treatment in group A 110

32. Comparison of PPBS before and after the treatment in group B 110

33. Comparison of US before and after the treatment in group A 111

34. Comparison of US before and after the treatment in group B 112

35. Showing the result of group A 113

36. Showing the result of group B 114

37. Showing the total result 115

List of Photographs

1. Photograph showing the Avartaki pushpa and beeja 04

2. Photograph showing the steps of preparation of medicine 62

Introduction


Introduction 1

INTRODUCTION

Madhumeha is a chronic metabolic disorder and the symptom appears in

relation with a mootravaha samsthana. Diabetes mellitus is a chronic metabolic

endocrinal disorder, which has similar pathogenesis as the madhumeha .Thus the

comparison between madhumeha and DM is justifiable 1.

Madhumeha has become a global problem in spite of much advancement in

modern medicine2. The World Health Organisation stated in 1998 that a 122 % rise in

the number of adults with diabetes is projected by 2005, to reach 300 million adults

worldwide. There are four reasons for this two-fold global increase: Firstly, we are

living longer; over-nutrition and lack of exercise are prevalent; the disease being

transmitted in a hereditary fashion; Such transformations have taken place within the

Indian population also. In India, it is estimated that 19 million cases occurred in 1995,

rising to a projected 57 million by the year 2025 (1/6th of the world total). According

to recent epidemiological studies there has been a 40% increase in diabetes prevalence

amongst urban during the last five years3. Even the NIDDM a commonest form of

DM is most common accounting for 85-99% of the patient depending on geography

and ethnicity, occurs in adults, more so over 35 years of age4. The prevalence of

NIDDM is on the rise more alarmingly in the developing nations, ranked 7th among

leading cause of death. It has been rated 3rd when all its micro vascular , macro

vascular, neuropathic complications5 are taken into account6. The cost of treating

diabetes an associated complication exceeds $ 100 billion per year7.

It has long been recognized that drugs represents only part of the management

of madhumeha and other intervention such as education , modification of diet and

promotion of physical health play a crucial role. If the dietary control and exercise


Introduction 2

programmes do not improve the condition then the medication is added. Many of

patients won’t have patience for long term therapies, complicated therapies like

exercise etc8. The OHA viz Sulfonylurea, Bigunides have associated with adverse

effect like nausea, vomiting, lactic acidosis, hypersensitivity etc. After long term

administration their action declines, up to 50% patients of NIDDM initially treated

with OHA ultimately need insulin.9 Hence we find no satisfactory remedies for

madhumeha in contemporary medical science.

Medicinal plants since time immemorial have been used virtually in all

cultures as a source of medicine. Several herbs have been described in ayurvedic

treasure of therapeutics, which have a beneficial effect in the management of

madhumeha. Avartaki (Cassia auriculata) is one such drug which act as mootra

sangrahaneeya and also reduces the high blood glucose 10. The seeds and flowers of

this plant are indicated in the management of madhumeha11 .Thus in the present study

an attempt is made to evaluate the hypoglycemic action of Avartaki, with a view to

find out a therapeutically efficacious, safer, cost effective and easily available drug.

Objectives


Objectives 3

OBJECTIVES

1. To evaluate the efficacy of Avartaki pushpa churna in the management of

madhumeha.

2. To evaluate the efficacy of Avartaki beeja churna in the management of

madhumeha.

3. To evaluate the comparative hypoglycemic effect of Avartaki pushpa and

beeja churna.

Review Of Literature Drug Review

Avartaki

(Cassia Auriculata)


Drug review- Avartaki 5

DRUG REVIEW

AVARTAKI ►►CASSIA AURICULATA

Avartaki is a plant with yellow flowers and auricule shaped stipules exists

abundantly in country like India got a wide range of significance in social as well as

medicinal field since immemorial time.

HISTORY12

In vanaspati shastra by Jay Krishnan, Avartaki is explained as it exist since the

period of Ramayana. When Lord Ram was wandering in search of Sita towards

Lanka, saw this plant with bloomed flowers and his mind is pleased with beauty,

asked for any information regarding Sita. But flower with proud of its beauty not

answered . Rama got angry and cursed the flower to loose its fragrance and become

unfit for the worship , thus it should be used by leather workers.

Ramasiya se garva kiya jo te nara jagame haryo

Garva kiyo avalake phoolade , to jaye chamara kadame daryo

Later the flower begged apology. Humble hearted Rama put his feet on its head and

there fore foot mark appears on the seeds

Apart from above evidence there are few more literature. A Persian poet has

given simile to the flowers with his beloved’s eyes. A fairy tale popular in Marawad

region , that Avartaki grows so densely for which it become a border for two

kingdom.



Meaning of Cassia auriculata ►

Cassia → Quetsiah (Hebrew):Kasia ( Greek ) – Old Name used for the plant ,

Auriculata→Auricula (Latin) –Ear of the lobe [large ear lobe shaped pair of stipules]

present on the stem 13 .

GANA/ VARGA

Table 1.1 Showing the varga according to different Nighantu :

Madhava dravya guna Vividhoushadhi varga14

Dhanwantari nighantu Oushadhi varga15

Kaiyadeva nighantu Oushadhi varga16

Raja nighantu

Guduchyadi varga17

& Shatavhadi varga18

Madanapala nighantu Abhayadi varga19

Nighantu adarsha Pootikaranja varga20



Synonyms of Avartaki with their meanings

1. Avartaki :Stipules are present on the stem

2. Peetapushpa : It bears yellow coloured flowers

3. Raktaphali : Legume is red in colour during riped condition

4. Peetakeela : Corolla or petals are yellow in colour

5. Shimbiphala : Legumes are present on the plant

6. Peetika : It bears a yellow coloured flowers

7. Supushpa : The flowers have beautiful appearance

8. Hemapushpa : The flowers have golden colour

9. Kanchanapushpa : The flowers have golden colour

10. Sharapushpa : Flowers blooms in the sharat ritu

11. Peetakeelaka : It bears yellow coloured flowers

12. Peeta pushpika : It bears yellow coloured flowers

13. Charmaranga : Its bark is used for dyeing the leather

14. Rangalata : A plant useful for leather dyeing

15. Mahajalini : The plant which form a network by their spread

16. Mahadadijali : The plant which form a network by their spread

17. Mahada : The plant which form a network by their spread

18. Tilapusphika : Flowers resembles like flowers of tila

19. Vamavarta : The legumes are often twisted in nature

20. Raktapushpika :The flowers bears red lines in it

21. Raktapushpa : The flowers bears red lines in it

22. Dantakashta :The twig is used for brushing



Some other synonyms are,

Mayhari ,Talopoda, Bindukini, Vibhandi, Tindukini, Vishanika, Manojna,

Ahulya, Avala, Tarawar, Halurakhya, kara, Tarawat, Arbar and Nripamangalyaka.

SYNONYMS ACCORDING TO DIFFERENT NIGHANTU Table 1.2 Showing synonyms according to different Nighantu

Sr.no Synonyms D.N K.N R.N M.N Ni.Ad Ni.R 1 Avartaki + + + + + + 2 Charmaranga + + + + + + 3 Peeta pushpa + - + - - - 4 Peetakeelaka + + - - + + 5 Vibhandi + + + + - - 6 Mahajalini + + - + - - 7 Bindukini + + - + - - 8 Raktaphali - + - - - - 9 Tindukini - - + - - - 10 Vishanika - - + - - - 11 Rangalata - - + - - - 12 Manojna - - + - - - 13 Raktapushpi - - + + - - 14 Mahadadijali - - + - - - 15 Peetakeela - - + - - - 16 Vamavarta - - + - - - 17 Tilapushpika - - - + - - 18 Ahulya - - + - + + 19 Halurakhya - - + - - - 20 Kara - - + - - - 21 Taravat - - + - - - 22 Shimbiphala - - + - - - 23 Supushpa - - + - - - 24 Arbar - - + - - - 25 Dantakashta - - + - - - 26 Hemapushpa - - + - - - 27 Kanchanapushpa - - + - - - 28 Nripamangalyaka - - + - - - 29 Sharapushpa - - + - - -



VERNACULAR NAMES

Latin : Cassia auriculata

English : Tanner’cassia , Mature tea tree, Tanner’s senna

Hindi : Taravar , Aval , Dantvan ,Tarota

Marathi : Tarabad ,Taroda , Tarawad

Gujarati : Avala, Aawar

Tamil : Avaram , Avarai , Avirae, Sadurguli, Semmara, Summai

Telagu : Tangedu, Avara gida, Merakatanageda ,tangeru

Malayalam : Avar , aveeram , Jimute ,Ponnaviram

Kannada :Tangedu, Taravara gida, Avarike, Chakusina gida,

Tangayaree, Avara, Tatwada , Olletanagida , Sakusina , Tangadi , Tangedi

Bengali :Taravar

Cutch : Aawala

Duk : Taravara , avala

Berara : Tarota

Burma : Peikthingata

Ceylon : Matura tea

Chines : Kiang Mang , Kiang Mang Kiue Min

Lambadi : Olaniyaro



KULA Shimbi Kula

UPAKULA Pootikaranja Upakula22

FAMILY Leguminosae

SUB –FAMILY Caeselpiniaceae

Taxonomical Classification of Cassia auriculata 23

Kingdom : Plantae

Division : Angiospermae

Class : Dicotyledonae

Series : Calciflora

Order : Rosale

Family : Leguminosae

Sub –family : Caesalpiniaceae

Genus : Cassia

Species : auriculata

FEATURES OF CAESALPINIACEAE 24

Diagnostic features►

Leaves paripinnate ; flowers zygomorphic ; Calyx and Corolla 5, ascending imbricate;

Stamens 10 or less, free, gynoecium monocarpellary with marginal placentation .

Distribution ►It is commonly called Cassia family. The sub –family contains 135

genera which are cosmopolitan in distribution. In India it is represented by 110

species and more than 21 genera.



Vegetative Characters►

Habit→ It shows great variation in habit , i.e, may be trees , shrubs ,

undershrubs or herbs. Besides this sometimes all types of plants occurs in

same genus.

Root→ Tap and branched

Stem→ Erect, woody, herbaceous or climbing , branched , glabrous or

covered with prickles and spines.

Leaf→Alternate, leaf base pulvinate, compound unipinnate, bipinnate or

rarely simple ; stipules.

Floral Characters ►

Flower –Pedicellate, bractate , zygomorphic, complete , hermaphrodite,

slightly perigynous, pentamerous

Calyx – Sepals 5 , free, or connate, odd sepal anterior , imbricate aestivation.

Corolla – Petals 5.

Androecium – Stamens 10, free, reduction in number of stamens by the

formation of staminodes. In Cassia there are 3 posterior staminodes.

Gynoecium –Monocarpellary , ovary superior or slightly inferior , unilocular

with marginal placentation , straight or curved, hairy ; Style long ; Stigma

simple.

Fruit – Legume and never breaks up into one seeded parts

Seed – Non endospermic

Pollination – Entomophilous



MORPHOLOGY OF CASSIA AURICULATA25

A tall much-branched shrub; bark smooth, reddish-brown; branchlets finely

pubescent. Leaves 3/4 inch long; rachis densely fulvous-pubescent with an erect linear

gland between each pair of leaflets; stipules foliaceous, reflexed, very large,

rotundato-reniform, produced at the base on the side next the petiole into a long

subulate point, persistent. Leaflets 8-12 pairs, 1-1 by -3/8-1/2 inch, slightly

overlapping, oblong-obovate, obtuse or emarginate, mucronate, glabrous or finely

downy, dull green above, paler beneath, base usually rounded; petiolules 1/20 inch

long. Flowers large, reaching 2 inch across, in terminal and axillary corymbose

racemes; pedicels 3/4-1 inch long; bracts ovate, acuminate, caducous. Calyx glabrous;

segments leathery, concave, the 2 outer much smaller than the other 3. Petals with

long claws, crisped on the margin, bright yellow, veined with orange. Stamens 10, of

which the 3 upper are reduced to staminodes, the remaining 7 perfect, of which the 3

lower are larger than the 4 lateral ones. Pods 3-5 by 1/2-5/8 inch, flat, thin, papery,

oblong, obtuse, mucronate, pale brown, deeply depressed between the seeds, having a

crumpled appearance, transversely veined, pubescent. Seeds 10-20. Every leaf has an

ear-shaped leafy structure at the base of the stalk. Fruit turns brown when dry.

HABITAT

Avartaki is found in Maharastra , Gujarat ,Rajasthana and Madhya Pradesh 26. A tree

of height of 1-3 meters with yellow flowers grows wild in the central provinces,

western coast , South India and Ceylon 27.Apart from India it also grows in Ceylon or

Srilanka and Indomalaysia 28. A fairy tale popular in Gujarat states that it grows in

such a fashion that the King make over the border for his kingdom29.



PHYTOCHEMISTRY

Plant contains pyrrolizidine, alkaloids. Root contains flavone glycoside. Bark

contains tannin 25% and ash 5%30. Flowers contain Beta – sitosterols , kaempferol .

Seeds yield fatty oil consisting of palmatic oleic linoleic acids31.

A new leucoanthocyanin- goratensidine, characterized as 4`, 5, 7-

trihydroxyflavan-3, 4-diol; Ariculacacidin characterized as 5, 2` 4`- trihydroxyflavan-

3, 4-dial 32.

It posses constituents like polysaccharides, flavonoids, anthracene derivatives

and some dimeric procyanidins33

Leaves contains saturated higher fatty keto alcohols and emodin. The leaves

were found to contain quinines, anthraquinones ( carmine , cascara, mitxanthobe),

benzoquinones, naphthaquinones34.

Recent research on cassia auriculata stem bark revealed the presence of sterol ,

triterpenoid glycosides like O-B- D- xylopyranosides35.

4.8% of light –yellow oil and oil has about 75% unsaturated fatty acids.

Palmatic and oleic acid are the major components of fatty acids. Oligosaccharides and

galactomanose were detected from seeds 36.



PROPERTIES ACCORDING TO DIFFERENT NIGHANTU

Table 1.3 Showing properties according to different Nighantu

PROPERTIS D. Ni K.Ni R.Ni M.D Ni. R Ni. Ad

Kashaya + + + + + +

Tikta - + + + + +

RASA

Amla - - + - - -

VEERYA Sheeta + - + + + +

Rechaka - - - + + +

PRABHAVA Grahi - - - - + +

Vata + - - - + +

Pitta + + + + + +

DOSHAGHNATA

Kapha + + - + + +

Summarising all the properties 37

Guna- Laghu ,Rooksha

Rasa – Kashaya ,Tikta

Vipaka – Katu

Veerya – Sheeta

Doshaghnata- Kapha vata shamaka



THERAPEUTIC ACTIONS ACCORDING TO DIFFERENT NIGHANTU

Table Showing therapeutic action according to different Nighantu

Sr. no Karma D.Ni K.Ni M.Ni M. D Ni.R Ni. Ad R.Ni

1 Kustahara + - - - - - -

2 Urdhwabhagahara + - - + - - -

3 Adhobhagahara + - + + - - -

4 Shukravardhana + - - - - - -

5 Varnya - + - - + + -

6 Pramehahara - + - - + + -

7 Vamihara - + - - + + -

8 Krimihara - + - - + + -

9 Trishnahara - + - - + + -

10 Chakshushya - - - - + + +

11 Ruchya - - - - + + -

12 Vishahara - - - - + + -



THERAPEUTIC USES ACCORDING TO DIFFERENT NIGHANTU

Table Showing therapeutic uses according to different Nighantu

Sr.no Roga M.D D.Ni K.Ni M.Ni Ni.Ad Ni.R R.Ni

1 Kusta + + + + + + +

2 Atisara - + - - + + -

3 Shopha - + - + + + -

4 Gulma - + + - - - -

5 Udara - + + + - - -

6 Anaha - + + + - - -

7 Krimi - + + + - - +

8 Shotha - - + - + + -

9 Trishna - - + - - - -

10 Kandu - - + - + + +

11 Visha - - + - - - -

12 Vamana - - + - + + -

13 Shwasa - - + - - - -

14 Daha - - + + - - -

15 Rakta vikar - - + - - - -

16 Jwara - - + + + + -

17 Prameha - - + - - - -

18 Raktapitta - - + - - - -

19 Shukrakshaya - - + - - - -

20 Mukha roga - - - - + + +

21 Shoola - - - - + + +

22 Vrana - - - - + + +



USES

1. Decorticated seeds in fine powder or paste or valved local application to purulent

ophthalmia or conjunctivitis known as country sore eye.

2. Seeds with testa and their kernels are finely powered and blown into the eye or the

powder mixed with coconut or gigelly oil is applied to the sore eyes.

3. Seeds are also used in Diabetes and chylous urine.

4. The plant is used in the form of a powder mixed with honey or decoction

especially of flower buds, is administered in chylous urine and diabetes with

excellent results38.

5. Twigs are used as tooth brushes.

6. In the south of Ceylon, leaves are used as a substitute for tea

7. Coffee made from powdered seed or leaves is good substitute for coffee made

from seeds of coffee arabica and is prescribed in giddiness due to heart disease.

8. Flowers are used as pessaries in Gujarat to check excessive menstrual flow.

9. Infusion of bark is used for enemas, gargles etc as substitute for tannic acid or oak

galls.

