Hand Dermatitis Eczema Current Management

REVIEW ARTICLE

Hand dermatitis/eczema: Current managementstrategy

Virendra N. SEHGAL,1 Govind SRIVASTAVA,2 Ashok K. AGGARWAL,2

Alpna D. SHARMA2

1Dermato-Venereology (Skin ⁄ VD) Center, Sehgal Nursing Home, Panchwati, Delhi, and 2Skin institute and School of Dermatology,

Greater Kailash, New Delhi, India

ABSTRACT

Ever since its inception a couple of centuries ago, hand dermatitis ⁄ eczema has been in the reckoning. Idiosyncra-

sies continued to loom large thereafter, till it acquired its appropriate position. Dermatitis ⁄ eczema are synonymous,

often used to indicate a polymorphic pattern of the inflammation of the skin, characterized by pruritus, erythema

and vesiculation. A spectrum delineated into acute sub-acute and chronic dermatitis of the hands. Pompholyx,

recurrent focal palmer peeling, ring, wear and tear and fingertip eczema, apron, discoid eczema, chronic acral der-

matitis, gut and patchy papulosquamous eczema are its clinical variants. Occupational dermatitis ⁄eczema may be

contributory. Etiological definitions are clinched by detailed history of exogenous and endogenous factors. However,

scientific confirmation of the entity is through patch testing by using available antigens.

Key words: hand dermatitis ⁄ eczema: clinical classification, occupational dermatitis ⁄ eczema.

INTRODUCTION

Hands are an integral part of our life from execution of

day-to-day activities to earning a livelihood. They are

also of great aesthetic and cosmetic value. The hands

when diseased or incapable of work, become a seri-

ous disability, responsible for loss of manpower and

large scale loss of national productivity. Besides, it

causes individual psychosocial trauma and affects

quality of life.

Hand dermatitis (HD) ⁄eczema is mainly confined to

the hands. Dermatitis ⁄eczema are often used synon-

ymously to indicate a polymorphic pattern of the

inflammation of the skin, characterized by pruritus,

erythema and vesiculation. Hand eczema is a fre-

quently encountered problem, affecting individuals

from all walks of life, involved in different fields of

work. In the absence of required care and therapy, it

may turn into a chronic, distressing disease largely

influencing an individual’s daily life. Both endogenous

and exogenous factors may contribute to the devel-

opment of HD ⁄eczema. Endogenous factors refer to

conditions like atopic dermatitis, hyperkeratotic pal-

mer dermatitis and the like, while exogenous factors

include both systemic and topical irritants, allergens,

inhalants, ingestants and infections.

In situations where an inflammatory response of

the skin occurs following exposure to exogenous

substance ⁄allergen ⁄ irritant, it is designated as con-

tact dermatitis. Also, irritant and ⁄or allergic contact

dermatitis, phototoxic and photo-allergic contact der-

matitis, an immediate type of contact reaction, are

also included in the category. Contact dermatitis is an

alarming problem all over the world. Whole popula-

tion studies and examinations of random samples of

people have put its incidence at 1.5–6%, whereas in

an occupational environment contact dermatitis

accounts for approximately 90% of dermatoses.1,2 In

Correspondence: Virendra N. Sehgal, M.D., FNASc, FAMS, FRAS, A-6 Panchwati, Delhi 110 033, India. Email: [email protected]

Received 17 September 2009; accepted 1 November 2009.

doi: 10.1111/j.1346-8138.2010.00845.x Journal of Dermatology 2010; 37: 593–610

� 2010 Japanese Dermatological Association 593

trades like construction work, chemical and metal

industries, the incidence is particularly high.3 Approxi-

mately two-thirds of all cases of contact dermatitis

affect the hands, the most important site for allergic

and ⁄or irritant contact dermatitis (ICD).4 Contact der-

matitis of the hands particularly forms an occupa-

tional hazard in housewives, hairdressers, dental and

medical personnel, metal workers and laborers.

Established important risk factors5 include history of

childhood eczema, female sex, occupational expo-

sure, atopic mucous membrane symptoms and a

service occupation. In yet another study from the

Netherlands, comprising 1900 people over a period

of 3 years, ICD was revealed as a cause of hand

eczema in half of the cases, whereas allergic contact

dermatitis accounted for another 15%.6 Rhus, nickel,

chromate, formaldehyde, ethylenediamine, merca-

ptobenzothiazole, thiurams and paraphenylene

diamine7 were the eight most common allergens

identified in the USA. In contrast, vegetables were the

most common implicated allergens in India.8

Assessment of the etiology and pathogenesis of

contact dermatitis largely depends on the patient’s

history, examination and certain investigations. An

important investigative procedure that aids in the

diagnosis is the ‘‘patch test’’. Proper evaluation of

the patch test results provides an accurate and

relatively simple means of diagnosis, allowing the

physician to initiate appropriate management for

alleviation of the patient’s suffering at the earliest.9

Patch testing also proves essential in distinguishing

allergic from ICD.10 Large scale screening of a series

of allergens yields a more complete evaluation of

patients with more relevant allergens identified. Sup-

plemental allergens that are added to screening

series based on patient’s history provide additional

relevant information.11

DEFINITION

Eczema literally means ‘‘boil out’’, is an inflammatory

skin reaction pattern characterized histologically by

spongiosis with varying degrees of acanthosis and a

superficial perivascular lymphocytic infiltrate. Clinical

features of eczema include itching, redness, scaling

and clustered papulovesicles.

The term ‘‘hand eczema’’ refers to predominant

involvement of the hands, and it has been specified

that if the eczema is widespread and the hands

appear to be involved coincidentally it is preferable to

speak of ‘‘hand involvement’’.12

Contact dermatitis is an inflammatory response of

the skin to an exogenous agent. Classical contact

dermatitis originates from external contact of the skin

with an irritant of allergic noxious agent13 according to

the mechanism of elicitation. Contact dermatitis may

be classified as: (i) ICD; (ii) allergic contact dermatitis;

(iii) phototoxic and photo-allergic contact dermatitis;

and (iv) immediate type contact dermatitis ⁄contact

urticaria syndrome (CUS).

Hands are an important site for irritant and allergic

contact dermatitis leading to fulminant hand eczema.