10. Compound syrup is prescribed for nocturnal emission.

11. The infusion is used as a cooling drink in fever.

12. Kwatha prepared of root bark and stem bark is used for Andavriddhi.

13. In ancient period the people while roaming use as antidiarrhoeal ,they used to

chew the root bark and suck 2-3 drops of juice

14. The root bark is chewed with lavana and juice is sucked to get relief from the

Cholera, Ajeerna , Shoola , Vamana , Atisara.

15. If the animals suffers with Adhmana, Chichaka or Khasara, then the kwatha of

patra is given. In Atisara and Adhmana the patra kalka with lavana is given.



16. Patra are tied over the abdomen in udarashoola.

17. The juice of stem bark is instilled into eyes in chakshu peeda.

18. The paste of patra, sarjikshara and tamarind leaves is applied in sprain and

inflammation.

19. The bhashpita patra is tied over the shotha

20. A bed covered with leaves and covered with a lining, angara is kept under that bed

and seka is given in Angasthabdata and any traumatic inflammation.

21. The patra swarasa is used as gandoosha in mukhapaka 39.

Useful parts

Root, Leaves, Flowers, Legume, Bark and Seeds.40

Posology

Churna – 3-6 gms41

Infusion of leaves (1 in 20 ) – 1-2 ounces

Infusion of bark - 2- 4 drachms

Compound syrup (of flower, mixed with Mocha Rasa & Sarsaparik) – 3-4 drachms

Decoction of root (1 in 2 ) - 2-8 drachms

Electuary of seed - 2-4 drachms

Medicated baths of leaves42



RECENT RESEARCHES ON AVARTAKI43

1.Antihyperglycaemic and antioxidant effect of hyponidd, an ayurvedic

herbomineral formulation in streptozotocin-induced diabetic rats. Babu PS,

Stanely Mainzen Prince P. Department of Biochemistry, Annamalai University,

Annamalai Nagar-608002 Tamil nadu, India.

Hyponidd is a herbomineral formulation composed of the extracts of ten medicinal

plants ( Momordica charantia, Melia azadirachta, Pterocarpus marsupium, Tinospora

cordifolia , Gymnema sylvestre, Enicostemma littorale, Emblica officinalis, Eugenia

jambolana, Cassia auriculata and Curcuma longa). We have investigated hyponidd for

its possible antihyperglycaemic and antioxidant effect in diabetic rats. Rats were

rendered diabetic by streptozotocin (STZ) (45 mg kg(-1) body weight). Oral

administration of hyponidd (100 mg kg(-1) and 200 mg kg(-1)) for 45 days resulted in

significant lowered levels of blood glucose and significant increased levels of hepatic

glycogen and total haemoglobin. An oral glucose tolerance test was also performed in

experimental diabetic rats in which there was a significant improvement in blood

glucose tolerance in the rats treated with hyponidd. Hyponidd administration also

decreased levels of glycosylated haemoglobin, plasma thiobarbituric acid reactive

substances, hydroperoxides, ceruloplasmin and alpha-tocopherol in diabetic rats.

Plasma reduced glutathione and vitamin C were significantly elevated by oral

administration of hyponidd. The effect of hyponidd at a dose of 200 mg kg(-1) was

more effective than glibenclamide (600 microg kg(-1)) in restoring the values to near

normal. The results showed that hyponidd exhibits antihyperglycaemic and

antioxidant activity in STZ-induced diabetic rats.

2.alpha-Glucosidase inhibitory activity of some Sri Lanka plant extracts, one of

which, Cassia auriculata, exerts a strong antihyperglycemic effect in rats



comparable to the therapeutic drug acarbose. Abesundara KJ, Matsui T,

Matsumoto K.Division of Food Biotechnology,Department of Bioscience and

Biotechnology, Faculty of Agriculture, Graduate School of Kyushu University, 6-10-1

Hakozaki, Higashi-ku ,Fukuoka 812-8581, Japan.

Some Sri Lanka plant stuffs were examined regarding in vitro and in vivo alpha-

glucosidase (AGH) inhibitory actions. According to the results, water extracts and

methanol extracts of dried fruits of Nelli (Phylanthus embelica), methanol extracts of

dried flowers of Ranawara (Cassia auriculata), and water extracts of latex of

Gammalu (Pterocarpus marsupium) were found to have a potential AGH inhibitory

activity. In particular, Ranawara methanol extract showed the strongest AGH

inhibitory activity in vitro preferably on maltase giving an IC(50) value of 0.023

mg/mL and inhibited the maltase activity competitively. As a result of single oral

administration of Ranawara (C. auriculata) methanol extract in Sprague-Dawley rats,

a significant and potent lowering of blood glycemic response toward maltose

ingestion was observed at 30 min after dosing of 5 mg/kg, thus, concurrently

suppressed insulin activity. The ED(50) of the extract (4.9 mg/kg) clearly indicated

that the antihyperglycemic effect was as potent as that of therapeuticdrug

acarbose(ED(50)3.1mg/kg).

3.The effects of Cassia auriculata and Cardiospermum halicacabum teas on the

steady state blood level and toxicity of carbamazepine.Thabrew I, Munasinghe J,

Chackrewarthi S, Senarath S.Department of Biochemistry and Clinical Chemistry,

Faculty of Medicine, University of Kelaniya, 6, Talagolla Road, Ragama, Sri Lanka.

[email protected]

A study was conducted using male Wistar rats as the experimental model, to compare

the effects of concurrent administration of herbal tea prepared from dried flowers of



Cassia auriculata or aerial parts of Cardiospermum halicacabum and carbamazepine,

on (a). steady state serum levels of the prescription drug, and (b). changes in toxicity

(as assessed by changes in general behaviour, haematological parameters, and liver

and kidney function) that may occur due to drug interaction. Results demonstrate that

in rats receiving the Cassia auriculata tea and carbamazepine, the blood levels of the

prescription drug were significantly enhanced by 47.1% (P<0.04), when compared

with the levels in animals receiving only carbamazepine for the same time period,

with no apparent changes in toxicity. In animals receiving the Cardiospermum

halicacabum tea, there were no significant changes in the blood levels of

carbamazepine or drug-related toxicity. Cassia auriculata tea has therefore the

potential to influence the bioavailability of carbamazepine, and hence its therapeutic

actions. Concurrent ingestion of carbamazepine with herbal teas containing Cassia

auriculata is therefore best avoided by patients under treatment for epilepsy.

4.Possible interaction of herbal tea and carbamazepine.Thabrew MI, Munasinghe

TM, Chackrewarthi S, Senarath S.Department of Biochemistry and Clinical

Chemistry, Faculty of Medicine, University of Kelaniya, Ragama, Sri Lanka.

[email protected]

A study was conducted using Wistar rats to determine the effect of concurrent

administration of a herbal tea prepared from dried flowers of Cassia auriculata and

carbamazepine on (a) blood levels of the prescription drug and (b) changes in toxicity

(as assessed by changes in hematological parameters, liver and kidney function, and

histology of major body organs) that may occur due to drug interaction. Results

demonstrate that in rats receiving the herbal tea and carbamazepine, the blood levels

of the prescription drug were significantly enhanced by 47.1% (p <0.04) when

compared with the levels in animals receiving only carbamazepine, with no apparent



changes in toxicity. Concurrent ingestion of the herbal tea prepared from Cassia

auriculata flowers with carbamazepine may therefore influence the bioavailability of

the prescribed drug and hence its therapeutic potential

5.Activity of Cassia auriculata leaf extract in rats with alcoholic liver injury.

Kumar Rajagopal S, Manickam P, Periyasamy V, Namasivayam N. Department of

Biochemistry, Annamalai University, Annamalainagar 608 002, Tamilnadu,India.

This study was undertaken to investigate the effect of Cassia auriculata leaf extract on

tissue lipid peroxidation and antioxidant status in experimental hepatotoxicity.

Administering ethanol to rats for 60 days resulted in significantly elevated levels of

serum total bilirubin, aspartate transaminase (AST), alanine transaminase (ALT) and

alkaline phosphatase (ALP) as compared with those of the experimental control rats.

Significantly elevated levels of tissue thiobarbituric acid reactive substances

(TBARS), hydroperoxides and lowered activities of superoxide dismutase (SOD),

catalase (CAT) and reduced glutathione (GSH) were also observed on alcohol

treatment as compared with those of experimental control rats. Concentration of

serum non-enzymic antioxidants such as vitamin E and vitamin C were also

significantly lowered on alcohol supplementation. Treatment with Cassia auriculata

leaf extract at a dose of 250 mg kg(-1) body weight and 500 mg kg(-1) body weight to

rats administered alcohol, lowered the levels of TBARS and hydroperoxides and

elevated the activities of SOD and CAT and the levels of reduced GSH in the liver,

brain, kidney and intestine significantly compared to unsupplemented alcohol treated

rats. Cassia auriculata leaf extract treatment restored the serum vitamin E, and vitamin

C levels also to near those of the experimental control animals. Our data indicate that

supplementation with Cassia auriculata leaf extract can offer protection against free

radical mediated oxidative stress in experimental hepatotoxicity. In addition,



histopathological studies of the liver and brain confirmed the beneficial role of Cassia

auriculata leaf extract.

6.Effect of Cassia auriculata flowers on blood sugar levels, serum and tissue

lipids in streptozotocin diabetic rats.Pari L, Latha M.Department of Biochemistry,

Faculty of Science Annamalai University, Annamalai Nagar Tamil Nadu-608 002,

India.

AIM OF THE STUDY: The main aim was to demonstrate the effects of Cassia

auriculata flowers on blood glucose and lipid levels in experimental diabetic rats.

METHODOLOGY: Aqueous extract of Cassia auriculata flowers was administered

orally and different doses of the extract on blood glucose, haemoglobin, glycosylated

haemoglobin, serum and tissue lipids, hexokinase and glucose-6-phosphatase in

streptozotocin-induced diabetic rats were studied. Glibenclamide was used as standard

reference drug. RESULTS: Cassia auriculata flower extract (CFEt), at doses of 0.15,

0.30 and 0.45 g/kg body weight for 30 days, suppressed the elevated blood glucose

and lipid levels in diabetic rats. Cassia auriculata at 0.45 g/kg was found to be

comparable to glibenclamide. CONCLUSION: Our findings indicate that the Cassia

auriculata flowers possess antihyperlipidaemic effect in addition to antidiabetic

activity

7.Preventive effects of Cassia auriculata L. flowers on brain lipid peroxidation in

rats treated with streptozotocin.Latha M, Pari L.Department of Biochemistry,

Faculty of Science, Annamalai University, Annamalai Nagar, Tamil Nadu, India.

The effect of aqueous extract of the flowers of Cassia auriculata were examined on

antioxidants and lipid peroxidation in the brain of streptozotocin diabetic rats.

Significant increase in the activities of superoxide dismutase, catalase, glutathione

peroxidase, glutathione-S-transferase and reduced glutathione were observed in brain



on treatment with Cassia auriculata flower extract (CFEt) and glibenclamide. Both the

treated groups showed significant decrease in thiobarbituric reactive substances

(TBARS) and hydroperoxide formation in brain, suggesting its role in protection

against lipid peroxidation induced membrane damage. Since the study of induction of

the antioxidant enzymes is considered to be a reliable marker for evaluating the

antiperoxidative efficacy of medicinal plant, these findings are suggestions of possible

antiperoxidative role played by Cassia auriculata flower extract.

8. Antihyperglycaemic effect of Cassia auriculata in experimental diabetes and

its effects on key metabolic enzymes involved in carbohydrate metabolism. Latha

M, Pari L. Department of Biochemistry, Faculty of Science, Annamalai University,

Annamalai Nagar, TamilNadu, India.

1. In experimental diabetes, enzymes of glucose and fatty acid metabolism are

markedly altered. Persistent hyperglycaemia is a major contributor to such metabolic

alterations, which lead to the pathogenesis of diabetic complications. To our

knowledge, there are no available reports on the enzymes of hepatic glucose

metabolism of Cassia auriculata flower against diabetes. The present study was

designed to study the effect of Cassia auriculata flower extract (CFEt) on hepatic

glycolytic and gluconeogenic enzymes. 2. Streptozotocin diabetic rats were given

CFEt (0.15, 0.30 and 0.45 g/kg) or 600 microg/kg glibenclamide for 30 days. At the

end of 30 days, blood glucose, plasma insulin, haemoglobin, glycosylated

haemoglobin, glycolytic and gluconeogenic enzymes were assessed. 3.

Administration of CFEt at 0.45 g/kg significantly decreased blood glucose,

glycosylated haemoglobin and gluconeogenic enzymes and increased plasma insulin,

haemoglobin and hexokinase activity. Similarly, administration of glibenclamide

showed a significant effect; however, CFEt at 0.15 and 0.30 g/kg did not show any



significant effect. 4. In conclusion, the observations show that the aqueous extract of

CFEt possesses an antihyperglycaemic effect and suggest that enhanced

gluconeogenesis during diabetes is shifted towards normal and that the extract

enhances the utilization of glucose through increased glycolysis. The effect of CFEt

was more prominent than that of glibenclamide.

9.Effect of Cassia auriculata leaf extract on lipids in rats with alcoholic liver

injury. Kumar RS, Ponmozhi M, Viswanathan P, Nalini N. Department of

Biochemistry, Annamalai University, Annamalainagar, Tamilnadu, India.

We studied the effect of administering Cassia auriculata leaf extract to rats with

experimentally induced liver damage. Hepatotoxicity was induced by administering

9.875 g/kg bodyweight ethanol for 30 days by intragastric intubation. C. auriculata

leaf extract was administered at a dose of 250 mg/kg bodyweight daily in one group

and 500 mg/kg bodyweight daily in another group of alcohol-treated rats. All rats

were fed with standard pellets. The control rats were also given isocaloric glucose

solution. The average bodyweight gain was significantly lower in alcohol-treated rats,

but improved on supplementation with C. auriculata leaf extract. Alcohol

supplementation significantly elevated the cholesterol, phospholipid and triglyceride

concentration in the liver, brain, kidney and intestine, as compared with those of the

normal control rats. Treatment with C. auriculata leaf extract and alcohol significantly

lowered the tissue lipid levels to almost normal levels. Microscopic examination of

alcohol-treated rat liver showed inflammatory cell infiltrates and fatty changes, which

were reversed on treatment with C. auriculata leaf extract. Similarly, alcohol-treated

rat brain demonstrated spongiosis, which was markedly reduced on treatment with C.

auriculata. In conclusion, this study shows that treatment with C. auriculata leaf

extract has a lipid-lowering effect in rats with experimentally induced, alcohol-related



liver damage. This is associated with a reversal of steatosis in the liver and of

spongiosis in the brain. The mechanism of C. auriculata leaf extract lipid-lowering

potential is unclear.

10.Effect of Cassia auriculata Linn. on serum glucose level, glucose utilization by

isolated rat hemidiaphragm.Sabu MC, Subburaju T.Amala Cancer Research Center,

Amala Nagar, Thrissur 680 553, Kerala, India. [email protected]

An aqueous leaf extract of Cassia auriculata (C. auriculata) was found to lower the

serum glucose level in normal rats. Maximum reduction in serum glucose level was

observed after 4 h at a dose levels of 100, 200, 400 mg/kg body weight of the extract.

In normal rats the serum glucose level reduction at 4th h was 23% by 100 mg/kg body

weight and 31% by 200 mg/kg body weight. In alloxan-induced diabetic rats, chronic

administration of the extract significantly reduced the serum glucose level from third

day to till the end of the experiment. The extract was also found to inhibit the body

weight reduction induced by alloxan administration. Glucose uptake and glycogen

deposition studies suggest that C. auriculata leaf extract probably has no direct insulin

like effect which can enhance the peripheral utilization of glucose.

11.Antihyperglycaemic effect of Diamed, a herbal formulation, in experimental

diabetes in rats. Pari L, Ramakrishnan R, Venkateswaran S.Department of

Biochemistry, Annamalai University, Tamil Nadu, India. [email protected]

Diamed is a herbal formulation composed of the aqueous extracts of three medicinal

plants (Azardirachta indica, Cassia auriculata and Momordica charantia). We have

investigated Diamed for its possible antihyperglycaemic action in rats with alloxan-

induced experimental diabetes. Oral administration of Diamed (1.39 (0.25 g), 1.67

(0.30 g) or 1.94 (0.35 g) mL kg(-1)) for 30 days resulted in a significant reduction in

blood glucose, glycosylated haemoglobin, and an increase in plasma insulin and total



haemoglobin. The effect was highly significant after administration of the 1.94 mL

(0.35 g) g(-1) body weight dose. Diamed also prevented a decrease in body weight.

An oral glucose tolerance test was performed in experimental diabetic rats in which

there was a significant improvement in glucose tolerance in the animals treated with

Diamed. The effect was compared with 600 microg kg(-1) glibenclamide. The results

showed that Diamed had antihyperglycaemic action in experimental diabetes in rats.

12.Constituents of Cassia auriculata.Nageswara Rao G, Mahesh Kumar P,

Dhandapani VS, Rama Krishna T, Hayashi T. Department of Chemistry, Sri Sathya

Sai Institute of Higher Learning, Prasanthi Nilayam 515 134, Andhra Pradesh, India.

The isolation and spectral data of di-(2-ethyl) hexyl phthalate (1) from Cassia

auriculata leaves are reported.