ICD is a non-immunological local inflammatory reac-

tion characterized by erythema, edema or corrosion,

following single or repeated applications of a sub-

stance to an identical cutaneous site. Inflammatory

or immunological mediators may be activated but

no memory cell T cells function or antigen-specific

immunoglobulins are involved.14

Allergic contact dermatitis is a T-cell-mediated

immunological reaction that requires prior sensitiza-

tion. It is a delayed type hypersensitivity (type IV)

reaction that occurs from exposure of sensitized indi-

viduals to contact allergens. Distinction between irri-

tant and allergic contact dermatitis is not always

easy.

HISTORICAL BACKGROUND

Captain John Smith recognized the effect of poison

ivy (Toxicodendron) as early as 1609. In the 17th cen-

tury, idiosyncratic reactions to various substances

were identified. Ddakin observed the selectivity of

Rhus dermatitis in 1829, while in 1884 Nisser

described idiosyncratic reactions while referring to

iodoform dermatitis. Furthermore, the 18th century

witnessed primitive versions of patch testing when

Stadler devised a method of reproducing lesions pro-

duced by Anacardium occidentale on human skin

using blotting paper strips. Collins, an ophthalmolo-

gist, applied patches of atropine to his patients who

were having reactions to atropine instillation. Josley

Jadasson in 1896, made a major advancement by his

success in reproducing the clinical lecture of contact

dermatitis from iodoform mercury salts by topical

application of the same in sensitized subjects. He

594 � 2010 Japanese Dermatological Association

V.N. Sehgal et al.

thus established the role of patch testing in dermatitis

medicamentosa. The term ‘‘allergic’’ was first coined

in 1906.

Allergic sensitization of the skin was first proved

experimentally by Bloch and Steiner-Worlich using

Primula extract on humans. However, monumental

contributions were made by Landsteiner and

Jacobs in 1935 when they showed that simple sub-

stances could cause contact reactions after conju-

gation with protein carriers. This was followed by

demonstration of passive transfer of delayed hyper-

sensitivity with lymphocytes by Landsteiner and

Chase. Other developments in patch testing

included a grading system for patch test reactions

and the concept of a standard series of allergens15

introduced by Basel.

In the context of hand eczema, dermatologists in

the 19th century described several morphological

variants of hand eczema like eczema solare, rubrum,

impetiginoides, squamosum, papulosum and margin-

atum.16 Radcliff Crocker emphasized the role of

external irritants in development of hand eczema.

EPIDEMIOLOGY

Contact dermatitis of the hands is a common dis-

order. The incidence of HD varied from 10.9–15.8%

in different studies.8 Reports from the Indian subcon-

tinent revealed that 5–10% of the patients attending

dermatology outpatient departments were affected

by allergic contact dermatitis17 and two-thirds of

these cases had hand involvement(s).18

In a study conducted in an industrial city in Swe-

den, 11.8% of the population under observation con-

sidered themselves to have had hand eczema at

some time during the past 12 months; approximately

two-thirds of them were women.19

In another part of Sweden, Agrup established the

minimum prevalence of hand eczema to be 1.7%

with one-third of these having a diagnosis of allergic

contact dermatitis.20 HD is more commonly seen in

women as compared to men21–23 with predilection

for younger age groups. It was postulated that

approximately 20% of women will suffer from hand

eczema at some point in their life.24

Clinical examination of a random sample of people

living in the Netherlands found the prevalence of HD

to be 5.2% in men and 10.6% in women.25 Contact

exposure to wet work, detergents and other house-

hold work probably predisposes women.

Young women tend to have more cosmetic and

occupational contact sensitizers. In older people,

many sensitizers will be of past relevance only and

there will be higher prevalence of medicament sensiti-

zation. Considering contact dermatitis in the occupa-

tional scenario, it has been observed to account for

40–60% of days lost at work.26

It has also been observed that patients of atopic

dermatitis and those with nickel sensitivity have a

poorer prognosis. In a recent survey of occupations

at a higher risk of dermatitis, positive cases included

75% construction workers 72% hairdressers and

barbers, and 20% food industry workers. In Finland,

44% of 617 hospital personnel engaged in wet work

had past or present history of hand eczema. Contact

irritants are the commonest cause of hand eczema.

Meding and Swanbeck27 also observed that in 35%

(a)

(b)

Figure 1. (a,b) Hand dermatitis ⁄eczema fungal infection ofthe palms and paronychia.


Hand dermatitis ⁄ eczema

irritant dermatitis was the commonest cause of hand

eczema followed by atopic dermatitis.

Other factors observed as important are predictive

factors for hand eczema such as history of childhood

dermatitis followed by sex, occupational exposure,

asthma, hay fever, service occupation and age. In a

recent study,28 the authors found a high frequency of

personal and familial atopy, 58% prevalence of con-

tact allergy, 67.4% history of hay fever, 25.6% cases

of asthma and 44% incidence of fungal infection

(Fig. 1), which was one of the most common coexis-

ting conditions.

In a study to identify factors of importance for long-

term prognosis of hand eczema, the main determi-

nant for a poor long-term prognosis was widespread

HD at the initial examination along with low age of

onset, history of childhood eczema and contact

allergy.29

ETIOLOGY

Hand dermatitis is usually multifactorial, where exog-

enous as well as endogenous factors may play a sig-

nificant role. The former (exogenous) factors refer to

influences of the external environment, where as

the latter (endogenous) factors refer to constitutional

influences upon skin function. Exogenous factors

may either be irritants and ⁄or allergens, coming into

contact with the skin.