13.Antibacterial activity of some folklore medicinal plants used by tribals in

Western Ghats of India. Samy RP, Ignacimuthu S. Entomology Research Institute,

Loyola College, Chennai, India

A series of 30 Indian folklore medicinal plants used by tribal healers to treat

infections, were screened for antibacterial properties at 10 mg/ml concentration by

using disc diffusion method against Bacillus subtilis, Escherichia coli, Klebsiella

aerogenes, Proteus vulgaris, Pseudomonas aerogenes and Staphylococcus aureus.

Twenty plant species showed activity against one or more species of bacteria used in

this assay; among them the leaf extracts of Cassia occidentalis and Cassia auriculata

exhibited significant broad spectrum activity against B. subtilis and S. aureus. Ten

plant species were not found active against all tested bacteria. These results were

compared with results obtained using standard antibiotics, chloramphenicol (30

microg/disc) and streptomycin (30 microg/disc) which served as a reference for

inhibition zone diameter.



14.Studies on medicinal plants of Sri Lanka: occurrence of pyrrolizidine

alkaloids and hepatotoxic properties in some traditional medicinal herbs.

Arseculeratne SN, Gunatilaka AA, Panabokke RG.

There is a paucity of data on the occurrence of hepatotoxic and hepatocarcinogenic

pyrrolizidine alkaloids in medicinal plants, and there are no data on the hepatotoxic

properties of herbal medicines that are used in the traditional pharmacopoiea of Sri

Lanka and other Asian and African countries. In view of the extensive consumption of

these herbs and the occurrence of chronic liver diseases including hepatocellular

cancer in this and other countries of South Asia, we have screened fifty medicinal

plants for pyrrolizidine alkaloids and have obtained positive results with three species,

namely Crotalaria verrucosa L., Holarrhena antidysenterica (L.) Br., and Cassia

auriculata L. Feeding trials in rats with materials from these three species produced

liver lesions--disruption of the centrilobular veins, congestion or haemorrhage in the

centrilobular sinusoids, centrilobular or focal hepatocellular necrosis--and

histopathology in the lungs and kidneys which were compatible with the action of

pyrrolizidine alkaloids. The presence of alkaloids in C. auriculata has not been

previously reported nor has the presence of pyrrolizidine alkaloids in H.

antidysenterica. It is suggested that the consumption of herbal medicines that contain

pyrrolizidine alkaloids could contribute to the high incidence of chronic liver disease

including primary hepatocellular cancer in Asian and African countries.

15.Chemical and spectral studies of novel keto-alcohols from the leaves of Cassia

auriculata.Varshney SC, Rizvi SA, Gupta PC.

16.[Presence of leucoanthocyanic chromogens in Cassia auriculata and C.

goratensis Fres., adulteration of official sennas.][Article in French]PARIS R,

CUBUKCU

Review Of Literature

Disease Review

Madhumeha


Disease review- Madhumeha 29

DISEASE REVIEW

MADHUMEHA

Madhumeha is a disease itself manifesting in one of the trimarma namely

basti. Though it is a endocrinal problem, disorder of metabolism it is included under

mootravaha srotovikara, because its manifestation is seen in mootravaha srotas 44.

Prameha literally formed by two words , Pra means the excessive, Meha

means the discharge. It means the frequent excretion of excessive urine45 , disease

where excessive dirty or contaminated (turbid ) urine is excreted46.

Synonyms for prameha

Meharoga,

Mehagada

Mehovikara

Bastiroga

Characteristics of prameharoga

1. Chirakaleena : chronic illness

2. Anushangitwa : relapsing type of illness

3. Mahagada : one of 8 mahagada mentioned by Sushruta

4. Beejadoshat-kulajavyadhi :may be congenital, hereditary inherited disease,

Nirukti for Madhumeha:

madhu upadan bhuto madhumeha

Madhumeha is also comprised of two words. Madhu- like honey, meha- discharge.

The patient passes urine similar in colour and taste of honey 47.



HISTORY 48

In India the history of the disease madhumeha is recorded since immemorial

time. Purana etc. have defined the condition in which the whole body become sweet.

Vedic literature a oldest literature of the world, named the disease as Astravam

which means mutratisara. i.e. excessive micturation as in the Atharva veda.

In later period, all the Samhitas from Charaka to Vagbhata’s deal with the

aetiology symptomology, pathology, prognosis, complication , principles of the

treatment , and different kind of management , under the different contexts mainly in

the nidana and chikitsa sthana.

Further literatures of late period, Madhava, Sharngadhara, Bhvaprakash etc

have explained the different treatment modalities with the existing. After the 16th

centuray several books related to the Madhumeha are published with its advanced

treatment.

NIDANA

Nidana of the Prameha are expressed as general those are common for all

kinds of prameha. Specific nidana manifests the particular kind of prameha such as

madhumeha.

General :

Sedentary habits, excessive sleep, excessive use of curds, soup of meat of

domestic animals or aquatic or marshy animals, milk derivatives (processed milk)

new curds, drinks, various processed jaggery etc and kapha promoting regimes are the

aetiological factors of prameha 49.

Sushruta recognizes, day sleep, lack of exercise, sitting idle, cold intake of

cold, unctuous, sweet, fatty liquid food and drinks in excess gradually lead to the

occurrence of prameha50.



Vagbhata’s, describes in a nut shell, that whatever food and regimes

promotive of kapha, meda, mootra are to be regarded as prameha hetu 51.

Specific nidana to madhumeha

As Charaka has stated in sutra sthana, the excessive intake of heavy,

unctuous, saline substances, use of new rice (freshly harvested crop) , fresh wine,

excessive sleep, injudicious use of varieties of dishes, who has given up physical and

mental exercise and taken to inactiveness, abandonment of elimination of procedures,

etc are the specific aetiological factors for madhumeha 52.

SAMPRAPTI

General :

Charaka had clearly explained the samprapti of the kaphaja prameha in the

prameha Nidana . Even though the disease prameha is stated to be due to the vitiation

of tri-doshas, the specific factors of the dosha is excessive fluidity of kapha . The

special features of the susceptible body elements (dushyas) are excessiveness and

diminished viscouness of Medas, Mamsa, Shareerakleda, Shukra, Rakta, Vasa, Majja,

Lasika, Rasa and Ojus.

When there is the simultaneous congress of these three pathological

conditions, the kapha is suddenly provoked since it is already in chaya stage. The

vitiated kapha quickly spreads throughout the body which is already in deranged

condition. In the path of its circulation the kapha first encounters and mixes with the

meda, owing to the pathological changes in the meda viz. excessiveness and

diminished viscous ness and also owing to the great similarity of the qualities

between the kapha and medas. Due to this combination of vitiated kapha and medas,

the latter is vitiated. The vitiated kapha coupled with the vitiated medas now comes in

contact with the shareera kleda and mamsa which are in excessive increase in the



body. The vitiated body fluid is changed into urine. The orifices or pores of the

mootravahasrotas, represented by the kidney and bladder are in a state of dilatation

due to the actions of vitiated medas and shareera kleda. The vitiated kapha , upon

reaching the mootravaha srotas gets localised there and thus develops the disease

called Prameha54.

The shareera kleda combined with the kapha and the medas while being

converted into urine on its entrance in to the mootrashaya acquires the following ten

pathological characteristics of kapha. They are unctuousness, heaviness, sweetness,

denseness and slowness. Then it acquires a special name accompanied with the

qualities of one or more of the other conditions by which it has been mainly

modified55.

The vitiated pitta and vata produces vataja and pittaja Prameha by the same

process as described above56.

If vata by its rooksha quality changes the ojus which is naturally of sweet

taste, in to one of astringent taste and carries it to the mootrashaya, then it causes the

condition called Madhumeha57.

Charaka in Prameha Chikitsa has explained the samprapti in brief 58. “The

kapha having vitiated the medas and mamsa dhatus and the body fluid, becomes

localised in the genito – urinary system and causes Pramehas59. The pitta, too, which

is provoked by ushna dravyas vitiating those very tissues, causes in the same manner

other varieties of prameha. On the diminution of the other two doshas the morbid vata

draws into the genito – urinary system the essential dhatus, and give rise to the third

group of Prameha. In every case the morbid humor, having reached the genitor

urinary system, vitiates the urine and generated Prameha corresponding to its specific

nature.



In a person who indulges in the mithya ahara vihara the three doshas which are

vitiated and in an↓ immature state join the medas and travel to the mootravaha srotas,

gets localised at the entrance of the basti, when they are emitted through the urethra

the disease is known as Prameha.

“The deranged kapha, in conjunction with the (morbid) pitta, vayu and medas,

gives rise to all kaphaja types of Prameha. The deranged pitta, in conjunction with the

deranged vayu, kapha, rakta and medas produced the pittaja ones; while the deranged

vayu, in union with the deranged kapha, pitta ,medas ,majja and vasa, engenders the

types of vataj prameha60.



Samprapti charka 61

Nidana sevana

↓ Kapha pradhana tridosha prokopa

↓ Agnimandya

↓ Amotpatti

↓ Samadosha kaphasthana anupravesha

↓ Rasam prapya (Oja sthana)

↓ The aggravated morbidity readily disperses as it can not be digested and assimilated

↓ due to deficient resistance or disintegrated body mechanism

↓ Augments while spreading and localizes where there is weakness

↓ Morbidity combined with medas, comes in contact with body fluids and muscles

↓ Increased quantity and decreased viscosity of medas, the intensified derangement of

kapha with more and identical proportion of medas

↓ This deranged dosha reaches the urinary system

↓ Exceed in normal quantity

↓ Apanadusti occurs due to obstruction and vitiates the vruk and brings about excessive

discharge of urine.

↓ diseased named as Prameha



Specific samprapti of Madhumeha 62

Charaka and Vagbhata’s have described the pathogenesis of Madhumeha as

separate from Prameha .Constant use of the specific nidana , leads to augmentation of

pitta kapha meda and mamsa which obstructs the vata in its route. Thus enraged vata

carries ojus along and drives it down through the urinary system giving rise to

madhumeha. The sign and symptoms pertaining to vata or avruta doshas which occur

and disappear indefinitely (but the recurrence is in more severe form) and frequently.

Vagbhata’s state that the pathogenesis of Madhumeha is of two varities63

1. The depletion of the dhatu leading to the vitiation of vata

2. Obstruction to the normal circulation of vata by the other doshas leading to the

vitiation of the former

This particular information leads us to include that Madhumeha is mainly due to

the vitiation of vata. Even according to Charaka, madhumeha is enumerated as one of

the vataja Pramehas. Vagbhata’s has also stated that any prameha if not treated and

attended to at the outset, will ultimately develop into Madhumeha. He has also clearly

stated that there is an increase in the sweetness in the body, which is expressed

through the physical qualities of urine, being the colour and taste resembles honey 64

According to Vagbhata’s, there is an increase in the sweetness or sweet substances

in the body of a Madhumeha patient 65. This particular fact is noticed by the sweetness

of the urine that can be observed and recognised by attraction and assemblage of ants

near the urine66. The urine of a normal or healthy person is not sweet in taste. This

sweetness of the urine of a Madhumeha patient is due to the madhura dravya, which is

filtered by the mootravaha srotas.



POORVARUPA

The state of prodroma or poorvarupa is expressed as when vitiated doshas

become localised due to srotovaigunya leading to the dosha-dushya-sammurchana.

Kapha predominant tridoshas and dhatus along with ojus are chiefly affected in

Prameha.

The following are the prodroma of Prameha.

1. Burning sensation of the palms of hands and the soles of the feet67.68,69 2. Sweet taste in the mouth.

3. Increased excretement in the body, increased discharged from the orifices in

the body70,71

4. Dryness in Coldness or sliminess of the skin and limbs, thermalgia and

numbness in the body.

5. Raw-meet odour in the body.

6. Somnolence and continuous torpor and lassitude.

7. Attraction of insects and ants to the body and urine72.

8. Matting of the hair and inordinate growth of the finger and toe nails73.74

9. Dryness in the mouth, palate and throat and thirst.

10. Slimy mucous deposit on the tongue, palate, pharynx and teeth.

11. Heaviness of the body.

12. Sweetness and whiteness of urine.

13. A bad odoured breath and shortness of breath75.

Vagbhata’s has mentioned additional prodroma for Prameha76

1. Excessive perspiration.

2. Laziness.

3. Liking of cold comforts.



ROOPA In the Roopavastha or actual manifestation of the disease, dosha dushya sammurchana

completes, and the onset of the disease will be commenced. The Roopa may change

from time to time and certain symptoms may newly appear or some may disappear.

Madhumeha

Clinical features of the present disease Madhumeha are divided into two groups.

1. General features of Prameha

2. Specific features of the Madhumeha

Charaka has not described the general features of Prameha where as

Sushruta77 and Vagbhata78 have described the general features as

a. Avila mootrata

b. Prabhoota mootrata

Specific Lakshanas of Madhumeha

It is one among the four Vataja Pramehas. Charaka states that ojus is sweet by

instinct. The rookshata of aggravated vata transforms sweetness into astringent taste

and carries along to urinary system and brings about madhumeha. The person with

Madhumeha thus passes urine which is astringent and sweet in taste, yellowish or

whitish in colour. The urine contains similar properties of Honey79.80.81.Even some of

the poorvaroopa lakshana may present in this condition.

Apart from the above lakshanas, Sushruta described typical lakshanas for Madhumeha

rogi82, that he prefers-

1. To stay while walking.

2. To sit while staying

3. To take rest on bed while sitting

4. To go to sleep while taking rest.



BHEDHA

Though Prameha is stated to be developed due to the vitiation

of all three doshas, the disease is mainly divided into three groups.

1. Kaphaja Pramehas – which are again subdivided into 10 types 83.

2. Pittaja Prameha – which are again subdivided into 6 types 84.

3. Vataja Prameha – which are again subdivided into 4 types 85.

Even though the three Ayurveda authorities Charaka, Sushruta And Vagbhata’s agree

the same number of Prameha in each group, there seems to be difference in the

nomenclature used by them. Increased quantity of urine and increased turbidity in the

urine are the main features in all varieties of Prameha.

The name of each variety of Prameha is based on the combination of dosha and

dushya, and the physical characters of the urine.

Kaphaja Prameha

Table showing Kaphaja prameha according to Brihatrayees

C.S86 S.S87 AS88

Udakameha Udakameha Udakameha

Ikshumeha Ikshumeha Ikshumeha

Sikatameha Sikatameha Sikatameha

Sanairmeha Sanairmeha Sanairmeha

Sandrameha Sandrameha Sandrameha

Sukrameha Sukrameha Sukrameha

Sandraprasadmeha ------------ -------------

Shuklameha Pishtameha Pishtameha

Sheetameha ------------ Sheetameha

Alalameha ------------ Alalameha

-------------- Surameha Surameha

-------------- Lavanameha Lavanameha

------------- Phenameha ---------------



Pittaja Prameha

Table showing Pittaja prameha according to Brihatrayees

CS 89 SS 90 AS 91

Ksharameha Ksharameha Ksharameha

Kalameha --------------- Kalameha

Neelameha Neelameha Neelameha

Lohitameha Shonitameha Raktameha

Manjishtameha Manjishtameha Manjishtameha

Haridrameha Haridrameha Haridrameha

--------------- Amlameha --------------

.

Vataja Prameha

Table showing prameha according to Brihatrayees

CS 92

SS93 AS94

Vasameha Vasameha

Vasameha

Majjameha -----------

Majjameha

Hastimeha Hastimeha Hastimeha

Madhumeha Kshoudrameha

Madhumeha

---------- Sarpirmeha -------------



MADHUMEHA:

Madhumeha can be sub classified mainly into two types.

Type one a) Kulaja or Sahaja (Hereditary)

b) Doshaja or Apathya nimittaja (acquired) 95

Type two a) Dhatu kshaya janya Madhumeha96

b) Doshavruta janya Madhumeha

Charaka has divided the Madhumeha patient into two varieties based on the line of

treatment 97.

1. Sthoola (stout or strong)

2. Krisha ( emaciated or week)

Sushruta accepts Sahaja rogi as krisha and the Apathya nimitaaja rogi as sthoola rogi

in his classification

SADHYASADHYATA

As discussed earlier, Prameha is classified in to three verities i.e.

1. Kaphaja Pramehas - 10

2. Pittaja Prameha - 6

3. Vataja Prameha - 4

The ten kaphaja Prameha are said to be sadhya (curable) 98,99.

Because

The medas having homogenous properties is affected

The Kapha is dominant

Both these factors are amendable to the same type of treatment.



The six pittaja Pramehas are only Yapya (palliable) 100,101 owing to the

proximity of the seat of the vitiated doshas and that of the medas and owing to the

antagonism involved in their treatment.

The four varieties of Vataja Prameha due to the vitiation of Vata are known to

be incurable 102, 103, because of their seriousness and also because of the contradiction

involved in their treatment.

Vagbhata’s adds to the above

• The kaphaja and Pittaja groups of Prameha if they are developed after full

expression of prodroma too are incurable104

• Kaphaja Pramehas gradually develops into pittaja pramehas and they both

transforms into vataja pramehas that are incurable

• If kaphaja pramehas gradually turns into pittaja pramehas these are yapya

• Even the pittaja pramehas are curable if there is no severe vitiation of medas

even this is applicable for vataja mehas 105

Charaka has stated that this disease is relapsing in nature .Though certain varieties

are stated to be curable they appear to be so only for certain period and relapse is

definite.

Madhumeha, which is a variety of vataja prameha is also to be considered, as

incurable but with specific line of treatment these can be palliable. Jata pramehi or

beeja doshaja are incurable due to leenata of dosha and as they themselves influence

on prakriti of patient.

Sushruta stated that if prameha patient suffering with pidikas and complications

like Hridgraha, then he should be considered as incurable106.



UPADRAVA

If all the Prameha are not treated properly and attended, they may ultimately

develop into Madhumeha107. Madhumeha is considered to be one of the 20 Prameha

by Charaka. Apart form this charaka has been described the updravas of Prameha in

general. Where as Sushruta and Vagbhata’s have mentioned upadravas separately for

each doshik group.

The general upadravas of Prameha according to Charaka are as follows108.

Trishna, Atisara, Jwara, Daha, Dourabalya, Arochaka, Avipaka, Putimamsa, Pidika,

Alaji, Vidradhi.

Charaka mentioned the upadravas (complications) of Madhumeha as 109

Trishna, Shwasa, Mamsakotha, Moha, Hikka, Mada, Jwara, Visarpa among them

many of upadravas are seen in patient.

CHIKITSA

Madhumeha is a chronic disease and may also develop as a hereditary disease.

Madhumeha patients are divided in two varieties.

1.Sthoola and 2. Krisha

Sthoola patient are capable of withstanding the shodhana karma and the krisha patient

are incapable of withstanding it. Therefore a sthoola patient has to be treated with the

shodhana chikitsa and krisha with shamana chikitsa110.

Shodhana

For every Shodhana procedure the patient should undergo poorva karma. But

the Madhumeha patient is prohibited from undergoing sweda karma111. In sthoola

patient after completion of sneha karma the doshas should be eliminated through

sodhana vamana and virechana karma respectively.



After the completion of the shodhana karma the patient has to be subjected for

samsarjana karma. Even though the Madhumeha is santarpana janya roga, the patient

should not be subjected to Apatarpana kriya, because it may result in to Gulma,

Kshaya, Mehanashoola, Vasti shoola and Mootra graha. The Brimhana chikitsa

should be carried out considering the strength of the individual patient112. A krisha or

emaciated, and Durbala or weak patient who is not capable of standing the shodhana

karma requires Bhrimhana chikitsa113.

Even though the vataja Pramehas are stated to be incurable the duty of

physician is to treat the patient and prevent the future complications. Therefore vataja

Prameha should be treated.

Samshamana Chikitsa

Samshamana chikitsa is indicated for a prameha patient who is not fit for

shodhana chikitsa, and also the patient who has completed the shodhana karma.

Many varieties of decoctions, choornas and lehyas have been described for the

treatment of the twenty varieties of Pramehas by all Ayurvedic authorities. Vyayama,

udvarthana, snana, jala sechana and the lepas with Twak, Ela, Agar and chandana are

useful in Prameha patient114.

Avoiding the causative factors (Nidana) is also treatment115. In our trial we

have used only shamana therapy, which has yielded a significant result.

The patient of Prameha who is not fit for evacuation should be subjected to

pacificator management for alleviation of the disease such as mantha (churned drink),

extracts, linctuses made of barley powder and light edibles. He should eat rough food

articles such as boiled barley, barley cakes, flour of parched grains and apupa with

palatable meat – soup of wild birds particularly gallinaceous and peckers. He should

take old shali rice with soup of mudga etc, and bitter vegetables added with oil of



danti and or linseed and mustard. In cereals, he should use shashtika and wild rice.

The diet of the patient of Prameha should consist mainly of barely. One suffering

form kaphaja Prameha should consist mainly of barley added with honey. Barley

grain dipped in decoction of Triphala for the whole night make a saturating food taken

with honey. The patient may also take them regularly mixed with vinegar for

alleviation of Prameha. He should use flour of parched grains, bolus, purchased

grains and other various edibles made of barley impregnated with decoction of drugs

prescribed in kaphaja Prameha, various preparations of barley mixed with the meat of

ass, horse, bull . Swan and spotted deer should be prescribed. The seeds of bamboo

and wheat may also be used in forms similar to those of barley116.

PRAMEHA NIVRUTTI LAKSHANA

The person is said to be free from prameha when his urine is devoid of

casts/deposits, but is clear ; non unctuous non dense, normal bitterness, pungent and

characteristically aromatic117.

Review Of Literature

Disease Review

Diabetes

Mellitus

(NIDDM)


Disease review-Diabetes mellitus (NIDDM) 45

DIABETES MELLITUS

Diabetes mellitus is a clinical syndrome characterised by hyperglycemia due

to absolute or relative deficiency of insulin118. Diabetes means the excessive discharge

that of urine119. DM comprises a group of common metabolic disorders that share the

phenotype of hyperglycemia. Several distinct types of DM exist and are caused by a

complex interaction e.g. genetics, environmental factors and life-style choice.

The metabolic deregulation associated with DM cause secondary

pathophysiologic changes in multiple organ system that impose a tremendous burden

on the individual with diabetes and on the health care system. With an increasing

incidence world wide, DM will likely continue to be a leading cause of morbidity and

mortality for the foreseeable future.

CLASSIFCATION120:

Recent advance in the understanding of the aetiology and pathogenesis of

diabetes have lead to a revised classification though all forms of DM are characterized

by hyperglycemia, the pathogenic mechanisms by which hyperglycemia arises differ

widely. Some forms of DM are characterized by an absolute insulin deficiency or a

genetic defect leading to defective insulin secretion, where as other forms share

insulin resistance as their underlying etiology.

The two broad categories of DM are designated as type 1 and type 2 . DM

results from autoimmune beta cell destruction, which usually leads to insulin

deficiency. Type 1A DM is also characterized by insulin deficiency as well as a

tendency to develop ketosis. However, individuals with type 1B DM, lack

immunologic markers indicative of autoimmune destructive process of the beta cells.

The mechanisms leading to beta cell destruction in these patients are unknown.



Type 2 DM is a heterogeneous group of disorders usually characterized by

variable degrees of insulin resistance, impaired insulin secretion, and increased

glucose production. Distinct genetic and metabolic defects in insulin action and or

secretion give rise to the common phenotype of hyperglycemia in type 2 DM .The

identification of distinct pathogenic process in type 2 DM has important potential

therapeutic implications, as pharmacologic agents that target specific metabolic

derangements become available.

Two features of the current classification of DM diverge from previous

classifications, first, the terms insulin-dependent diabetes mellitus (IDDM) and non

insulin-dependent diabetes mellitus (NIDDM) are obsolete. These previous

designations reflected the observation that most individuals with type 1 DM

(previously IDDM) have an absolute requirement for insulin treatment, whereas many

individuals with type 2 DM (previously NIDDM) do not require insulin therapy to

prevent ketoacidosis. However, because many individuals with type 2 DM eventually

require insulin treatment for control of glyceamia, the use of the latter term generated

considerable confusion.

A second difference is that age is no longer used as a criterion in the new

classification system. Although type 1 DM most commonly develops before the age

of 30, an autoimmune beta cell destructive process can develop at any age. In fact, it

is estimated that between 5 and 10% of individuals who develop DM after age 30

have type 1A DM. Likewise, although type 2 DM more typically develops with

increasing age, it also occurs in children, particularly in obese adolescents .



Aetiologic classification of Diabetes mellitus 121

I. type 1 diabetes (b-cell destruction, usually leading to absolute insulin deficiency) A. Immune-mediated B. Idiopathic II. type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretary defect with insulin resistance) III. Other specific types of diabetes

A. Genetic defects of B-cells function characterized by mutations in: 1. Hepatocyte nuclear transcription factor (HNF) 4a(MODY !) 2. Glucokinase (MODY 2) 3. HNF-alpha (MODY 3) 4. Insulin promoter factor (IPF) 1(MODY 4) 5. HNF-1 Beta (MODY 5) 6. Mitochondrial DNA 7. Proinsulin or insulin conversion

B. Genetic defects in insulin action

1. Type A insulin resistance 2. Leprechaunism 3. rabson-Mendehall syndrome 4. Lipoatrophic diabetes

C. Diseases of the exocrine pancreas-pancreatitis, pancreatectomy. Neoplasia, cystic fibrosis, hemochromatosis, fibrocalculous pancreatopathy

D. Endocrinopathies—acromegaly, Cushing’s syndrome, glucagonoma.

Pheochromocytoma, hyperthyroidisom, somatostatiomnoma. Pheochromocytoma, hyperthyroidism somatostatinoma aldosterodnoma

E. Drug or chemical induced —Vacor, pentamidine, nicotinic acid, glucocorticoids,

thyroid hormone , diazoxide, B-adrenergic agonists, thiazides, phenytoin, a-interferon, protease inhibitors, clozapine beta blockers.

F. Infections—congenital rubella, cytomegalovirus, coxsakie

G. Uncommon forms of immune-mediated diabetes –“stiff-man” syndrome, anti-

insulin receptor antibodies. H. Other genetic syndromes sometimes associated with diabetes-Down’s

syndrome, Klinefelter’s syndrome, Turner’s syndrome. Wolfram’s syndrome, Friedreich’s ataxia. Huntington’s chorea, Laurence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader.Willi syndrome

IV. Gestational diabetes mellitus (GDM)



Pathophysiology of DM

Diabetes mellitus is a chronic disease. It results due to disturbance in

carbohydrate metabolism and deficiency of insulin 122 secreted by the Beta cells of

islets of Langerhan of pancreas, but hormones of pituitary and adrenal glands are also

intimately related to the development of diabetes mellitus. Liver plays an important

role in the metabolism for carbohydrate. It stores glucose in the form of glycogen

under the influence of insulin. Any alteration in this function leads to diabetes 123 .

PANCREAS124

The pancreas is a compound alveolar gland. It has got both endocrine and

exocrine functions. It lies against the posterior abdominal wall behind peritoneum.

The whole organ is about 15 cm long with the right margin of the head is in contact

with the descending part of the duodenum and the tail is in contact with the spleen.

The disease diabetes mellitus is considered only to its endocrine secretion that is

insulin, so it is more important to go through its endocrine part.

ISLETS OF LANGERHANS

The islets of Langerhans are composed of various components that are

organized to form micro-organs. The mass of islets within a pancreas is dynamic and

changes both with growth and development and with functional challenges.

Islets function both singly and in concert. Recent work has revealed greater

diversity in islets than that previously recognized. There is functional heterogeneity

between islets and beta cells within the same islet. Numerous peptides other than the

four main islet hormones (insulin, glucagon, somatostatin, and pancreatic

polypeptide) have been immuno-localized in islets.



The islets Langerhans are clusters of endocrine tissue scattered throughout

the exocrine pancreas. In the adult mammal, the islets are 1 to 2% of the pancreatic

mass and thus comprise around 1 gm of tissue in the adult human. Islets are a

complex mixture of cells and function both separately as micro organs and in concert

as the endocrine pancreas. Although the direct secretion of insulin and glucagon from

islets into the portal vein has obvious advantages with respect to influence on hepatic

function. The islet mass is dynamic, adjusting to meet the changing needs of

individual, whose size and level of activity vary at different stages of life. When the

islet mass cannot adjust to meet the demand, diabetes results.

The pancreas of the adult human contains about 200 units, or 8mg, of insulin. The

size of an islet can range from only a few cells and less than 40 micrometer in

diameter to about 5000 cells and 400 micrometer in a diameter.

GROWTH OF ISLET

The growth capacity of the beta cell depends on the stimulus and the ability if

the cell to recognize the stimulus as well as the number of beta cells that can enter the

cell cycle and undergo mitosis. There is an increased incidence of polyploid beta cells

in the diabetic human. Although there may be numerous stimuli for beta-cell growth,

three major stimuli are known. Glucose has been shown to stimulate modest growth

of either neonatal or adult pancreatic beta-cells in culture. Pregnancy has been shown

to cause both increased replication and mass of beta – cells. As a parallel finding, in

vitro studies have shown that prolactin, placental lactogen and growth hormone can

stimulate replication of beta - cells. Diabetes results only if increased cell loss or

functional demands cannot be met.



COMPONENTS OF THE ISLETS OF LANGERHANS

There are three major endocrine cell types in islets : the insulin producing

beta – cell, the glucagon producing alpha – cell, the somatostatin producing delta –

cell.

Alpha – cell

The alpha cells are usually smaller and more columnar than the beta cell and

well granulated with granules 200 to 250 nm in diameter. The granules are electron

dense with narrow halo of less – dense material and a tightly fitting granule – limiting

membrane.

Beta – cell

The beta cell are polyhedral, being truncated pyramids, and are usually well

granulated with secretary granules 250 to 350 nm in diameter.

Delta – cell

The delta-cells are usually smaller than either alpha or beta cells, are well

granulated and are often dendritic in shape. Within a delta cell the electron density of

granules varies greatly. Each granule 200 to 250 nm in diameter. contains material of

homogenous moderate density that fills the granule – limiting membrane

Table showing cells of islet of Langerhan and their relative hormones

Cell type Size of secretary granule (nm) % of cells Hormone

Beta 250 – 350 60 – 80 Insulin

Alpha 200 – 250 15 – 20 Glucagon

Delta 200 – 250 5 – 10 Somatostatin

Factors regulating islet blood flow may effect islet hormone secretion. High

concentrations of glucose have been shown to enhance pancreatic blood flow and to

preferentially increase islet blood flow125.



Functions of hormones :

INSULIN:

The insulin is hypoglycemic, anti diabetic factor and the protein bound

hormone that regulates the blood glucose, It also increases the oxidation of glucose to

CO2 in the tissues and depresses gluconeogenesis i.e., formation of glucose from the

sources other than carbohydrates.

Insulin increases combustion of sugar in the tissue and also helps in the

treatment of glucose in the cells. It increases synthesis of glycogen from sugar and

lactate both in the liver and muscle. This is called the directive effect of insulin.

Insulin promotes the uptake of glucose inside the cells and the intercellular

phosphorylation of glucose to glucose-6-phosphate itself also appears to be a specific

activator of glycogen synthesis.

Insulin effect on protein metabolism:

In prevents gluconeogenesis, Glucose is normally formed from proteins and

lipids in the liver. In diabetes this process is enhanced. High blood sugar level in

diabetes is due to over production of glucose. In the starving diabetes dextrose

nitrogen ratios is fairly constant. This shows that both sugar and nitrogen are coming

from the same source i.e., proteins. When insulin is given both sugar and nitrogen

excretion fails, showing that formation of new glucose from proteins has been

interfered.

It prevents formation of ketone bodies (anti ketogenic). In advance diabetes,

excess ketone bodies are formed in liver, due to incomplete combustion of fatty acids.

After the administration of insulin more sugars burn and liver glycogen increases

displacing the lipids. Hence lipid combustion is discouraged and ketosis disappears.



Insulin decreases the cholesteremia and lipademia. It also prevents accumulation of

excess lipid in the liver and breakdown of lipid in Adipose tissue.

METABOLIC ACTIONS OF INSULIN 126

Increase (anabolic effects) Decrease (anti catabolic effects)

Carbohydrate metabolism

Glucose transport(muscle, adipose tissue)

Glucose phosporylation

Glycogenesis

Glycolysis

Pyruvate dehydrogenase activity

Pentose phosphate shunt

Gluconeogenesis

Glycogenolysis

Lipid metabolism

Triglyceride synthesis

Fatty acid synthesis (liver)

Lipoprotein lipase activity

(adipose tissue)

Lipolysis

Lipoprotein lipase (muscle)

Ketogenesis

fatty acid oxidation (liver)

Protein metabolism

Amino acid transport

Protein synthesis

Protein degradation

GLUCOGON 127

The Alpha cells of the islets of Langerhans secrete Glucagons. It is a

polypeptide hormone with 29 amino acids having molecular weight of 3.485. This

polypeptide has been completely synthesized Glucagons causes glycogenolysis in the

liver and antagonist to liver by depriving the action of Insulin.



The blood sugar level chiefly controls the secretary activity of Alpha and Beta

cells Hyperglycemia stimulates the release of Insulin where as, hypoglycemia will

release the glycogen. There is no good evidence that a tropic hormone secreted by the

pituitary, directly influences the secretary activity of the pancreatic islets, through

secretions derived form other endocrine glands for example, the adrenal gland have

some effects.If the islets are completely removed or extensively damaged. The lack of

or reduced Insulin formation results in hyperglycemia and the condition of diabetes

mellitus (Madhumeha). Relatively normal carbohydrates metabolism can then be

restored by supplementation of insulin.

It is necessary to point out however that though a deficiency of insulin

production and release may result in Diabetes, not all cases of Diabetes are due to a

deficiency in Insulin production. Even pituitary, Liver and Adrenals are also involved

in this process Clinical syndromes involving abnormal carbohydrate metabolism and

abnormal blood sugar levels may result from either deficiency or excess production of

insulin and Glycogen. The latter when injected result in an increase in blood

hypoglycemic and attains neurological changes, excess production of Gastrin, acidity

and peptic ulceration.

LIVER

Functions of liver in carbohydrate metabolism are :-

1. Storage of Glycogen

2. Conversion of Galactose and fructose into glucose

3. Gluconeogenesis

4. Formation of many important chemical compounds from the intermediate

products of Carbohydrate Metabolism.