Irritants

An irritant is any agent, physical or chemical that

is capable of producing cell damage if applied for a

sufficient period of time, and in adequate concen-

tration.30

Acute irritant dermatitis is recognized first by expo-

sure to irritants in a vulnerable population. However,

in general, the intensity of reaction to irritants is

directly proportional to the concentration of the

incriminating irritant and exposure time.31 Dermati-

tis ⁄eczema arise without previous sensitization when

the repair capacity of the skin is impeded or

exhausted when penetration of the chemical pro-

vokes an inflammatory reaction.13

Irritants are a frequent cause of hand eczema.32

Although the irritant affects almost everyone, its sus-

ceptibility varies considerably. Incidence of ICD

declines with age and is reported to be higher in

women than in men.6 A high prevalence was also

seen among workers exposed to moist conditions, as

wet work causes prolonged and repeated exposure

to water in combination with various chemicals. Eighty

percent of female cleaners with hand eczema

revealed that they had wet hands more than a quarter

of the working day.33 Others who are at risk of ICD are

hairdressers, hospital workers, agriculturists, painters,

printers, metal workers, laborers and people involved

in food preparation. Common irritants include indus-

trial cleaning agents like solvents, abrasives, alkalies,

cutting oils, oxidizing and reducing agents, and desic-

cant powders. Detergents, especially the anionic

types, are also well-known irritants, and widely used

in cleaning products. They are capable of exerting a

direct toxic effect on the skin and may disturb its

barrier function. Furthermore, physical factors such

as friction, micro-trauma, heat, cold and low humidity

are implicated to enhance an irritant effect.34

Irritant contact dermatitis has been delineated into

several clinical types. Primary ⁄acute ICD is caused

by one overwhelming external exposure to irritant of

short duration and is often accidental. Chronic ICD on

the other hand, may be the result of too frequent

exposure (repetition) of an impairing factor or is

often the result of the influence of a variety of subse-

quent stimuli, each one perpetuating the previous

episode.35

Clinical spectrum of acute ICD ranges from mild

reaction to transient erythema and chapping to florid

dermatitis with pain, inflammation, edema, vesicula-

tion, exudation and necrosis. In contrast, in chronic

ICD, an eczematous condition persists for more than

6 weeks causing redness edema, scaling and fissur-

ing on thin and exposed skin of the hands.

Allergens

Contact allergens are almost invariably small sub-

stances of less than 500 D, which because of their

small size penetrate the otherwise impermeable skin

barrier and reach the living layers of the skin. Further,

antigenicity is accomplished by conjugation of small

molecules with autologous proteins present in the

skin. Allergens vary greatly in their capacity to sensi-

tize. Prior sensitization is a salient prerequisite for

allergic contact dermatitis. In a sensitized individual,

acute contact dermatitis (ACD) appears or is exa-

cerbated 24–96 h after contact with the causative


V.N. Sehgal et al.

allergen and its initial localization is at the site of con-

tact.13 Agrup’s study found metals, balsam, phenol,

formaldehyde, resin, colophony, mercaptobenzo-

thiazole and wood tar to be the most frequent sensi-

tizers in Sweden.20 A study from Britain found

balsams, nickel, medicaments, cobalt, rubber, chro-

mate, benzocaine and paraphenylene diamine as the

commonest allergens.36 Indian studies established

vegetables,23,37 soaps, detergents, topical drugs21,

metals, condiments,38 industrial agents2 and nuts39

as the major allergens responsible for ACD.

The preceding studies also elaborate the sites

affected by the implicated allergens, namely house-

wives who show ACD to garlic and onion have

involvement of the thumb, index and middle finger of

the dominant hand and only the thumb of the other

hand. Fingertip dermatitis is also commonly seen with

vegetables.37 The dorsal aspect of the hands and

forearms is affected more due to soaps and deter-

gents.21 Rubber dermatitis may be sharply limited,

giving a clear indication of the object or garment

(glove, boot, mask) that caused the dermatosis.40

Dermatitis on the fingers, characteristically as ‘‘tulip

fingers’’, is seen in bulb growers and gardeners who

peel the tulip bulbs.41

Oral ingestion of allergens such as nickel,

chromium,42 balsam of Peru and even drugs like

neomycin and hydroxyquinolines43 may promote or

aggravate HD in sensitized individuals.

Again, acute form allergens cause erythema,

edema, followed by appearance of papule vesicles,

oozing and crusting, whereas on chronic exposure

lichenification, fissuring and pigmentation persist.

Allergens cause more of pruritus as compared to

burning and pain in contrast to irritants.

Immediate type contact dermatitis/CUS

In addition to erythema, edema vesiculation and exu-

dation an urticaria (wheal) may be a presenting fea-

ture. The urticaria begins at the site of contact with

allergens. Proteinous products like fish and other sea

foods are commonly implicated.44 Even rubber latex

protein causes contact urticaria.45,46

Endogenous factors

Hand dermatitis due to endogenous causes may

either be idiopathic (as in hyperkeratotic palmer der-

matitis) or may be due to an immunological or meta-

bolic defect (as in atopics) or it may be aggravated

by psychosomatic stress or could be enhanced by

physiological factors (like sweating as in dyshidrosis.

Atopic diathesis has been considered the common-

est cause of HD,47 and in adults the most frequent

site to be involved in atopic dermatitis are the

hands. Several studies demonstrate a higher risk for

atopics to develop ICD, because of lower threshold

for irritation and slower healing.48 An epidemiological

study also established that even individuals with

apparently healthy skin who only had a history of

atopy were at greater risk for developing hand

eczema later in life. The conclusion made after a

study of 777 patients of atopic dermatitis for hand

involvement, was that the hands are frequently

involved in patients with active atopic dermatitis and

present unique physical, social and therapeutic chal-

lenges for the patients. On evaluation of these

patients, it was found that involvement of dorsal

hand surfaces and the volar wrist may suggest

atopy as a contributing etiological factor.49 Atopic

hand eczema probably has the worst prognosis of

all types of hand eczema.32 Even in an occupational

setup, when employees performing wet work in hos-

pitals were studied, it was found that HD occurred

in 65% of persons with atopic symptoms.50 In yet

another five studies on the predictive factors for

hand eczema, it was found that history of childhood

eczema was most important. Of those individuals

who reported history of childhood eczema, 27%

had had hand eczema on some occasion in a

12-month period. Female sex and history of hay

fever and asthma were also shown to be of signifi-

cant predictive value.

PATHOGENESIS

Irritant contact dermatitis is a non-immunological

inflammatory reaction. It occurs following an expo-

sure to an irritant, without prior sensitization. It has a

twofold pathogenic mechanism. Chronic irritant der-

matitis is related to a disturbed barrier function, and

an increased epidermal cell turnover leading to liche-

nification, whereas an acute ICD is more of an inflam-

matory reaction caused by release of mediators and

cytokines like tumor necrosis factor-a, interleukin (IL)-

1, IL-6, IL-8, c-interferon (IFN-c), IL-2 and granulocyte

monocyte-colony stimulating factor.51



Allergic contact dermatitis

Allergic contact dermatitis is a delayed hypersensitiv-

ity reaction mediated by T cells. Under ordinary con-

ditions, exposure to contact allergens sets in motion

two competing mechanisms, the one mediated by

effecter T-lymphocytes leading to a state of hyper-

sensitivity that becomes clinically manifest as an

eczematous skin reaction, while the other is mediated

by regulatory T cells leading to a relative or complete

tolerance of allergen. The balance between effecter

and suppressor cells is determined by the state of

reactivity of the skin.