Liver is especially important for maintaining a normal blood glucose

concentration. For instance storage of glycogen allows the liver to remove excess



glucose from blood, store it and then return it in to the blood when the blood glucose

concentration begins to fall too low. This is called the glucose buffer function of the

liver. As an example, immediately after a meal containing large amounts of

carbohydrates the blood glucose concentration raises about three times as much in the

person with a non functional liver as in a person with a normal liver.

Gluconeogenesis in the liver is also concerned with maintaining a normal blood

glucose concentration for glucose exogenesis occurs to a significant extent only when

the glucose concentration begins to fall below normal. In such case large amount of

amino acids are converted in to glucose, there by helping to maintain a relatively

normal blood glucose concentration.

TYPE 2 DIABETES 128

Type 2 diabetes commonly occurs in subjects who are obese and insulin-

resistant, but these two factors alone are two factors alone are insufficient to cause

diabetes unless accompanied by impaired beta cell function.

Genetics

Genetic factors are more important in the etiology of type 2 than type 1 diabetes. As

shown by studies in monozygotic twins where concordance rates for type 2 diabetes

approach 100%.

Environmental factors

Life styles

Overeating , especially when combined with obesity and under activity is associated

with the development of this kind. Middle aged people with diabetic eat, less active

acts as the diabetogenic factor.



Malnutrition in utero

Malnutrion in utero may programme beta cell development and metabolic function at

a critical period ,so predisposing to type 2 diabetes in later period. smoking during the

pregnancy has also been implicated.

Age

Type 2diabetes is principally a disease of the middle aged and elderly.

Pregnancy

Repeated pregnancy may increase the like hood of developing irreversible diabetes,

particularly in obese women ; thus women with the gestational diabetes ultimately

develop permanent clinical diabetes.

Pathogenesis of type 2 diabetes

Insulin resistance

Increased hepatic production of glucose and resistance to the action of insulin

in muscle are invariable in both obese and non-obese patients with type 2 diabetes.

Insulin resistance may be due to any one of three general causes; an abnormal insulin

molecule, an excessive amount of circulating antagonists, or target tissue defects. The

last is the most common cause of insulin resistance in type 2 diabetes and seems to be

the predominant abnormality in those with more severe hyperglycemia

A characteristic feature of type 2 diabetes is that it is often associated with

other medical disorders including obesity. Hypertension and hyperlipidaemia. It has

been suggested that this cluster of conditions, all of which predispose to

cardiovascular disease, is a specific entity (the insulin resistance syndrome’ or

‘metabolic syndrome’ )



Pancreatic beta cell failure

In type 2 diabetes there is only moderate reduction in the total mass of pancreatic islet

tissue which is consistent with a measurable fall in plasma insulin concentration when

related to the blood glucose level. However, some pathological change are typical of

type 2 diabetes, the most consistent of which is deposition of amyloid. This is

accompanied by atrophy of the normal tissue, particularly islet epithelial cells, Islet

amyloid is composed of insoluble fibrils formed from islet amyloid polypeptide(also

known as amylin). Small quantities of islet amyloid are very common in elderly non-

diabetic patients, and the role of islet amyloid in the pathogenesis of type 2 diabetes is

uncertain. Deposition of amyloid is probably not a cause of diabetes but rather a

pathological process which is increased in type 2 diabetes. More extensive

amyloidosis is, however, found in patients who have progressed to insulin

replacement therapy, suggesting that islet function may become compromised by

amyloid deposition.

While beta cell numbers are reduced by 20-30% in type 2 diabetes, alpha cell

mass is unchanged and glucagon secretion is increased, which may contribute to the

hyperglycemia. Insulin resistance tends to raise blood glucose and this stimulates

insulin secretion to prevent hyperglycemia. When the maximal insulin secretary

capacity has been exceeded, any further increase in fasting blood glucose levels

caused a decline in insulin generation. Possible mechanisms for beta cell

decompensation include glucotoxicity, an intrinsic failure of insulin production, a

witch to abnormal processing pathways producing biologically inactive products and

chronic degranulation of the beta cells



Some people with type 2 diabetes, most of whom are not overweight have

advanced pancreatic beta cell failure at the time of presentation and require early

treatment with insulin.

The American Diabetes Association (ADA) 1997 revised criteria for diabetes129

The ADA-revised criteria for diagnosis are:-Typical symptoms of diabetes -

polydipsia, polyuria, and unexplained weight loss - plus a casual serum glucose level

greater than 200 mg/dl - "casual" meaning any random glucose obtained at any time

of the day without respect or non-fasting.

A fasting serum glucose greater than or equal to 126 mg/dl after no caloric

intake for at least 8 hours. Two hours serum glucose greater than or equal to 200

mg/dl during a 75-gram oral glucose tolerance test is also diagnostic of diabetes.

Any of these initial findings confirmed on a subsequent day can be considered

as diagnostic of diabetes, and any combination of the findings can be used for

confirmation. For example, a physician may observe a casual serum glucose greater

than 200 mg/dl in a patient with symptoms of diabetes on one day, and subsequently

document a fasting serum glucose greater than 126 mg/dl on another day. This

satisfies the requirement for confirmation by repeat testing.

The ADAs new criteria for diagnosing diabetes mellitus de-emphasize the glucose

tolerance test and favor diagnosis by fasting serum glucose.

HYPERGLYCAEMIA130

Hyperglycaemia is a very common biochemical abnormality. It is frequently

detected on routine biochemical analysis of asymptomatic patients. And is found

during conditions which impose a burden on pancreatic beta cells, such as pregnancy,

severe illness or treatment with drugs such corticosteroids (‘stress hyperglycaemia’)



Symptoms of hyperglycemia associated with diabetes The diabetes diagnosed accidentally, usually asymptomatic but shows the symptoms

of hyperglycemia accordingly. Thus the symptoms related to the hyperglycemia are

of DM.

Table showing the symptoms of hyperglycemia:

• Thirst, dry mouth

• Polyuria

• Nocturia

• Tiredness, fatigue, irritability, apathy

• Recent change in weight

• Blurring of vision

• Pruritus vulvae, balanitis (genital candidiasis)

• Nausea; headache

• Hyperphagia; predilection for sweet foods



Complications of DM131

Table showing the complications of DM

Microvascular/ neuropathic Macrovascular

Retinopathy, cataract

• Impaired vision

Nephropathy

• Renal failure

Peripheral neuropathy

• Sensory loss

• Motor weakness

Autonomic neuropathy

• Postural hypotension

• G I problems

Foot disease

• Ulceration

• Arthropathy

Coronary circulation

• Myocardial ischaemia/ infarction

Cerebral circulation

• Transient ischaemic attack

• Stroke

Peripheral circulation

• Claudication

• Ischaemia

Risk factors for type 2 DM132

Table showing the risk factors for type 2 DM

Family history of diabetes(i.e., parent or sibling with type 2 diabetes)

Obesity(i.e., > 20% desired body weight or BMI> 27 K\m2)

Age>45 years Race\ethnicity(e.g. African American, Hispanic American native American, Asian American, Pacific Islander)

Previously identified IFG of IGT History of GDM or deliver of baby over 9 lbs

Hypertension blood pressure > 140\90 mm, Hg

HDL. Cholesterol level > 0.90 mmol\L (35 mg\dl) and\ or a triglyceride level > 2.82 mmol|l (250mg\dl)

Polycystic ovary syndrome



MANAGEMENT OF DIABETES133

Three methods of treatment are available for diabetic patients; viz diet,

exercise, OHA and insulin.

The importance of life style changes such as taking regular exercise, observing

a healthy diet and reducing alcohol consumption should not be under-estimated in

improving glycaemic control, but many people, particularly the middle-aged and

elderly, find them difficult to sustain. Patients should also be encouraged to stop

smoking.

AIMS OF DIETARY MANAGEMENT

• Abolish symptoms of hyperglycemia

• Reduce overall blood glucose and minimise fluctuations

• Achieve weight reduction in obese patients to reduce insulin resistance,

hyperglycemia and dyslipidaemia

• Avoid hypoglycaemia associated with therapeutic agents (insulin, sulphonylureas)

• Avoid weight gain associated with therapeutic agents(insulin, sulphonylureas,

thiazolidinediones)

• Avoid ‘atherogenic’ diets or those which may aggravate diabetic complications

(e.g. high protein intake in nephropathy)

Low-energy, weight-reducing diets: Dietary prescriptions which cause a daily

deficit of 500 Kcal provide a realistic diet and induce a weekly weight loss of around

0.5 kg. Rapid weight reduction may provoke loss of lean body tissue. And care must

be taken in the elderly to avoid the omission of essential nutrients, vitamins and

minerals. Caloric restriction is essential for the obese diabetic patient treated with

insulin and most oral agents, to try to minimize the weight gain which these can

promote.



Exercise:

Exercise is necessary for the reduction of the weight. An acute bout of

exercise can place numerous metabolic demands on the human organism. To maintain

homeostasis, a person must meet increased requirement for the oxygen and metabolic

substrates through the precise functioning of several regulatory system. Typically,

circulating glucose concentration fall modesty during the exercise in person with the

NIDDM because insulin secretion is not inhibited while the peripheral utilization of

glucose is increased.

Oral hypoglycemic agents:

Various drugs are effective in reducing hyperglycemia in patients with type 2

diabetes. Although their mechanisms of action are different mostly depend upon a

supply of endogenous insulin and they therefore have no hypoglycaemic effects in

patients with type1 diabetes. The sulphonylureas and the Bigunides have been the

mainstay of treatment for many years but novel agents are now available, such as the

insulin enhancing agents , the thiazolidinediones, the alpha glucosidase inhibitors,

which delay carbohydrate digestion and absorption of glucose, and the prandial

glucose regulators which stimulate endogenous insulin secretion.

Educating the patients:

It is essential that people with diabetes should be made to learn to handle all

aspects of their management as quickly as possible , and this can be done on an OPD.

It is wise precaution for diabetic patients who are taking insulin or OHA to carry a

card stating their identity and about their medication. They should be aware about

their condition and the management of emergencies. They should be posses the

knowledge regarding complication and their preventive aspects.

Insulin:Insulin is the ultimate and final treatment for the DM, if OHA fails to control.

Methodology


Methodology 63

MATERIALS

Source of Data

1.Literary source:

Literary aspect was collected from classical Ayurvedic texts , Modern texts,

Journals and those updated information regarding the study were collected from

internet search.

2.Drug :

Avartaki beeja (Cassia auriculata – seeds )

and Avartaki pushpa ( Cassia auriculata – flowers )

were taken for clinical trial .

Collection of raw materials

Botanically identified Avartaki pushpa and beeja were personally collected during

seasons (September –December ) respectively from the local areas.

Method of Preparation

• The flowers of Avartaki were collected and completely dried under the shade.

Then the fully dried flowers were finely powdered.

• The dried legumes of Avartaki were collected and seeds were separated from

them. These seeds were air dried and later finely powdered.

Place of Preparation of medicine

The preparation of medicine was done in PGR&S Dept of Dravya guna vijnana, Shri

D. G. M. Ayurvedic medical College Gadag


Methodology 64

Form of medicine

The Avartaki pushpa and beeja were subjected for churna kalpana as per classics and

then finely powdered drug was filled within capsules.

METHODS

The trial drugs were subjected for the evaluation of physical contents. They found to

be as follows:

Avartaki beeja

1. Foreign matter : 0.36%w/w

2. Total ash : 9.05%w/w

3. Acid insoluble ash : 1.25%w/w

4. Water soluble ash : 6.48%w/w

5. Water soluble extractive : 65.2%w/w

6. Alcohol soluble extractive : 7.12%w/w

1.Foreign matter:

Weight of paper + sample : 10.6480gms

Weight of paper : 0.6480gms

Weight of paper + residue : 10.6120gms

= 100X 0.0360 10 = 0.36%w/w

2.Total ash :

Weight of dish + sample : 28.1670gms

Weight of dish : 26.1670gms

Weight of dish + residue : 26.3480gms

Weight of sample : 2.000gms

Weight of residue : 0.1810gms


Methodology 65

= 100X 0.181 2 = 9.05%w/w

3. Acid insoluble ash :





= 100X 0.00250 2 = 1.25 %w/w

4.Water soluble ash :


Weight of ash : 0.1810gms



Weight of insoluble matter : 0.0514gms

Weight of soluble matter : 0.1296gms

= 100X0.1296 2

=6.48%w/w

5.Water soluble extractive:

Weight of the sample : 5gms




= 100X100X0.8150 25X 5 = 65.2% w/w


Methodology 66

6.Alcohol soluble extractive:

Weight of the sample : 5.00gms




= 100 X 100 X 0.0890 25 X 5 = 7.12 % w/w

Avartaki pushpa

1. Foreign matter : 0.45 %w/w

2. Total ash : 8.2%w/w

3. Acid insoluble ash : 0.93%w/w

4. Water soluble ash : 5.63%w/w

5. Water soluble extractive : 65.92%w/w

6. Alcohol soluble extractive : 7.312 %w/w

1.Foreign matter:

Weight of paper + sample : 10.6480gms

Weight of paper : 0.6480gms

Weight of paper + residue : 10.6030gms

= 100X 0.0450 10

= 0.45%w/w

2.Total ash :

Weight of dish + sample : 28.1670gms





Methodology 67


= 100X 0.1640 2 = 8.2%w/w

3. Acid insoluble ash :





= 100X 0.01860 2 = 0.93%w/w

4.Water soluble ash :


Weight of ash : 0.1640gms



Weight of insoluble matter : 0.0514gms

Weight of soluble matter : 0.1126gm

= 100X0.1126 2 =5.63%w/w

5.Water soluble extractive:

Weight of the sample : 5gms




= 100X100X0.8240 25X 5


Methodology 68

= 65.92% w/w

6.Alcohol soluble extractive:

Weight of the sample : 5.00gms




= 100 X 100 X 0.09140 25 X 5 = 7.312 % w/w

Selection of a sample

Patients suffering from Madhumeha were randomly selected from OPD/IPD of

PGR&S. Dept of Dravya guna vijnana Shri D. G. M. Ayurvedic medical college

Gadag.

Criteria for selection of patients

1. The patients diagnosed as the madhumeha as per the classics

2. Both male and female patients were selected

3. The patients aged in between 25- 65 years

Inclusive criteria

1. The patients diagnosed as the Madhumeha depending on the signs and

symptoms as mentioned in the texts

2. The non insulin dependent patients

3. both obese and non-obese were included

4. NIDDM without complication


Methodology 69

Exclusive criteria

1. Patients within 25 years and above 65 years of age

2. Insulin dependent ( type -1)

3. Patients associated with any other systemic disorders

4. Patients with upadrava of madhumeha

5. Non diabetic glycosuria

6. Malnutritional DM

7. Gestational DM

8. Secondary DM

Laboratory Investigations

The included patients were subjected for the following laboratory investigations

US

FBS

PPBS

Glucose tolerance test in case of border line sugar

Diagnostic criteria :

Diagnosis was made on the basis of subjective parameters mentioned in the

classics and objective parameters ( lab investigations ).

Table showing normal values of objective parameters.

Lab investigation Normal values

FBS 70-110 mg/dl

PPBS 110-140 mg/dl

Urine sugar Nil


Methodology 70

Methods of lab investigations

1.Blood glucose

Blood glucose is determined by using Gluzyme glucose reagent set

Procedure

A blood sample is collected from patient into a sterilized container. Serum is

separated from the cells at the earliest possible time (within 30 minutes), then the

serum blood is mixed with the reagent ( working solution ) and heated at 37 0 c for 15

minutes . Then observed in colorimeter under 520 nm .

Pipetting scheme for determination of blood sugar

Blank Standard Test

Working enzyme reagent (ml) 3.0 3.0 3.0

Distilled water (ml) 0.025 - -

Standard ( ml) - 0.025 -

Sample (ml) - - 0.025

Calculation

Glucose in mg/ dl = Absorbance of sample x 100 Absorbance of standard

The same procedure is applied for both FBS and PPBS . The FBS is done with empty

stomach and on the same day the PPBS is calculated after 2 hours of food and the

results are recorded in case sheet.

2.Urine sugar

A fresh urine sample is collected from the patient. 5 ml of Benedict solution is taken

in a test tube and 5-6 drops of urine sample in put in that. Then the test tube is heated

till until a boil in the solution and cooled at room temperature. The change is

observed for the presence of sugar.


Methodology 71

Observations

Colour of test solution Urine sugar

Blue

Green

Yellow

Orange

Brick red

Nil

0.5 %

1.0 %

1.5 %

2.0 %

Study design

Prospective comparative clinical study

Sample size

A minimum of 30 patients were selected and grouped randomly in two with 15 in

each. The grouping was as follows

Group A- Avartaki beeja churna

Group B- Avartaki pushpa churna

Posology

2gms in divided dose , 1 cap = 500 mg so 2 cap bid, Anupana ─ Sukhoshna jala

Study duration

Duration of the study was 30days

The patients were asked to report on every 10 days

1st assessment – before treatment

2nd assessment – 10th day after initiation of medicine

3rd assessment – 20th day after initiation of medicine

4th assessment – 30th day after initiation of medicine

These assessment were considered for the progressiveness of medication clinically.

But to asses the overall results 1st and 4th assessment are taken.


Methodology 72

Diet

Patients were asked to take their regular diet .

Assessment of results

Results of the treatment were assessed on the basis of difference between baseline

data and assessment data of both subjective and objective parameters. These

differences were subjected for the statistical analysis by applying student ‘t’ test and

paired / unpaired ‘t’ test

Subjective parameters

1. Prabhoota mootrata

2. Avila mootrata

3. Trishna

4. Ashaktata

Objective parameters

1. US

2. FBS

3. PPBS


Methodology 73

Gradation for subjective parameters to asses the result

Sr. no Subjective parameter Gradation according to state

1 Prabhoota mootrata 0-no complaints

1- patient is not aware of complaint

2-patient is aware of complaint

3-patient is disturbed by the complaint

2 Avila mootrata 0-clear urine

1- turbid urine +

2-turbid urine ++

3-turbid urine +++

3 Trishna 0- no complaint

1-mild ( desire for water)

2-moderate ( frequently drinks water)

3-severe ( strongly needs water)

4 Ashaktata 0- no complaints

1- feels weakness

2- routine activities are not affected

3- routine activities are affected


Methodology 74

Results

Results of the study are given as follows:

1. Relieved

2. Palliative

3. Not responded

To categorise the result as above following criteria are taken into consideration

1. Relieved

All the subjective parameters attain grade 0 after the treatment.

The FBS appears in the normal value or difference in baseline and

assessment data is more than or equal to 100.

2. Palliative

Two or more subjective parameters attain the grade 0.

The FBS level is decreased from the previous one.

3. Not responded

No subjective parameters attain the grade 0.

The blood sugar level is raised with the difference of the baseline data and

assessment data is 100 or more.

Result


Results 75

Master charts

Demographic data

Sr.no A

(yrs) S R O S e

s D o I C

(yrs)

Fh T h

D Ag V Pr G Results

1. 59 M H A Hc 20.01.04 20 P Y V V AS Vp B P 2. 54 F H A Mc 04.03.04 5 M Y V V No K B P 3. 48 F H A Hc 08.03.04 10 A Y V V Bl Pk B P 4. 56 F H L Mc 15.04.04 1 A N M T Bl K B R 5. 48 F H A Hc 18.04.04 10 M Y V V Bl Pk A R 6. 54 F H A Mc 18.04.04 5 A Y V V No K A R 7. 56 F H L Mc 20.04.04 1 A N M T Bl K A R 8. 60 M H L P 17.05.04 1 A N M V No V B Nr 9. 49 M H A Mc 20.05.04 4 A Y M V At K B Nr 10 52 M M A Mc 20.05.04 1 A Y M T As P B R 11 49 M H A Mc 27.06.04 4 A Y M V At K A R 12 54 M M A Mc 30.06.04 1 A Y M T As P A Nr 13 53 M H L Mc 04.06.04 1 A Y V V T Pk B R 14 52 M H L Mc 19.06.04 1 A Y M T T Vp B P 15 60 M H L P 20.07.04 1 A N M V No V A Nr 16 53 M H L Mc 04.06.04 1 A Y V V T Pk A R 17 52 M H A Mc 30.07.04 1 A Y M T T Vp A P 18 56 M H A Hc 02.08.04 1 A N V V No K B P 19 55 M H A Mc 02.08.04 2 M Y V T S Vk B P 20 56 M H A Hc 12.09.04 1 A N V V No K A P 21 55 M H A Mc 12.09.04 2 M Y V T S Vk A R 22 48 M H A Hc 02.10.04 5 M Y V V No K B P 23 57 F H A Mc 09.10.04 8 P Y V V Bl K B R 24 46 M H A Mc 26.10.04 2 A N M T No K B P 25 48 F H A Hc 20.11.04 5 M Y V V No K A R 26 46 M H A Mc 01.12.04 2 A N M T No K A R 27 57 M H A Mc 20.12.04 8 P Y V T Bl K A R 28 44 M M A Mc 28.12.04 2 A Y M T A K B R 29 54 M H A Mc 30.12.04 4 A Y V T A Vk A P 30 50 F H A Hc 19.01.04 8 P Y V V No Vk A P

Key words: A- Age in years, S –Sex (M- Male, F – Female) R – Religion (H – Hindu. M – Muslim ,O – Others), O – Occupation ( L – Labour, A – Active) S e s- Socio Economic State ( Hc-high class, Mc –middle class , P – Poor )D o I – Date of initiation), C –Chronicity in years , Fh – Family history ( M- Maternal- Paternal, A – absent ) , Th- Treatment history( Y- Yes , N –No), D –Diet ( V- Vegetarian, M – mixed), Ag- Agni(V- Vishama, T- Teekshna ) ,V-Vyasana ( A- Alcohol, S-Smoking, T- Tobacco, B – Betal nut ), Pr – Prakruti ( V- Vataj , P- Pittaja, K- Kaphaja, VP- Vataj Pittaja , VK- Vataj Kaphaja ,PK - Pittaja Kaphaja ),G- group , Results ( R- Relived, P – Palliative, NR- Not respond


Results 76

Data related to complaints

Sr .no Prabhoota mootrata

Avila mootrata

Ashaktata Sharira bhara hani

Janga mansa graha

Trishna

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. + + + - + + 26. + + + - + + 27. + + + - - + 28. + + + + - + 29. + + + + - + 30. + + + - + +


Results 77

Data related to personal history

Ahara Vihara Sr .no M Sh Sn G

N

Du Da G .V D.V Ma Av A Ds Ss Mnasika chinta

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. + + + + + + + + + + + + - + - 26. + + + - + - + + + + - + + + - 27. + - + + + + + - - - - + + + - 28. + - + + + - + - - + + + + + + 29. + + + + + + + - - - + + - + - 30. + + + + + + + - - - + + + + -

- Key notes: M- Madhura , Sh – Sheeeta ,Sn - Snigdha, G – Guda ,N – Navanna , Du- Dugdha , Da – Dadhi, G.V – Guda vikruti ,D.V –Dugdha vikruti, Ma – Mamsa Av- Alpa vyayama, A – Avyayama ,Ds – Diwaswapna ,Ss – Swapna sukha


Results 78

Data related to the srotodusti before and after the treatment

Udakavaha srotas Medovaha srotas Mootravaha srotas 1 2 3 4 5 6 7 8 9 10 11 12 13 14

Sr. no

B A B A B A B A B A B A B A B A B A B A B A B A B A B A 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 + - + - - - - - + - + - + - - - + - - - + - - - - - - - 26 + - - - - - - - + - - - - - - - + - - - + - - - - - - - 27 + - - - - - - - + - + - - - - - + - - - + - - - - - - - 28 + - + - + - - - + - + - + - - - + - - - + - - - - - - - 29 + - + - + - - - + - + - - - - - + - - - + - - - - - - - 30 - - + - + - - - + - - - - - - - + - - - + - - - - - - -

Key words :-1.Jihwashosha ,2-Talushosha, 3- Ostashosha, 4- Klomashosha;5- Pipasa,

6-Sweda,7- Snigdhangata,8- Pipasa ,9-Alpalpa mootrata, 10-Mootrarodha ,11-Adhika

mootrata, 12-Sashoola mootrata, 13-Bastistabdhata


Results 79

Subjective parameters of group A

Prabhoota mootrata Avila mootrata Trishna Ashaktata Sr.no BT AT BT AT BT AT BT AT

5 3 1 3 0 2 0 1 0 6 3 1 2 0 2 0 1 0 7 1 0 1 0 1 0 1 0 11 2 0 2 0 1 0 1 0 12 1 1 1 1 1 1 1 0 15 3 1 3 3 3 1 3 1 16 1 0 1 0 1 0 0 0 17 3 1 2 1 2 1 2 1 20 2 1 2 1 2 0 2 1 21 2 1 1 0 1 0 1 0 25 2 0 1 0 2 0 1 0 26 2 0 2 0 1 0 0 0 27 2 1 2 0 1 0 0 0 29 2 2 2 2 2 1 2 0 30 2 1 2 0 2 0 2 1

Subjective parameters of group B

Prabhoota mootrata Avila mootrata Trishna Ashaktata Sr.no BT AT BT AT BT AT BT AT

1 2 1 2 1 2 0 1 0 2 2 1 2 0 3 0 2 0 3 3 1 3 1 2 0 1 0 4 1 0 2 0 1 0 1 0 8 3 2 3 3 3 2 3 2 9 2 1 1 1 2 1 1 0 10 1 0 1 0 1 0 1 0 13 1 0 1 0 1 0 0 0 14 3 1 3 1 3 1 2 1 18 2 1 2 1 2 0 1 0 19 2 1 1 0 1 0 2 0 22 2 1 2 1 2 0 1 0 23 2 0 2 0 2 0 1 0 24 2 1 2 1 2 0 1 0 28 2 1 1 0 2 0 1 0


Results 80

Objective parameters of group A

FBS in mg/dl PPBS in mg/dl US in % Sr.no BT AT BT AT BT AT

5 214 196 260 253 1 0.5 6 240 138 330 210 1.5 1 7 107 97 159 164 0 0 11 142 90 152 130 0 0 12 99 100 131 160 0 0 15 348 369 500 499 2 2 16 120 90 210 150 0 0 17 280 160 330 215 1.5 1 20 238 126 369 154 1.5 1 21 161 131 242 162 0.5 0 25 89 85 193 140 0 0 26 193 115 248 150 0.5 0 27 210 120 290 154 0.5 0 29 143 237 336 365 1 1.5 30 200 164 350 249 1.5 1

Objective parameters of group B

FBS in mg/dl PPBS in mg/dl US in % Sr.no BT AT BT AT BT AT

1 270 200 330 270 1.5 1 2 251 158 359 241 1.5 1 3 228 168 259 206 1 0.5 4 162 107 184 159 0 0 8 344 500 500 500 2 2 9 117 142 162 152 0.5 0.5 10 196 99 242 131 0.5 0 13 150 95 290 180 0.5 0 14 240 160 380 290 1.5 1 18 210 130 340 260 1.5 1 19 104 161 199 242 0 0.5 22 146 113 259 212 0.5 0 23 190 110 260 170 0 0 24 228 142 312 236 0.5 0 28 204 163 300 201 1 0.5


Results 81

OBSERVATION

In the present study 30 patients were selected randomly and grouped as ‘A’ and ‘B’

each of fifteen each. All patients were observed closely during course of the

treatment. Changes both in subjective and objective parameters were recorded

according to the case sheet proforma. The data were collected as follows:

Section A- Demographic data

Section B- Data related to disease madhumeha

Section C – Data related to the response to the treatment

Section A – Demographic data

Age:

In the present study 30 patients of Madhumeha were included have age group of 25-

65 years. Maximum 20 (67%) were in between the age of 46-55 years , followed by 9

(30%) in between the 56-65 years and only 1(3%) falls in the age of 36-45 years .

Table showing the age ratio

Age (in years) No. of patient Percentage 26-35 0 0% 36 – 45 01 3% 46 – 55 20 67% 56 – 65 09 30%

Showing age ratio

26-350%

36 – 453%

46 – 5567%

56 – 6530%

26-3536 – 4546 – 5556 – 65


Results 82

Sex:

Table showing the sex ratio

Sex No .of patient Percentage

Male 21 70%

Female 9 30%

Among the 30 patients , 21 ( 70%) patients were male and 9 (30 % ) were female

ones. This indicates the incidence of madhumeha is more in male.

Showing sex ratio

Male70%

Female30%

MaleFemale


Results 83

Religion incidence

The data shows among 30 patients 27 (90%) belongs to religion Hindu, 3 (10% )

belongs to the Muslim category . It dos not mean that Hindus are more prone for this

disease. This may be due to the area from where sampling is being done.

Table showing the incidence of religion

Religion No . of patient Percentage

Hindu 27 90%

Muslim 3 10%

Others 0 0%

Showing the incidence of religion

Hindu90%

Muslim10%

Others0%

HinduMuslimOthers


Results 84

Occupation This data shows among 30 patients 22 (73%) were belonging to active and 8(27%)

were belonging to the labour kind of occupation. This shows the less laborious work

might have more susceptibility to this disease.

Table showing the nature of occupation

Occupation No . of patient Percentage

Sedentary 0 0%

Active 22 73%

Labour 8 23%

showing the nature of occupation

Sedentary0%

Active73%

Labour27%

SedentaryActiveLabour


Results 85

Socio economic state

Data related to socio economic state indicates that maximum 20 (66% ) falls in

middle class and 8 (27%) falls in the higher class. Only 2 (7%) falls in the category of

poor class. It suggest that poor class patient are not have the incidence of madhumeha

as compare to middle and higher class because chronic diet intake and less utility.

Table showing the socio economic state

Socio economic state No . of patient Percentage

Higher class 08 27%

Middle class 20 66%

Poor 02 7%

Showing the socio economic state

Higher class27%

Middle class66%

Poor7%

Higher classMiddle classPoor


Results 86

Diet

The food habit distribution in the locality of research has more percentage of

vegetarians in comparison to mixed diet.

The ratio between vegetarian and mixed diet is 17:13 i.e., 57%:43% respectively.

Table showing the diet

Diet No . of patient Percentage

Veg 17 57%

Mixed 13 43%

Showing the diet

Veg57%

Mixed43% Veg

Mixed


Results 87

Section B-Data related to disease Chronicity

The occurrence of disease varies for 0 years to more than 20 years. The incidence of

chronicity is not discriminate. The maximum 24 (80%) patients are have the

chronicity of 5years. 5 (16.67%) patients with the chronicity of 6-10 years and 1

(3.33%) with the 20 years chronicity.

Table showing the chronicity of madhumeha

Chronicity in years No . of patient Percentage

0-5 years 24 80%

6-10 years 05 16.67%

11-15 years 00 0%

16-20 years 01 3.33%

showing the chronicity of madhumeha

24

5

0 10

5

10

15

20

25

30

0-5 years 6-10years

11-15years

16-20years

No.

of p

atie

nts

Series1


Results 88

Complaints

The data shows the 30(100%) patients with prabhoota mootrata, Avila mootrata and

trishna. 26(86.66%) patients shows Ashaktata, 10(33.33%) shows Janga Mansa

graham and only 5(16.66%)patients were with the sharira bhara hani. These

complaints drags the patients towards the disease.

Table showing the complaints

Complaints No . of patient Percentage

Prabhoota mootrata 30 100%

Avila mootrata 30 100%

Ashaktata 26 86.66%

Sharira bhara hani 5 16.66%

Janga mamsa graham 10 33.33%

Trishna 30 100%

30 3026

510

30

05

1015202530

NO. of patients

1

Complaints of Patient

Showing the complaints

PrabhootamootrataAvila mootrata

Ashaktata

SharirabharahaniJanga mansagrahamTrishna


Results 89

Family history

The data related to family history shows maximum 20 (67%) patients without any

family history. 6(20%)patients were with maternal history and 4(13%) patients are

with the paternal history. These data suggest that the incidence of the disease not

depended on the hereditary factor but develops on aetiological factors.

Table showing the family history

Family history No . of patient Percentage

Maternal 06 20%

Paternal 04 13%

Absent 20 67%

showing the family history

Maternal20%

Paternal13%Absent

67%

MaternalPaternalAbsent


Results 90

Treatment history

The data shows the presence of previous antidiabetic treatment confirms the disease

as madhumeha. Among 30 patients maximum 22(73%) shows the treatment history

different antidiabetic therapy and 8(27%) were freshly diagnosed and not shows any

medication.

Table showing the treatment history

Treatment history No . of patient Percentage

Present 22 73%

Absent 08 27%

Showing the treatment history

Present73%

Absent27%

PresentAbsent


Results 91

Agni The data shows among the 30 patients 16(53%) are having Vishama Agni and

14(47%) are having Teekshna Agni. The involved both kind of are suggestive of the

disease as vikrutagnikruta(metabolic disorder).

Table showing the ratio of involved Agni

Agni No . of patient Percentage

Vishama 16 53%

Teekshna 14 47%

showing the involvement of agni

Vishama53%

Teekshna47% Vishama

Teekshna


Results 92

Vyasana

Among the 30 patients maximum 13(44%) shows the Vyasana of tobacco and betal

nut, 10 (33%) are without any Vyasana , and 7 ( 23%) are having the Vyasana of

alcohol and smoking. The data suggest that vyasana are one the cause for the loss of

strength thus produce the disease.

Table showing the vyasana in relation with disease

Vyasana No . of patient Percentage

Alcohol & smoking 7 23%

Tobacco & betal nut 13 44%

No habit 10 33%

Showing the vyasana in relation with disease

Alcohol & smoking

23%

Tobacco & betal nut

44%

No habit33%

Alcohol & smoking

Tobacco & betalnutNo habit


Results 93

Prakruti

In this study of 30 patients , maximum 15( 50%) are found of kapha prakruti,

pittakaphaj 5(16.67%) , vatapittaja and vatakaphaja 3(10%) each and vataja , pittaja

of 2(6.67%) each This data suggest that initially the madhumeha is found in kaphaja

Prakruti which is later makes avarana over the vata.

Table showing the prakruti

Prakruti No . of patient Percentage

Vataj 02 6.67%

Pittaj 02 6.67%

Kaphaja 15 50%

Vatapittaja 03 10%

Vatakaphaja 03 10%

Pittakaphaja 05 16.67%

0

5

10

15

no of patient

No . of patient

prakruti

showing the prakruti of the patient

VatajPittajKaphajaVatapittajaVatakaphajaPittakaphaja


Results 94

Personal history

To asses the nidanas of the disease , detailed personal history is taken with more

concentration drawn towards ahara and vihara of the patients

1. Ahara

The data related to ahara for 30 patients shows that 26 (86.66%) consume

madhura ahara, 23(76.66%) sheeta, 28(93.33%) snigdha, 16(53.33%) guda,

26(86.66%) navanna , 21 (70%) dugdha , 28(93.33%) dadhi, 19(63.33%)

gudavikruti , 12(40%) dugdha vikruti ,13 (43.33%) Mamsa as a regular diet. All

these are prone to produce madhumeha.