Antigenicity is accomplished by the conjugation of

the small molecules with autologous proteins present

on the skin. Most of these proteins are the cell mem-

brane proteins.

It is not possible for T-lymphocytes to interact

directly with the contact antigen even when they pos-

ses the appropriate surface receptors for that anti-

gen. The antigen must first be processed and then be

presented in a suitable form in which it associates

with major histocompatibility complex class II mole-

cules, coded in the human leukocyte antigen-differ-

entiation region (HLA-DR) genes present in dendritic

cells, Langerhans cells (LC) or antigen-presenting

cells. Epidermal LC have properties that make them

particularly suitable for this function. Epicutaneously

applied allergen molecules attach with their antigen-

presenting cells within 6 h.52 Within 24 h of antigen

application, LC migrate to regional lymph nodes

where they present the antigen to the compatible

T-lymphocytes within the lymph nodes. Certain

T-lymphocytes like CD4+ and CD45 RA+ become

physically apposed to the LC, thus facilitating the

transfer of antigen. Ever since the role of LC in skin

immunity was established it has been investigated

extensively.53–55 Recent data deriving from trans-

genic animals that are deficient in LC have begun to

challenge the dogma that there is a universal require-

ment for these cells in the development of skin sensi-

tization. Accordingly, relationships between LC

mobilization, draining lymph node activation, and skin

sensitization using immunomodulators agonistic for a

family of sphingosine-1-phosphate (S1P) receptors

have been highlighted in a recent commentary.56

Many mediators or cytokines are released by this

apposition, namely, IL-1 by antigen-presenting cells

and IL-2 by T-lymphocytes.57 Other cytokines that

are important at this stage are IL-6, transforming

growth factor-b and IL-12. The cytokines cause

clonal proliferation of antigen-specific T-helper 1,

CD4+ lymphocytes which might be capable of

responding to a particular antigen when future

exposure occurs.

The cellular response seem to be based on an

increased frequency of T cells with a given specificity

throughout the body of a sensitized individual, and

takes 7–10 days before there are sufficient numbers

of T-lymphocytes to cause contact dermatitis. On

subsequent exposure, antigen-presenting cells and

specific T cells meet locally, leading to cytokine pro-

duction within the skin, thus leading to development

of an erythematous reaction, which reaches a maxi-

mum in 18–48 h.

Cytokines that play a major role in the development

of allergic contact dermatitis are those with a major

stimulatory effect on other lymphocytes (MIP-1b, IL-2,

IFN-c), on mononuclear phagocytes (chemotactic

factor, migration inhibitory factor, IFN-a) and on mast

cells and vasculature (skin reactive factor, IFN-c).

CLINICAL CLASSIFICATION

The etiological classification of HD has already been

described (vide supra). However, no single classifica-

tion of hand eczema is completely satisfactory. A sim-

ple method is to classify it according to the stage of

eczema:

1 Acute: clinical features range from erythema, chap-

ping to a florid dermatitis with edema, inflammation,

vesiculation, pain, exudation, bullae formation and

tissue necrosis.

2 Subacute: milder, characterized by erythema, pap-

ules and crusting.

3 Chronic: lichenification characterized by thickening

of the skin, exaggerated skin marking, scaling and

pigmentation.

The preceding classification is easy to comprehend

and facilitates treatment approach.

However, an anatomical classification is useful in

defining the etiology of HD. A morphological classifi-

cation of hand eczema is often suggested. Although

most cases are of a patchy vesiculosquamous nature

without any special characteristics, one-third of cases

present particular patterns that deserve recognition

and are outlined below.


V.N. Sehgal et al.

Pompholyx

Pompholyx is a frequent deep-seated vesicular erup-

tion of idiopathic ⁄unknown origin affecting the palm

and soles recognized as palmoplantar pompholyx.58

It has been assumed to be a disturbance of sweat

gland function. Pompholyx is of the hands (cheiro-

pompholyx) (Figs 2,3) and of the soles (podopompho-

lyx). It accounts for 5–20% of all cases of hand

eczema.20,32

The role of sweat glands is disputed, although dis-

tribution of lesions corresponds to emotionally acti-

vated palmoplantar sweating and hot weather.

However, hyperhidrosis is not a constant feature.

Role of atopy may be significant. Lodi et al.58 found

personal and family history of atopy in 50% of their

patients as compared to 12% controls. Primary irri-

tants may cause pompholyx, for example in metal

workers exposed to soluble oils.59 Contact allergens

known to cause pompholyx are primin, isopropyl para

phenylene diamine, benzisothiazol ones, dichro-

mates, perfumes, fragrances, balsam and even nickel

sulfate. It was found that many nickel-sensitive

patients presented with this pattern of hand eczema

and produced flares on ingesting oral nickel sulfate.60

Chromium61 and cobalt have also been implicated,

and dermatophyte infection is another factor causing

‘‘id’’ reaction in the form of symmetrical vesicular

eruption. Aspirin ingestion, oral contraceptives and

regular smoking also increase the risk of pompholyx.

Clinically, an episode of pompholyx is character-

ized by sudden onset of crops of clear vesicles, which

appear deep-seated and sago-like. There is no ery-

thema, but a sensation of heat and prickling of the

palms may precede the attacks. Vesicles may

become confluent and present as large bullae. Reso-

lution with desquamation occurs in 2–3 weeks.

Rubbing and inappropriate treatment may produce

secondary eczematous changes. Nails can be

involved. The attacks can occur at intervals of

3–4 weeks for months or years; and there may also

be a pattern of summer aggravation.

Recurrent focal palmer peeling

This condition is probably a mild form of pompholyx,

presenting with small areas of superficial, white

(a)

(b)

Figure 2. (a,b) Hand dermatitis ⁄eczema: pompholyx show-ing multiple vesicles on the thenar eminence of the palmsextending to dorsa of the hands.