Table showing the kind of ahara

Ahara No . of patient Percentage

Madhura 26 86.66% Sheeta 23 76.66% Snigdha 28 93.33% Guda 16 53.33% Navanna 26 86.66% Dugdha 21 70% Dadhi 28 93.33% Gudavikruti 19 63.33% Dugdhavikruti 12 40% Mamsa 13 43.33%

2.Vihara

2623

28

16

2621

28

19

12 13

05

1015202530

No. of patients

1

Ahara

showing the kind of ahara

MadhuraSheetaSnigdhaGudaNavannaDugdhaDadhiGudavikrutiDugdhavikrutiMamsa


Results 95

2. Vihara

The data related to vihara shows among 30 patients 19 (63.33%) are performing

the alpavyayama,11 (36.33%) are avyayama. Lack of vyayama is leading the

condition towords the disease. About the state of nidra 12(40%) with diwaswapna

and 28 (93.33%) with the swapnasukha. This suggest the peaceful sleep may

agrrevate the diseased condition.

Table showing the vihara

Vihara No . of patient Percentage

Alpa vyayama 19 63.33%

Avyayama 11 36.33%

Diwaswapna 12 40%

Swapnasukha 28 93.33%

showing the vihara

19

11 12

28

05

1015202530

Alpa vy

ayam

a

Avyay

ama

Diwasw

apna

Swapna

sukha

vihara

No.

of p

atie

nts

Series1


Results 96

3.Manasika chinta

When we notice the mental state , maximum27(90%) patients were noticed without

any mansaika chinta and only 3(10% ) patients were noticed with the manasika chinta

. It suggests that the happy life without any worries are causative factors for the

Madhumeha.

Table showing the involvement of manasika chinta

Manasika chinta No . of patient Percentage

Yes 3 10%

No 27 90%

showing the involvement of manasika chinta

Yes10%

No90%

YesNo


Results 97

Section C-Data showing the response to the treatment

Data related to srotas

The three major srotas i.e, udakavaha , medovaha and mootravaha are generally

involved in the manifested disease. The srotodusti lakshana are usually found .

Udakavaha srotas

Among the 30 treated cases, Jihwashosha is in 28(93.33%) before treatment

and not found (0%) after the treatment. Talushosha is in 18 (60%)before treatment

and 2(6.66%)after the treatment. Ostashosha is in19(63.33%)before treatment and

3(%)after the treatment. Kloma shosha is not found. All 30(100%) suffer with pipasa

before treatment and only 2 (6.66%) are found after the treatment. Pipasa and

jihwashosha takes major improvement by the treatment.

Table showing the comparison of udakavaha srotodusti lakshana before and

after the treatment.

Before treatment After treatment Laxana No . of patient

Percentage No . of patient

Percentage

Jihwashosha 28 93.33% 00 0% Talushosha 18 60% 02 6.66% Ostashosha 19 63.33% 03 10% Klomashosha 00 0% 00 0% Pipasa 30 100% 02 6.66%

28

0

18

2

19

3 0 0

30

20

102030

No. of patients

Jihwashosha Klomashosha

Srotodusti laxana

Comparison of udakavaha srotodusti laxana before and after the treatment

BTAT


Results 98

Medovaha srotas

The data related to medovaha srotas shows among 30 treated

patient,28(93.33%)are with sweda before treatment and 4(13.33% )after the treatment.

Snigdhangata is in 17(56.66 %) before treatment and only 2(6.66 %) after the

treatment. Pipasa is found in all 30(100 %) before treatment and only in 2 (6.66 %)

after the treatment. Thus the medovaha srotas is responded with the medication.

Table showing comparison of medovaha srotodusti lakshanas before and

after the treatment

Before treatment After treatment Laxana No . of patient Percentage No . of patient Percentage

Sweda 28 93.33% 04 13.33% Snigdhangata 17 56.66% 02 6.66% Sthoola shophata 00 0% 00 0% Pipasa 30 100% 02 6.66

28

4

17

2 0 0

30

2

05

1015202530

No. of patients

Sweda Sthoolashophata

srotodusti laxana

Comparision of medovaha srotodusti laxana before and after the treatment

BTAT


Results 99

Mootravaha srotas

Among 30 patients all 30(100%) show the adhika mootrata before treatment

and only 2(6.66 %) shows after the treatment

Table showing the comparison of mootravaha srotodusti lakshana before and


Before treatment After treatment Laxana No . of patient Percentage No . of patient Percentage

Alpalpa mootrata 00 0% 00 0% Mootrarodha 00 0% 00 0% Adhika mootrata 30 100% 02 6.66% Sashoola mootrata 00 0% 00 0% Basti stabdhata 00 0% 00 0%

0 0 0 0

30

2 0 0 0 005

1015202530

No. of patients

Alpalpamootrata

Adhikamootrata

bastistabdhata

srotodusti laxana

Comparision of mootravaha srotodusti laxana before and after the treatment

BTAT


Results 100

Data showing the intensity of disease before and after treatment

The data related to intensity are given the gradation particular to each complaints.

1.Prabhoota mootrata

Table showing the Prabhoota mootrata before treatment in group A and group B

Grade 3 Grade 2 Grade 1 Grade 0 Group No. of patient

% No. of patient

% No. of patient

% No. of patient

%

A 4 26.66% 8 53.33% 3 20% - - B 3 20% 9 60% 3 20% - - These data reveals the complaint Prabhoota mootrata has the Grade 3, within 4

(26.66%)

patients of group A and of 3 (20%) in group B. There are 8(53.33%) patients of

group A and 9 (60%) patients of group B are in Grade 2. 3(20%)patients of each

group are in Grade 1 during before treatment.

Table showing the Prabhoota mootrata after the treatment in group A and

group B

Grade3 Grade 2 Grade 1 Grade 0 Group No. of patient

% No. of patient

% No. of patient

% No. of patient

%

A 0 0 % 1 6.66% 9 60 % 5 33.33%B 0 0 % 1 6.66% 10 66.66

% 4 26.66%

After the completion of treatment , in15 patients of each group, there no patients at

Grade 3.1(6.66%)each patients are at Grade 2. maximum 9 (60%)of group A and

10(66.66%) of group B have reached the grade 1.Thus there are 5(33.33%) and

4(26.66%) patients of group A and B respectively at grade 0.


Results 101

0

0.5

1

1.5

2

2.5

3

Grades

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Patients

comparision of prabhoota mootrata before and after the treatment in group A

Series1Series2

0

0.5

1

1.5

2

2.5

3

grades

1 3 5 7 9 11 13 15patients

Comparision of Pabhoota mootrata before and after the treatment in group B

Prabhoota mootrata BTPrabhoota mootrata AT


Results 102

Avila mootrata

Table showing the Avila mootrata before treatment in group A and group B


% No. of patient

% No. of patient

% No. of patient

%

A 2 13.33% 8 53.33% 5 33.33% 0 0%B 3 20% 7 46.66% 5 33.33% 0 0%

Before treatment among 15 patients of each group, 2(13.33%) and 3(20%) of group

A and group B respectively are at grade 3. Maximum 8(53.33%) of group A

and7(46.66%) of group B are on grade 2.5(33.33%) of each group are at the grade 1.

Table showing the Avila mootrata after the treatment in group A and group B


% No. of patient

% No. of patient

% No. of patient

%

A 1 6.66% 1 6.66% 3 20% 10 66.66%B 1 6.66% 0 0% 8 53.33% 6 40% After the completion of the treatment , there are still 1 (6.66%) of each group are

resides at grade3. only 1(6.66%) patient of group A is on grade 2. Maximum

8(53.33%) patients of group B are at grade 1 and only 3 (20%) of group A at grade

1.Maximum 10 (66.66%) patients of group A are at grade 0, only 6(40%) of group B

are at this grade.


Results 103

00.5

11.5

22.5

3

Grades

1 3 5 7 9 11 13 15

Patients

Comparison of avila mootrata before and after treatment in group B

Avila mootrata BTAvila mootrata AT

00.5

11.5

22.5

3

grades

1 3 5 7 9 11 13 15

patients

comparison of avila mootrata before and after the treatment in group A

Avila mootrata BTAvila mootrata AT


Results 104

Trishna

Table showing trishna before the treatment in group A and B


% No. of patient

% No. of patient

% No. of patient

%

A 1 6.66% 7 46.66% 7 46.66% 0 0%B 3 20% 8 53.33% 4 26.66% 0 0% Before treatment the data relating to the trishna shows among the 15 patients of each

group ,at grade 3 there are 1 (6.66%) of group A and 3 (20%) of group B. Maximum

7(46.66%) of group A and 8 (53.33%) of group B are at grade2. 7 (46.66%) and 4

(26.66%) patients of group A and B are at grade 1 respectively.

Table showing trishna after the treatment in group A and B


% No. of patient

% No. of patient

% No. of patient

%

A 0 0% 0 0% 4 26.66% 11 73.33%B 0 0% 1 6.66% 2 13.33% 12 80% After the treatment there are no patients in grade 3 of both groups. Only 1(6.66%) of

group B is at grade2. 4(26.66%)and 2(13.33%) of group A and B respectively at grade

1.Maximum 11 (73.33%) and 12(80%) of group A and B have reached the grade 0.


Results 105

0

0.5

1

1.5

2

2.5

3

grades

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Patients

Comparision of trishna before and after the treatment in group A

Trishna BTTrishna AT

0

0.5

1

1.5

2

2.5

3

Grades

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Patients

Comparision of trishna before and after treatment in group B

Trishna BT

Trishna AT


Results 106

Ashaktata

Table showing Ashaktata before treatment in group A and B


% No. of patient

% No. of patient

% No. of patient

%

A 1 6.66% 4 26.66% 7 46.66% 3 20% B 1 6.66% 3 20% 10 66.66% 1 6.66% Before treatment among the 15 patients of each group , there are1 (6.66%) patient

from each group is at grade 3. 4(26.66%) of group A and 3 (20%) of group B are at

grade 2.Maximum 7(46.66%) patient of group A and 10(66.66%) of group B are at

grade 1.Finally 3(20%) and 1 (6.66%)of group A and B respectively are at gra

Table showing Ashaktata After treatment in group A and B

Grade3 Grade 2 Grade 1 Grade 0

Group No. of patient

% No. of patient

% No. of patient

% No. of patient

%

A 0 0% 0 0% 4 26.6% 11 73.33%B 0 0% 1 6.66% 1 6.66% 13 86.6% After treatment none are at grade 3,only 1(6.66%) of group B at grade 2.4(26.66%)

and 1(6.66%)patientsof group A nad B are at grade 1 respectively . Maximum

11(73.33%) of group A and 13(86.6%) of group B are at grade 0.


Results 107

00.5

11.5

22.5

3

Grades

1 3 5 7 9 11 13 15

Patients

comparision of ashaktata before and after the treatment in group A

Ashaktata BTAshaktata AT

0

0.5

1

1.5

22.5

3

Grades

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Patients

Comparision of ashaktata before and after the treatment in group B

BTAT


Results 108

Data showing the relief from complaint after treatment in both groups

Before treatment After treatment Parameters Group No. of patients

% No of patients(Relieved)

%

A 15 100% 05 33.33% Prabhoota mootrata B 15 100% 04 26.66%

A 15 100% 10 66.66% Avila mootrata B 15 100% 06 40% A 15 100% 11 73.33% Trishna B 15 100% 12 80% A 12 80% 08 66.66% Ashaktata B 14 93.33% 11 78.57%

To asses total relief the data collected as above shows that, among 15 patients of each

group , all 15( 100%)of each group are with the complaint of Prabhoota mootrata. In

this category, 5 (33.33%) of group A and 4 (26.66%) of group B are relieved . Avila

mootrata is found in all 15(100%) patients of each group before treatment, thus the10

(66.66%) patients of group A and 6 (40%) patients of group B are relieved after the

treatment. Trishna is also found with all 15(100%) patients of each group before

treatment, 11 (73.33%) of group A and 12(80%) patients of group B are relieved. But

Ashaktata is found in 12(80%) patients of group A and 14(93.33%) patients of group

B before treatment . After treatment the 08 (66.66%) are relieved from Ashaktata in

group A and 11 ( 78.57%) of group B are relieved from the complaint initially

suffering.

02468

10121416

no. of patients

A B A B A B A B

Prabhootamootrata

Avilamootrata

Trishna Ashaktata

complaints of both group before and after the treatment

Showing relief after the treatment

BT

AT


Results 109

Comparison of FBS before and after the treatment in group A :

The comparison of FBS in group A , before and after the treatment shows great

variations. Among 15 patients , 3 (20%) shows increase in the values, with the

difference of maximum 94 mg/dl and minimum 1mg/dl. Remaining 12 (80%) shows

decrease , with maximum difference 120 mg/dl and minimum 4mg/dl.

Comparison of FBS before and after the treatment in group B

Among 15 patients of group B , the FBS shows the raise in 3 (20%) with highest

difference 156 mg/dl. and lowest 25mg/dl.the reduction is found in remaining 12

(80%) with highest difference of 97mg/dl and the lowest 33 mg/dl.

0100200300400500

FBS

1 3 5 7 9 11 13 15

Patients

Comparison of FBS before and after the treatment in group B

FBS in mg/dl BTFBS in mg/dl AT

0

100

200

300

400

FBS

1 3 5 7 9 11 13 15

Patients

Comparison of FBS before and after the treatment in group A

FBS in mg/dl BTFBS in mg/dl AT


Results 110

Comparison of PPBS before and after the treatment in group A :

Among 15 patients of group A , the PPBS shows the raise in 3 (20%) with highest

difference 29 mg/dl. and lowest 5mg/dl.The reduction is found in remaining 12 (80%)

with highest difference of 215mg/dl and the lowest 1 mg/dl.

Comparison of PPBS before and after the treatment in group B

Among 15 patients of group B , the PPBS shows the raise in 3 (20%) with highest

difference 43mg/dl. and lowest 0mg/dl.The reduction is found in remaining 12 (80%)

with highest difference of 118 mg/dl and the lowest 10 mg/dl.

0100200300400500

PPBS

1 3 5 7 9 11 13 15

Patients

Comparision of PPBS before and after treatment in group A

PPBS in mg/dl BTPPBS in mg/dl AT

0

100

200

300

400

500

PPBS

1 3 5 7 9 11 13 15

Patients

comparision of PPBS before and after the treatnent in group B

PPBS in mg/dl BTPPBS in mg/dl AT


Results 111

Comparison of US before and after the treatment in group A :

Among 15 patients of group A , the US is present in 10(66.66%) patients only

before the treatment. Among these 10(66.66%) patient , 1(6.66%) has the US at 2 %

before which is not changing even after the treatment. One( 6.66%)patient with nil

US showed 5% after the treatment. One(6.66%) with US 1% before treatment has

raised to1.5% after the treatment.5(33.33%) patients with nil US before treatment

remains unaltered after the treatment. 4 (26.66%) patients with 1.5% US before

treatment reduced to 1% after treatment. 1(6.66%) with1% US before treatment gets

0.5% after treatment. 3 (20%) patient with 0.5% US before treatment attains nil


0

0.5

1

1.5

2

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Comparsion of US before and after treatment in group A

US in % BTUS in % AT


Results 112

Comparison of US before and after the treatment in group A :

Among 15 patients of group A , the US is present in 12(80%) patients only

before the treatment. Among these 12(80%) patient , 1(6.66%) has the US at 2 %

before which is not changing even after the treatment. One( 6.66%)patient with nil

US showed 5% after the treatment. One(6.66%) with US 0.5% before treatment has

remained to0.5% after the treatment.2(13.33%) patients with nil US before treatment

remains unaltered after the treatment. 4 (26.66%) patients with 1.5% US before

treatment reduced to 1% after treatment. 2(13.33%) with1% US before treatment gets

0.5% after treatment. 3 (20%) patient with 0.5% US before treatment attains nil


0

0.5

1

1.5

2

US

1 3 5 7 9 11 13 15

Patients

Comparision of US before and after the treatment in group B

US in % BTUS in % AT


Results 113

Results

Result of the study on the basis the subjective and objective parameters is given

as follows:

Group A

Table showing the result of group A

Results related to group A shows , among 15 patients suffering with madhumeha,

9(60%) are relieved, 4 (27%) are palliative and 2 ( 13 %) are not responded.

Results No. of patients Percentage

Relieved 9 60%

Palliative 4 27%

Not responded 2 13%

showing the result in group A

Relieved60%

Palliative27%

Not responded13%

RelievedPalliativeNot responded


Results 114

Group B

Table showing the result of group B


Relieved 7 47%

Palliative 6 40%

Not responded 2 13%

Among 15 patients , 7 (47%) are relieved, 6 (40%) are palliative and 2( 13%) are

found to be not responded in group B.

showing the results of group B

Relieved47%

Palliative40%

Not responded13%



Results 115

Total result

Table showing the total result

The total result can be given as follows. Among total 30 patients 16(54%) are found

to be relieved ,10 (33.33%) are found to be palliative and 4 (13%) are found to be not

responded.