Figure 3. Hand dermatitis ⁄eczema: pompholyx keratoticscaly lesions of the hands.



desquamation on the sides of fingers and on palms

or on feet, mainly during summer months. There are

usually no vesicles, but some patients may subse-

quently develop true pompholyx. The condition is rel-

atively asymptomatic.

Hyperkeratotic palmer/tylotic eczema

Hyperkeratotic palmer ⁄ tylotic eczema is a distinct

form with highly irritable, scaly fissured, hyperkera-

totic patches on the palms and palmer surfaces of

fingers (Fig. 4), seen frequently in men of middle age.

Etiology is unknown, and patch tests are usually neg-

ative. However, in an Indian study of 230 patients

who were patch tested, contact sensitivity was

detected in 130, mainly by vegetables (garlic, onion),

followed by detergents, metals, rubber, leather, plas-

tic, fertilizers and drugs.62

Ring eczema

In ring eczema, an irritable patch of eczema begins

under a ring and typically spreads to involve the adja-

cent side of the middle finger and adjacent area of

the palm. This characteristic pattern commonly

affects young women, more so after marriage or

childbirth. However, as may be commonly thought,

these patients do not show sensitivity to gold, copper

and rarely to white gold alloys. Nickel, cobalt and

chromium sensitivity are found on patch testing, but

this type of hand eczema is primarily by concentra-

tions of soap and detergents beneath rings, with

micro-trauma or friction also playing a role. Ring der-

matitis has also been described as a clinical presen-

tation of fragrance sensitization.63 The dermatitis

remains confined or may occasionally show discoid

patches elsewhere or a diffuse vesicular eczema.

Wear and tear/asteatotic dermatitis/eczema/

housewives’ dermatitis/dry palmer eczema/

dermatitis palmeris sicca

This variant is due to a combined effect of asteatosis,

exposure to mild irritants and trauma. It is commonly

seen in housewives and cleaners who frequently

immerse their hands in water and detergents.

Accordingly, the horny layer of the skin gets dam-

aged, the skin over the palms becomes dry, appears

crisscrossed with superficial cracks and loses its nor-

mal pliability. There may be associated dryness and

chapping of skin over dorsa of knuckle joints. Exuda-

tion and weeping are not usually seen. The condition

is usually bilateral (Fig. 5).

Fingertip eczema

As the name suggests, fingertip eczema is a condi-

tion that characteristically involves the palmer sur-

face of the tips of some or all of the fingers. Skin is

dry, cracked and glazed and breaks down into

painful fissures (Fig. 6). It usually remains localized.

Two clinical patterns have been described. The first

type involves most or all of the dominant hand, par-

ticularly thumb and forefinger, and worsens in win-

ter. It is most likely more of a cumulative irritant

dermatitis due to degreasing agents and to trauma.

The second pattern involves preferentially the

thumb, forefinger and the third finger of one hand

and is usually occupational. It may be irritant or

allergic, seen with colophony, formaldehyde, tulip

bulbs41 or certain vegetables like onion and garlic

held in the fingers. Patch tests are relevant in the

second pattern.

Apron eczema

Apron eczema is a type of hand eczema that involves

the proximal palmer aspect of two or more adjacent

fingers and the contiguous palmer skin over the

metacarpophalangeal joints, thus resembling an

apron. Rarely, it is caused by contact allergens, but

may reflect the effect of irritants. It is more common

in women and is largely endogenous.64Figure 4. Hand dermatitis ⁄eczema: hyperkeratotic palmer ⁄tylotic eczema and hyperkeratosis of the palms.


V.N. Sehgal et al.

Discoid eczema

Discoid eczema is characterized by circular and ⁄or

oval plaques of eczema with a clearly demarcated

edge and normal intervening skin. The plaques usu-

ally recur at the same site. Both sexes are equally

affected. Various possibilities regarding its etiology

include an atopic diasthesis,65,66 role of infection,

local physical and chemical trauma, sensitivity to spe-

cific allergens and emotional stress. Role of contact

allergens was shown in a study on 48 patients with

discoid eczema of whom eight had hand eczema. A

high percentage of these showed clinically-relevant

positive patch tests with rubber, chemicals and met-

als as the common allergens.67 In an Indian study on

50 patients with discoid eczema, patch testing analy-

sis showed a positive reaction to allergens in 56%,

with potassium dichromate as the most common

allergen (20%), followed by nickel (16%), cobalt chlo-

ride and fragrances (12% each).68 Discoid eczema

may be recognized in three different patterns:

(i) hands and forearms; (ii) limbs and trunk; and (iii) dry

discoid eczema.

Discoid eczema of the hands affects the dorsa of

the hands or the backs or the sides of individual fin-

gers. It often develops as a single plaque, occurring

at the site of a burn or local chemical ⁄ irritant reaction.

Secondary lesions may occur on the hands, fingers

or forearms. In the acute phase, lesions are dull red,

oozy, crusted and go on to become less vesicular

and more scaly as they progress, with a central clear-

ing and peripheral extension.

Chronic acral dermatitis

Chronic acral dermatitis is a distinctive syndrome

affecting middle-aged patients, and is characterized

by pruritic, hyperkeratotic papulovesicular eczema of

(a) (b) (c)

Figure 5. (a,b) Hand dermatitis ⁄eczema: housewives’ dermatitis. (c) Skin over the palms is dry, criss-crossed and hassuperficial cracks.

(a)

(b)

Figure 6. (a,b) Hand dermatitis ⁄eczema: fingertip dermatitis.Dry, cracked, glazed skin, breaking down into painful ero-sions, affecting the palmer surface of the fingers.



the hands and the feet. It is associated with grossly

elevated immunoglobulin (Ig)E levels without any per-

sonal or family history of atopy.

Gut/slaughterhouse eczema.

Gut ⁄slaughterhouse eczema is seen as a transient

vesicular eczema which begins from the webs of the

fingers and spreads to the sides. Each episode may

be mild and may clear spontaneously but recurs at

regular intervals. This specifically affects workers

engaged in evisceration of carcasses of animals in

slaughterhouses. Its pathogenesis is uncertain.

Patchy papulosquamous eczema

Patchy papulosquamous eczema is a mixture of

irregular, patchy, vesiculosquamous lesions occur-

ring on both hands, usually asymmetrically. The

degree of activity and distribution of lesions varies.

OCCUPATIONAL DERMATITIS/ECZEMA

This is by far the most frequently reported occupa-

tional hazard. Of all the occupational diseases, der-

matoses comprise 20–70% in different countries of

the globe, and contact dermatitis alone contributes

20–90%. Occupational contact dermatitis (OCD) is

an entity that may be an outcome of exposure to

agents at work (Fig. 7). The agents may either be the

cause or one of the factors contributing to its occur-

rence. ICD may account for 6.33% of all the cases

while the remaining are due to allergic contact

hypersensitivity. Predisposing factors could either

be job-related wet work, irritating chemicals and

temperature changes, host-related, dryness, aging

skin, sweating and atopic diathesis65,66 or related

indirectly, to drugs, seasonal changes, personal

hygiene and age.

The candidates for OCD as compared to non-

occupational contact dermatitis (NOCD) are younger,

less likely to be atopics, predominantly male, have

hand and arm dermatitis, and show positive patch

test responses to rubber, metals, paraphenylene dia-

mine, epoxy and resins. However, if subjects with

irritant occupational contact dermatitis (IOCD) are

compared with those with allergic occupational con-

tact dermatitis (AOCD), the latter are likely to be

women, atopic and have dermatitis of the hands,

arms and eyelids. Contradictory to this, a study in

Denmark claimed a higher prevalence of occupa-

tional allergic contact dermatitis in men than women,

incriminating chromium, rubber derivatives and nickel

from work tools and metal working industry as the

main causative agents. It showed an equal preva-

lence of occupational irritant dermatitis in both

sexes.69,70

Hands are the most common site affected and are

involved in 70–80% cases of OCD. In a study in Swe-

den, OCD was localized to the hands in 94% women

and 84% men. It occurred at any age, however, and

average age of onset varied from one occupation to

another.66 In some studies, two peaks of age were

recorded, one at each end of working life.71

Occupations that are at major risk for occupational

hand eczema include agriculture, hospital work, con-

struction, manufacturing, laundering, food handling,

(a)

(b)

Figure 7. (a,b) Hand dermatitis ⁄eczema: erythema, indura-tions erosions pigmentations, with prominent skin marking,affecting dorsal and palmer surface of the hands.


V.N. Sehgal et al.

gardening, automobile repairs and domestic work.

Various irritants and sensitizers implicated are rubber,

metals, cutting fluids, chemicals, resins, soldering

fluxes, solvents, soaps, detergents, foodstuffs and

plants. The Indian studies found housewives invol-

ved in domestic work to be the most commonly

affected.8,23 A study from Singapore found the con-

struction industry as the target source of OCD.1

Health-care personnel form a major risk group for

occupational hand eczema. In a study conducted to

assess the clinical relevance of contact dermatitis in a

group of 1391 employees of a hospital, 21.2% had

contact dermatitis of the hands and forearms.72

Hairdressers and beauticians are the other group

commonly affected by HD. HD was seen in 26.1%

amongst Indian beauticians in a study comprising a

total of 161, of which 59.3% were positive for patch

tests. Paraphenylene diamine (35.5%), rubber anti-

gens (22.6%), nickel (22.6%) and shampoos, ammo-

nium thioglycolate and ammonium persulfate73 were

the usual incriminating allergens. A study on hair-

dressers from abroad also implicated the same

allergens. Eighty percent were deemed to have

allergic contact dermatitis while another 16% had

ICD. The skin eruptions involved the hands in all

but one case.74 In another study, in an Australian

population of hairdressers and trainees, 60% had

experienced changes in their hands since commenc-

ing hairdressing.75

In a survey of automobile mechanics, 15% were

reported to have hand eczema. However, ICD was

more prevalent in this group than allergic contact der-

matitis, and the most frequent relevant reaction was

to nickel.76

Bakers also tend to show more ICD, infections and

infestations than allergic contact dermatitis. Flour can

produce contact urticaria of the baker’s hands that is

further scratched and excoriated.77

A study of 246 shoemakers showed contact der-

matitis in 36 individuals with hyperkeratosis of the fin-

gers as the primary morphological presentation. Most

common allergens seen were p-tert-butylphenol-

formaldehyde and mercaptobenzothiazole.78

Flower bulb growers (gardeners) had contact irrita-

tion with many skin irritants like hyacinth sap, bulbs

and pesticides. Skin of the hands was often dam-

aged, characterized by redness, itching, callous

formation and fissures.41

DIAGNOSIS

The diagnosis of ACD of the hands depends upon the

history, examination of the skin surface and labora-

tory investigations including patch test.

History

It is imperative to question the patient about the mode

of onset, frequency, duration of the symptoms and

their relation to a particular season or time of year.

Also, a detailed account of the patient’s hobbies,

work profile, occupational and home environment,

habits and use of medicaments is necessary to con-

sider various exogenous factors involved in the etio-

pathogenesis. Another significant history to be ruled

out is that of atopy (personal or family) or childhood

eczema.

Examination of the skin surface

The hands should be thoroughly examined for the

type of lesions, their distribution and any specific pat-

tern to grade the severity of eczema. Any simulta-

neous involvement of adjoining or other parts of the

body should be checked for, especially the feet. A

complete general examination is always important to

eliminate any underlying systemic cause.

Laboratory investigations

Depending on the clinical picture of the disease and

its severity, hand eczema may also require a few non-

specific and basic investigations to rule out systemic,

endogenous, infectious causes and other conditions

showing a close resemblance clinically:

1 Potassium hydroxide (KOH) mount prepared from

the scraping from the active border to exclude

tinea ⁄candidiacies which may mimic allergic con-

tact dermatitis. It may either be primary or second-

ary to pre-existing dermatitis ⁄eczema.

2 A skin biopsy from a representative lesion may be

required to microscopically differentiate conditions

like psoriasis of the palms from contact dermatitis,

which may otherwise be difficult to differentiate by

clinical examination alone.

3 In case of fulminant hand eczema, with oozing ⁄purulent discharge, a smear can be examined

microscopically after Gram staining to rule out sec-

ondary bacterial infection and infectious eczema-

toid dermatoses (IED).