Relieved 16 54%

Palliative 10 33%

Not responded 4 13%

showing the results

Relieved54%Palliative

33%

Not responded13%



Results 116

Statistical study of both groups is done to rule out the efficacy of both Avartaki

pushpa and avartaki beeja.

Individual study of Group A before and after the treatment

Parameters Mean S.D S.E t value P value Remarks

FBS 53.2 41.915 10.822 4.915 <0.001 H.S

PPBS 71.4 60.19 15.542 4.59 <0.001 H.S

US 0.3 0.253 0.065 4.615 <0.001 H.S

Prabhoota mootrata 1.33 0.723 0.186 7.15 <0.001 H.S

Avila mootrata 1.266 0.883 0.228 5.55 <0.001 H.S

Trishna 1.33 0.617 0.159 8.36 <0.001 H.S

Ashaktata 0.8 0.676 0.174 4.597 <0.001 H.S

Individual study of Group B before and after the treatment

Parameters Mean S.D S.E t value P value Remarks

FBS 71.66 32.23 8.323 8.609 <0.001 H.S

PPBS 67.466 37.26 9.62 7.013 <0.001 H.S

US 0.366 0.228 0.059 6.203 <0.001 H.S

Prabhoota mootrata 1.2 0.414 0.106 11.320 <0.001 H.S

Avila mootrata 1.2 0.676 0.174 6.896 <0.001 H.S

Trishna 1.533 0.743 0.191 8.026 <0.001 H.S

Ashaktata 1.0666 0.457 0.118 9.038 <0.001 H.S


Results 117

Comparative study of group A and group B after the treatment

Parameters Group Mean S. D S. E P.S. E t- value P value Remarks

A 147.86 74.55 19.249FBS

B 162.7 98.22 25.36

31.837 0.466 >0.05 N.S

A 210.333 100.93 26.061PPBS

B 230.0 87.85 22.68

34.54 0.569 >0.05 N.S

A 0.466 0.667 0.172 US

B 0.533 0.581 0.150

0.228 0.293 >0.05 N.S

A 0.733 0.593 0.153 Prabhoota

mootrata B 0.8 0.5606 0.144

0.21 0.067 >0.05 N.S

A 0.533 0.915 0.236 Avila

mootrata B 0.666 0.816 0.210

0.315 0.422 >0.05 N.S

A 0.266 0.457 0.118 Trishna

B 0.266 0.593 0.153

0.193 2.41 <0.05 H.S

A 0.266 0.457 0.118 Ashaktata

B 0.733 0.593 0.153

0.193 2.41 <0.05 H.S

When we compare group A and B , all the parameters shows non significant except

trishna and ashaktata. The mean effect of trishna in both the groups is same. The

parameters PPBS , prabhoota mootrata and avila mootrata are having uniform

effecting group B the mean effect of FBS is more in Group B and shows more

variations.

Individually the Group B is having more effect then group A in all symptoms.

The prabhoota mootrata is much significant than the other s parameter FBS the mean

net effect is more in group B . The objective parameter FBS the mean net effect is


Results 118

more in group B and correspondingly variance is more ( by using paired ‘ t’ test,

unpaired ‘t’ test, by comparing ‘t’ values, co- efficient of variation and ‘P’ value is <

0.05.

Discussion


119

DISCUSSION

The trail drug Avartaki is growing abundantly in the tropical country like

India, hence it is commonly found from Gujarat, Maharastra and southern India .The

drug is used commercially to dye the leather and medicinally in various disorders. The

different parts of the plant are used as medicine .Among them the flower, seeds and

leaves are frequently used . Most of the classical texts indicates the seeds in

conjunctivitis, chylous urine, etc. and flower in garbhasrava , kusta , trishna etc. But

both flowers and seeds are indicated in madhumeha.

The drug possesses the tikta, kashaya rasa, sheeta veerya , katu vipaka and

laghu , rooksha guna. Thus it may be said that its activity is based on these properties

can be mootrasangrahaneeya, as the most of mootrasangrahaneeya gana dravya with

such qualities do so.

Madhumeha is the disorder, where the madhura tatwa is discharged through

the urine giving sweetness to it. The pratyatma lakshana are Prabhoota mootrata and

Avila mootrata. Avilata is due to the presence of the madhura tatwa. Prabhoota

mootrata is the atipravrutti lakshana of the mootravaha srotas due to the accumulation

of vitiated dosha in the basti. Among the tridosha the kapha and pitta are causing

avarana to the vata leading to the disorder. Similarly in the NIDDM the beta cells of

the pancreas are acting deficiently thus due to increased secretion of glucogon as

proportional to insulin there is hyperglycemia. Thus the blood with high concentration

of glucose, undergone for filtration in the kidney, does not capable to regain the

filtrated glucose and the glucose thus passes out through the urine. Hence comparison

seems true and thus needs the alike medication. Avartaki is one such drug which

possesses the features that effective in madhumeha.

The line of the treatment in both condition can given as follows.


120

Madhumeha: It is a chiefly due to the dosha avarana to the vata, hence considered

under the vataja prameha. For this purpose the drug choosen should be capable of the

elimination of the avarana and mitigate the avarakas. The Prabhoota mootrata causes

the excessive loss of fluid which results into trishna , and Ashaktata due to the

madhura tatwa hani. The dosha mainly avruta i.e. kapha and pitta can be subsided by

the tikta kashaya rasa, i.e. kapha and pitta shamana. Katu vipaka and laghu, rooksha

guna subsides the kapha and sheeta veerya subsides the pitta.

To over rule, the loss of urine should be prevented , which can be performed

by the tikta and kashaya rasa because of rookshana of the drava and sangrahana,

sheeta veerya because of the sroto sankuchana, sangrahana, katu vipaka because of

baddhata of mootra, and finally by laghu , rooksha guna because of the rookshana

karma of the vayu mahabhuta. As the prabhoota mootrata is stopped the loss of

madhura tatwa is also be prevented that leads to the regain of energy. The sheeta

veerya also provides the balya and jeeveneeya function. The tikta also acts as the

trishnahara , dahaprashamana , those appears associating the condition. The

prevention of loss of fluid also reduces the trishna. Even the overeating , one of the

causative factor is mitigated due to the tikta rasa .as the pathogenesis involves the

meda vruddhi can corrected by the tikta rasa and laghu , rooksha guna.

DM ;NIDDM: The deficiency of the insulin is to be fulfilled, either by promoting the

beta cells function, reducing the alpha cell function. in order to lower the blood

glucose level

The trial drug Avartaki possesses the properties as tikta , kashaya rasa, katu

vipaka ,sheeta veerya and laghu , rooksha guna. Thus it can be interpretated that the

avartaki is effective in the management of madhumeha as it is fulfilling the

requirements said above. Although the classical reference for the management of


121

madhumeha by avartaki , two parts are mentioned ,i.e. avartaki pushpa and avartaki

beeja. The efficacy of these two parts are evaluated by the clinical trial.

The design of the study on madhumeha is a comparative clinical study. Thus

this trail is carried out with the 2 groups receiving two kinds of medicines.

1. Group A- Avartaki beeja churna

2. Group B- Avartaki pushpa churna

Many of the hypoglycemic activity studies are carried out with various herbal drugs

and even with the avartaki itself. In comparison to synthetics, the safest and

efficacious , evaluation of a drug on madhumeha is required. Hence two parts of the

avartaki are indicated and many experimental studies of avartaki in madhumeha ,

Avartaki beeja and avartaki pushpa were selected for the comparative clinical study.

Group A- Avartaki beeja

Clinical study of group A, is carried out by administration of avartaki beeja churna in

15 patients showed its significant values at the level of probability as < 0.001.The

avartaki beeja is effective in all the parameters. The research works have shown that

these seeds contain palmatic oleic acid, Oligosaccharides and galactomanos which

have role in the hypoglycemic activity. But compare to the other group the gradation

have not much improvement.

Group B – Avartaki pushpa

The clinical study of group B was carried out by the administering avartaki pushpa

churna in other 15 patients. The significant value at the level of probability as <0.001

.All the parameters are highly significant .The known component of the flower is the

beta sitosterol which is effective anti inflammatory, anti neoplasmic and immune

modulator. Thus it is capable of reducing the elevated blood sugar level to the

normal. Hence avartaki pushpa seems to more effective than the beeja.


122

Observations regarding the study are indicating the prevalence of the disease

in the following conditions among the study of 30 patient of madhumeha.

The disease is diagnosed on the subjective and objective parameters as

mentioned in the methodology. The data related to age suggests that middle aged

persons are more prone (67%) to Madhumeha. The male (70%) showed the incidence

of the disease. The majority of patients are of active (73%) with less laborious work

might have more susceptibility to the disease. All patients shows the vitiated agni

which suggests the disease manifestation due the vikrutagni. The family history is

absent 20 (67%) giving the clue for manifestation of the disease due to the

aetiological factor. The maximum 50% Kaphaja Prakruti of the patient gives hint for

the manifestation of by avarana. The data relating the personal history are identical to

the aetiological factor mentioned the texts for the madhumeha.

The data related to the response to the treatment showed the effectiveness of

both drug in all parameters with varying degree. In group A 9 (60%) are relieved , 4

(27%) are palliative and 2 ( 13%) are not responded. In group B 7 (47%) are relieved,

6 (40%) are palliative and 2(13%) are not responded. The selection of the patient is

randomised for both groups. The comparison of results indicates that group A is

efficacious on first look. But when the gradation of the parameters are subjected for

the statistical analysis the group B is found efficacious. The mean net effect of FBS is

more in group B and correspondingly variances are more .

Therefore the comparative study showed non significant but comparatively

the avartaki pushpa is extremely efficacious than the avartaki beeja.

Conclusion


Conclusion 123

CONCLUSION

The dissertation entitled ‘Evaluation of efficacy of Avartaki in madhumeha

(NIDDM)’ is concluded as below:

Madhumeha is becoming a epidemic with high rate of morbidity and mortality.

The various kinds of managements could not satisfactorily control this condition .

Medicinal plants used since immemorial time, in many disorder. Avartaki is one

such drug with multidimensional actions used as medicine.

Medicinal values of avartaki ranges varyingly by utilization of different parts

avartaki pushpa and avartaki beeja are used chiefly in madhumeha (prameha).

Madhumeha is one of 20 varieties of prameha. It is vata predominant, or due the

doshavarana to vata, considered under the vataja prameha.

DM is co- related with the madhumeha especially the NIDDM (Type -2) which

have the similar pathogenesis and the manifestation.

The classical affirmed pathogenesis and the signs and symptoms in madhumeha

(NIDDM) are stand still even in 21st centaury . The pratyatma lakshana are

Prabhoota mootrata and Avila mootrata.

The multidimensional action of avartaki promotes the comparative clinical study

over the 30 patients in 2 groups

• Group A- Avartaki beeja

• Group B- Avartaki pushpa

The result of the study showed both the drugs are efficacious in the madhumeha.

The parameters shows high significance rate with respect to both groups. In group

A 9 patients are relieved, 4 are palliative, and 2 are not responded. In group B 7

are relieved 6 are palliative and 2 are not responded.

Avartaki pushpa is more efficacious than the avartaki beeja.


Conclusion 124

As the classical literature the reason for the hypoglycemic effect is possible by the

property of tikta rasa and sheeta veerya of the drug. The antidiabetic activity may

be due to the presence of beta sitosterol, a phytosterol.

Finally the avartaki pushpa and avartaki beeja are the safer, therapeutically

efficacious, cost effective and easily available can be considered as the drug of

choice.

Future scope:

Though the clinical study shows high significance the study should be

conducted on the large sample.

The detailed phytochemical study is to be carried out.

The drugs should be evaluated in IDDM cases also.

Summary


Summary 125

SUMMARY

The dissertation entitled ‘Evaluation of efficacy of avartaki in madhumeha

(NIDDM)’ is summarized as follows:

Under the heading of introduction the necessity of the assortment of the

research , significance of the drug in the present work is mentioned .

Aims and objectives of the study are dealt in the objectives.

Review of literature consists of literary review of drug avartaki and disease

madhumeha. The drug review deals with the history, synonyms, varga, guna,

karma, prayoga , taxonomical classification, family description, morphology ,

phyotochemistry etc. in detail.

The majority of the references describe, the avartaki has properties as tikta ,

kashaya rasa, katu vipaka, sheeta veerya, laghu, rooksha guna and action as

pramehaghna, trishnahara, chardighna, krimighna etc. because of this one can

conceptualize that drug must effective in the madhumeha and other related

condition.

The disease review has the detailed description of madhumeha in ayurvedic

aspect and DM in modern aspect as those are co related in each angle .

Materials and methods are described in detail in methodology which is

followed in the present study.

Observation related to demography , disease, and effect of medication are

presented in tables and graphs, the statistical analysis and results are included

Discussion of the clinical study about the results was done over it.

The thesis is concluded under the conclusion .The efficacy of avartaki pushpa

and avartaki beeja are comparatively studied, that reveals that both are highly


Summary 126

significant and when compared the avartaki pushpa is found better than the

avartaki beeja.

Finally the essence of the thesis is summarized in the summary

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Lea and Febiger ; 1994.p.15-8.


Lea and Febiger ; 1994.p.26


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Bibliography 140









Graw Hill ; 2001. p.2112


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livingstone publication ; 2002.p .657.

Annexures


Case sheet 141

PROFORMA FOR THE EVALUATION OF EFFICACY OF AVARTAKI IN

MADHUMEHA

Post Graduation Studies and Research Dept. Of Dravya Guna Vignana

D.G.M. Ayurvedic Medical College Gadag

Guide: Dr. G.V. Mulagund M.D (Ayu) Co –Guide: Dr. Kuber . Sankh M.D.(Ayu) Scholar: Dr. S.B.Bani Name of the patient: Address: Sr. no: Age: OPD.No

Sex : M F D.O.I

Religion H M C O D.O.C Occupation Sedentary Active Labour Socio-economic state HC MC Poor Results Relieved Palliative Not responded Discontinued Consent: I here by giving my consent

to be included as a subject in the above study. I have been informed to my satisfaction

, by investigator about the purpose of the clinical trail, nature of the drug treatment

and its follow up. I am also aware of my right to quit at any time during the course of

the trail without having to reason for doing so.

Signature of investigator Signature of patient


Case sheet 142

CHIEF COMPLAINTS

No Complaints Duration Before treatment After treatment

1 Prabhoota mootrata 2 Avila mootrata 3 Ashaktata 4 Shareera bhara hani 5 Janga mamsa graham 6 Trishna

FAMILY HISTORY

Father Grand father Brother Uncle Mother Grand mother Sister Aunt

TREATMENT HISTORY Medication Dose Ayurvedic Specify

Glibendamide Sulfonylures Glipizide

Oral hypoglycemic agents Bigunides Metformin PERSONAL HISTORY

Veg Mixed Guda Gramya Mansa Navanna Dugdha vikruti Audaka

Form

Dugdha Dadhi Anupa Pramana Alpa Madhyama adhika Rasa Madhur Amla Lavana Tikta Katu Kashaya

Ahara

Guna Snigdha Sheeta Vyayama Alpa vyayama Avyayama Nidra Swapnasukha Diwaswapna Manasika chinta Yes No Agni Vishama Teekshna Vyasana ( if any)


Case sheet 143

GENERAL EXAMINATION Pulse BP Height Akruti Temp Resp Weight Heart sounds SROTO PAREEKSHA

L Jihwashosha

Talushosha Ostashosha Klomashosha Pipasa

B

Udakavaha

A L Alpalpa

mootrata Adhika mootrata

Sashoola mootrata

Mootrarodha Basti stabdhata

B

Mootravaha

A L Sweda Snigdhangata Sthoola shophata Pipasa B

Medovaha

A ATURA BALA PAREEKSHA

Deha V P K VP VK PK S Prakruti Mana R S T RS RT ST S

Sara Rasa Mansa Meda Sarva Samvahana Susnhita Madhyama

sanhita Avara sanhita

Satmya Pravara Madhyama Avara Satwa Pravara Madhyama Avara Vaya Bala Proudha Vruddha Desha Jangala Anupa Sadharana SUBJECTIVE PARAMETER No Parameters 0th day 10th day 20th day 30th day 1 Prabhoota mootrata 2 Avila mootrata 3 Trishna 4 Ashaktata


Case sheet 144

INVESTIGATIONS

Investigation Before After Urine sugar

FBS PPBS

Blood sugar

GTT TREATMENT PROTOCOL:

Medicine Dose Started on

INVESTIGATOR’ NOTE: Signature of scholar Signature of co-guide Signature of Guide


Case sheet 145

Gradation for subjective parameters to asses the result

Sr. no Subjective parameter Gradation according to state

1 Prabhoota mootrata 0-no complaints

1- patient is not aware of complaint

2-patient is aware of complaint

3-patient is disturbed by the complaint

2 Avila mootrata 0-clear urine

1- turbid urine +

2-turbid urine ++

3-turbid urine +++

3 Trishna 0- no complaint

1-mild ( desire for water)

2-moderate ( frequently drinks water)

3-severe ( strongly needs water)

4 Ashaktata 4- no complaints

5- feels weakness

6- routine activities are not affected

7- routine activities are affected

Documents

Madhumeha#dg01 gdg