4 A total and differential leukocyte count, an absolute

eosinophil count and serum IgE can be done to

establish or rule out atopic diathesis.

Patch testing

The execution of patch testing is generally required to

pinpoint ⁄ identify offending agents of ACD. Properly

applied and correctly interpreted patch tests are con-

sidered the only systematic ‘‘proof’’ of ACD.11 Patch

testing is based on the observation that primed

antigen-specific T-lymphocytes should be present

throughout the body, and so an allergen in the patch

test would produce a dermatitic reaction even when

applied to apparently normal looking skin.

The first patch test was carried out in 1896 by

Jadassohn and the word ‘‘patch test’’ was coined by

Cooke in 1910. Ever since, the test has been modified

and standardized many a times.

Indications for patch testing include eczematous

disorders where contact allergy is suspected or to be

excluded, eczematous disorders failing to respond

to treatment as expected, chronic hand and foot

eczema, persistent or intermittent eczema of the

face, eyelids, ears and perineum, and varicose

eczema.79,80

Methods

The basis of testing is to elicit an immune response

by challenging already sensitized persons to defined

amounts of allergen and assessing the degree of

response. The technique includes the application of

the antigen to the skin of the patient, usually the

upper back or lateral aspect of the arm under occlu-

sion for an approximate period of 48 h. Various types

of patches, discs and chambers are used in order to

ensure occluded contact with the skin. The earliest

method was pieces of cotton fabric soaked with

offending allergen solutions. This method may still be

used in a modified way using gauze strips ⁄patches

impregnated with proper concentrations of the aller-

gen. Later, filter paper discs were also introduced,

used in a similar way and taped to the skin under a

water impermeable cover. The Al test is a develop-

ment of this method.76 In this, filter paper discs of

1 cm diameter are attached to polythene-coated alu-

minum foil. It has the advantage over aluminum

chambers because aluminum is not inert and can

react with metals.81 However, the Finn chambers

are the commonest system to apply allergens and

consist of small aluminum discs, mounted on acrylic-

based adhesive, non-occlusive, hypoallergenic tape,

devised by Pirila in 1975. Advantages of this method

include localization of reaction to test site and small

area required. The major disadvantage is reaction of

metal salts like mercury, cobalt and nickel with alumi-

num.82 Other systems consist of square plastic

chambers (Van der Bend chambers) and oval plastic

chambers (Epicheck; SmartPractice, Phoenix, AZ,

USA).

The true test is the newest method of patch test,

introduced by Fischer and Maibach.83 It involves the

use of ready-to-apply polyester patches coated with

allergens in hydrophilic allergen and has the advan-

tage of exact dosage, thin surface spread, equal dis-

tribution and high bioavailability of the allergen. There

are other ready-to-use patch tests namely Accupatch

(SmartPractice) and Epiquick (SmartPractice).84

PRECAUTIONS THAT ARE TO BE TAKENWHILE PATCH TESTING

1 Only known antigens in standard concentrations

should be used, and the antigen should not be

contaminated.

2 Vehicles used for suspending ⁄developing the anti-

gens should be non-sensitizing and able to release

the test substance upon coming into contact with

the skin.

3 The test should not be done if dermatitis is acute.

The test site should be completely free of derma-

titis.

4 The patient should be educated so as not to wet

the patches, and avoid heavy work and exercise

that may result in heavy sweating.

5 Patches are to be left on for 48 h ideally, but in case

of severe burning or irritation in a patch site, they

can be removed without disturbing the others.

Readings and interpretation of patch tests

Patch tests can be read initially at 48 h after allowing

the initial reaction from the adhesive tapes to subside,

but an additional reading at 72 h is usually advised.

Once developed, positive patch test reactions persist

for several days.

Strong reactions of an allergic nature are erythema-

tous and infiltrated, commonly with minute papules or


V.N. Sehgal et al.

vesicles, which in severe reactions coalesce to form

bullae. This is accompanied by a thickening of the

dermis due to infiltration. The results are recorded as

recommended by the international contact dermatitis

research group.

Reasons for false-positive reactions include adhe-

sive tape reactions, improper concentration of the

antigen or improper vehicle (as these can act as irri-

tants), acute phase of dermatitis, dermatitis near a

test site and recent patch testing at same site.

Another cause is angry back85 or excited skin syn-

drome, where a strong positive reaction provokes

multiple false-positive reactions at other sites.

False-negative reactions refers to a negative patch

test in the presence of contact allergy, and important

reasons for this are insufficient penetration of the

allergen, early reading, previous treatment of the test

site with topical steroid or ultraviolet radiation or use

of systemic corticosteroids.

Adverse reactions to patch test include anaphylac-

tic reactions, flare-up of pre-existing dermatitis and

risk of sensitizing the tested individual. Rare side-

effects include secondary infection at test site, hyper-

pigmentation and depigmentation, pseudolymphoma

and keloid reactions.13

Open test

This test is applied while testing poorly defined or

unknown substances such as those brought by the

patients. The test substance is dropped on an area of

1 cm2 and allowed to dry. The time for reading and

characteristics of the reading are the same as closed

patch testing.

Repeated open application test

This is done when the test agent gives a negative

patch test result despite strong clinical suspicion of

contact allergy.86 Substances are applied twice daily

for 7 days, and an area of at least 5 cm2 on the upper

back, antecubital fossa or outer aspect of upper arm

is employed.

Usage test

If a patch test to a strongly suspected allergen is

negative, the patient is asked to use the prepara-

tion again routinely as before in order to detect

sensitivity. It is useful in detecting allergy to cos-

metics.

All the above tests also help in distinguishing

irritant reactions from allergens and confirm allergy to

a suspected contactant. For contact urticaria, prick

tests, scratch tests and scratch chambers are

employed.

Management strategy

Hand eczema ⁄dermatitis has always been a fascinat-

ing challenge for it is capable of remissions and exac-

erbation. Apparently, it is hard to avoid the allergens

incriminated for the condition, more so in the under-

privileged candidate of the disease. Nevertheless, it is

worthwhile to dwell on the modalities available thus

far to alleviate the symptoms and signs (Tables 1,2)

Hand dermatitis ⁄eczema is a chronic skin disorder.

Although topical corticosteroids are often used to

control the predominant symptoms of the disease,

the chronicity of the condition increases the risk of

long-term adverse effects. The advent of calcineurin-

blocking, non-steroidal topical immunomodulators

for effective management of eczema as a safer alter-

native95 is appreciated. Accordingly, local immuno-

modulator such as tacrolimus (calcineurin) and

pimecrolimus are breakthrough advances. The form-

ers’ pharmacokinetics, mechanism of action, drug

interaction dosage, side-effects, approved and

unapproved dermatological indications ⁄usages are

succinctly recounted elsewhere,93,94 while that of

pimecrolimus are described in another review.96

In an open-label pilot study to evaluate the safety

and efficacy of topically applied tacrolimus ointment

for the treatment of hand and ⁄or foot eczema, it was

concluded that 0.1% tacrolimus ointment is a promis-

ing corticosteroid alternative.99 Furthermore, topical

tacrolimus 0.1% was found to improve the induration

Table 1. Hand dermatitis ⁄eczema: acute

Acute Use ⁄ indication

Moist compresses Soothing effect and removalof crusts and debris

Antiseptics

Burrows solution

Condy’s solution

For control of secondary

infection, softening of crust

and debrisOral antihistamines Control of associated pruritus

Oral antibiotics87 Control of superimposed

bacterial infection

Systemic corticosteroids{pred. ⁄ beta ⁄ dexamethasone ⁄methylpred pulse88–90

Required for fulminant casesnot controlled by topical

corticosteroids



and scaling, and there was a trend to suggest that it

prolongs the time to recurrence in patients treated

with a prednisone taper.113 Topical tacrolimus might

also be an efficacious treatment option for chronic

occupational HD. However, blinded and randomized

controlled studies are necessary to confirm the

results.114

In addition, efficacy and safety of tacrolimus oint-

ment 0.1% and pimecrolimus cream 1% in adults

with moderate atopic dermatitis were compared in

another study. Tacrolimus ointment was found to be

more effective than pimecrolimus cream. However,

overall, reported adverse events occurred at a similar

frequency for both treatment groups.115 Long-term

efficacy of occlusive therapy with topical pimecroli-

mus in severe dyshidrosiform hand and foot eczema

has also been claimed.116 Similarly, successful treat-

ment of chronic persistent vesicular HD with topical

pimecrolimus ointment 1% has been reported.117,118

In addition to conventional treatment modalities,

the use of cyclosporin A, (CyA) an immunosuppres-

sant, has been mooted in chronic recalcitrant HD.

Table 2. Hand dermatitis ⁄eczema: sub-acute and chronic

Sub-acute ⁄ chronic Use ⁄ indication

Avoidance of allergen: use of gloves minimal,use of irritants like soaps detergents

In proven cases of allergic contact dermatitis to specificsubstances

Topical therapy

Emollients

BlandWith alpha hydroxy acids

First-line of treatment to decrease itching and reduce dryness and

scaling

For thick scaly plaques

Topical steroids

Low to medium strength

Potent and highly potenti.d. triamcinolone92

Prolonged use in chronic cases

Short-term; intermittent use91; hyperkeratotic eczema; refractory

casesRecalcitrant localized patches of eczema

Other applications like tar paste, salicylic

acid, propylene glycol

Mainly as adjuvants to topical steroids

Topical immunomodulators

Tacrolimus93–95

Pimecrolimus96–98

For erythema, scaling, induration, fissuring, pruritus

Used singly or in combination with topical steroids99

Topical Vitamin D3 derivatives100

Calcipotriol

Maxa-calcitriol

Recalcitrant hyperkeratotic eczema

Bexarotene gel101 Severe chronic cases

i.d. botulinum toxin102 Dyshidrotic eczemaSystemic therapy

H1 blocker (oral antihistamines): hydroxyzine

hydrochloride, cetirizine dihydrochloride

Alleviation of pruritus

H2 blocker: (cimetidine, ranitidine hydrochloride)103 Useful in atopic hand eczema. Suppressive effect on wheal, flare,

itching104

Oral corticosteroids Rarely required; only in cases with acute exacerbation

Oral immunosuppressantsCyclosporine105

Methotrexate98

Refractory cases not responding to above treatment

Oral retinoids Effective in recalcitrant hyperkeratotic hand eczema

Chelating agents like disulfiram60,106 Useful in allergic contact dermatitis of hands to metals (nickel)Phototherapy107

UV-B

PUVA

OralGel108

Bath109

Only UV-A110

Visible light111

Chronic stubborn cases not responding to treatment; dyshidrotic

eczema

Grenz rays112 Tried in refractory cases

PUVA, psoralen and ultraviolet A therapy; UV, ultraviolet.


V.N. Sehgal et al.

Accordingly, the efficacy of CyA was evaluated in

seven patients of chronic HD. It was administrated

at a daily dose of 2.5 mg ⁄kg in five, and 1.25 mg ⁄kg

in another two patients. In those who responded to

the treatment at 2.5 mg ⁄kg per day, the daily CyA

dose was reduced stepwise to the lowest mainte-

nance dose of 1.25 mg ⁄kg. In patients who did not

respond, the dose was increased to a maximum of

5 mg ⁄kg per day. The treatment was given for

2–16 weeks. In six of the seven patients, the derma-

titis responded to CyA treatment within a few weeks.

However, no response was seen with a starting dose

of 1.25 mg ⁄kg per day. In three of the five patients

with a starting dose of 2.5 mg ⁄kg per day, the daily

CyA dose could be reduced to 1.25–2 mg ⁄kg per

day. After stopping CyA treatment, the dermatitis

recurred during follow up in three patients, and three

had remission. CyA might be a useful treatment

modality101 for chronic HD not responding to con-

ventional therapy. Similar, observations were made

earlier.119

The efficacy and safety of oral alitretinoin (9-cis-

retinoic acid) taken at 10 or 30 mg once daily for up

to 24 weeks, compared with placebo control, in the

treatment of severe chronic hand eczema (CHE)

refractory to topical corticosteroids was assessed

through a double-blind, placebo-controlled, prospec-

tive, multicenter trial. It was claimed that alitretinoin

given at well-tolerated doses induced clearing of

CHE in a substantial proportion of patients with

severe disease refractory to standard therapy. How-

ever, the preceding observation needs confirmation

in the future studies on this invaluable addition to the

therapy of chronic HD ⁄eczema.120

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