doi: 10.1111/j.1346-8138.2010.00845.

Journal of Dermatology 2010; 37: 593610

REVIEW ARTICLE

Hand dermatitis/eczema: Current management strategy

Virendra N. SEHGAL,1 Govind SRIVASTAVA,2 Ashok K. AGGARWAL,2 Alpna D. SHARMA2
1

Dermato-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. Idiosyncrasies continued to loom large thereafter, till it acquired its appropriate position. Dermatitis eczema are synonymous, often used to indicate a polymorphic pattern of the inammation 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 ngertip eczema, apron, discoid eczema, chronic acral dermatitis, gut and patchy papulosquamous eczema are its clinical variants. Occupational dermatitis eczema may be contributory. Etiological denitions are clinched by detailed history of exogenous and endogenous factors. However, scientic conrmation of the entity is through patch testing by using available antigens. Key words: hand dermatitis eczema: clinical classication, 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 serious 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 conned to the hands. Dermatitis eczema are often used synonymously to indicate a polymorphic pattern of the inammation of the skin, characterized by pruritus, erythema and vesiculation. Hand eczema is a frequently encountered problem, affecting individuals from all walks of life, involved in different elds of work. In the absence of required care and therapy, it may turn into a chronic, distressing disease largely

inuencing an individuals daily life. Both endogenous and exogenous factors may contribute to the development of HD eczema. Endogenous factors refer to conditions like atopic dermatitis, hyperkeratotic palmer dermatitis and the like, while exogenous factors include both systemic and topical irritants, allergens, inhalants, ingestants and infections. In situations where an inammatory response of the skin occurs following exposure to exogenous substance allergen irritant, it is designated as contact dermatitis. Also, irritant and or allergic contact dermatitis, phototoxic and photo-allergic contact dermatitis, an immediate type of contact reaction, are also included in the category. Contact dermatitis is an alarming problem all over the world. Whole population studies and examinations of random samples of people have put its incidence at 1.56%, 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: drsehgal@ndf.vsnl.net.in Received 17 September 2009; accepted 1 November 2009.

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trades like construction work, chemical and metal industries, the incidence is particularly high.3 Approximately 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 dermatitis of the hands particularly forms an occupational hazard in housewives, hairdressers, dental and medical personnel, metal workers and laborers. Established important risk factors5 include history of childhood eczema, female sex, occupational exposure, 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, mercaptobenzothiazole, thiurams and paraphenylene diamine7 were the eight most common allergens identied 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 patients 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 patients 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 identied. Supplemental allergens that are added to screening series based on patients history provide additional relevant information.11

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 inammatory 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 classied 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 inammatory reaction characterized by erythema, edema or corrosion, following single or repeated applications of a substance to an identical cutaneous site. Inammatory or immunological mediators may be activated but no memory cell T cells function or antigen-specic immunoglobulins are involved.14 Allergic contact dermatitis is a T-cell-mediated immunological reaction that requires prior sensitization. It is a delayed type hypersensitivity (type IV) reaction that occurs from exposure of sensitized individuals to contact allergens. Distinction between irritant 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 century, idiosyncratic reactions to various substances were identied. 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 produced by Anacardium occidentale on human skin using blotting paper strips. Collins, an ophthalmologist, 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

DEFINITION
Eczema literally means boil out, is an inammatory skin reaction pattern characterized histologically by spongiosis with varying degrees of acanthosis and a supercial perivascular lymphocytic inltrate. 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 specied

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thus established the role of patch testing in dermatitis medicamentosa. The term allergic was rst coined in 1906. Allergic sensitization of the skin was rst 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 substances could cause contact reactions after conjugation with protein carriers. This was followed by demonstration of passive transfer of delayed hypersensitivity 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 marginatum.16 Radcliff Crocker emphasized the role of external irritants in development of hand eczema.

exposure to wet work, detergents and other household 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 sensitization. Considering contact dermatitis in the occupational scenario, it has been observed to account for 4060% 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%
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EPIDEMIOLOGY
Contact dermatitis of the hands is a common disorder. The incidence of HD varied from 10.915.8% in different studies.8 Reports from the Indian subcontinent revealed that 510% 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 Sweden, 11.8% of the population under observation considered 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 men2123 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

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

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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 contact 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 coexisting conditions. In a study to identify factors of importance for longterm prognosis of hand eczema, the main determinant 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 exogenous as well as endogenous factors may play a signicant role. The former (exogenous) factors refer to inuences of the external environment, where as the latter (endogenous) factors refer to constitutional inuences 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 sufcient period of time, and in adequate concentration.30 Acute irritant dermatitis is recognized rst by exposure 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 Dermatitis eczema arise without previous sensitization when the repair capacity of the skin is impeded or exhausted when penetration of the chemical provokes an inammatory reaction.13 Irritants are a frequent cause of hand eczema.32 Although the irritant affects almost everyone, its susceptibility 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 industrial cleaning agents like solvents, abrasives, alkalies, cutting oils, oxidizing and reducing agents, and desiccant 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 inuence of a variety of subsequent stimuli, each one perpetuating the previous episode.35 Clinical spectrum of acute ICD ranges from mild reaction to transient erythema and chapping to orid dermatitis with pain, inammation, edema, vesiculation, exudation and necrosis. In contrast, in chronic ICD, an eczematous condition persists for more than 6 weeks causing redness edema, scaling and ssuring on thin and exposed skin of the hands. Allergens Contact allergens are almost invariably small substances 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 sensitize. Prior sensitization is a salient prerequisite for allergic contact dermatitis. In a sensitized individual, acute contact dermatitis (ACD) appears or is exacerbated 2496 h after contact with the causative

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allergen and its initial localization is at the site of contact.13 Agrups study found metals, balsam, phenol, formaldehyde, resin, colophony, mercaptobenzothiazole and wood tar to be the most frequent sensitizers in Sweden.20 A study from Britain found balsams, nickel, medicaments, cobalt, rubber, chromate, 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 housewives who show ACD to garlic and onion have involvement of the thumb, index and middle nger 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 detergents.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 ngers, characteristically as tulip ngers, 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 lichenication, ssuring 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 exudation an urticaria (wheal) may be a presenting feature. The urticaria begins at the site of contact with allergens. Proteinous products like sh 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 dermatitis) 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 commonest 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 challenges 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 hospitals were studied, it was found that HD occurred in 65% of persons with atopic symptoms.50 In yet another ve 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 signicant predictive value.

PATHOGENESIS
Irritant contact dermatitis is a non-immunological inammatory reaction. It occurs following an exposure to an irritant, without prior sensitization. It has a twofold pathogenic mechanism. Chronic irritant dermatitis is related to a disturbed barrier function, and an increased epidermal cell turnover leading to lichenication, whereas an acute ICD is more of an inammatory 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

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Allergic contact dermatitis Allergic contact dermatitis is a delayed hypersensitivity reaction mediated by T cells. Under ordinary conditions, exposure to contact allergens sets in motion two competing mechanisms, the one mediated by effecter T-lymphocytes leading to a state of hypersensitivity 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 membrane proteins. It is not possible for T-lymphocytes to interact directly with the contact antigen even when they posses the appropriate surface receptors for that antigen. The antigen must rst be processed and then be presented in a suitable form in which it associates with major histocompatibility complex class II molecules, coded in the human leukocyte antigen-differentiation 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 antigenpresenting 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.5355 Recent data deriving from transgenic animals that are decient in LC have begun to challenge the dogma that there is a universal requirement for these cells in the development of skin sensitization. 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-specic 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 specicity throughout the body of a sensitized individual, and takes 710 days before there are sufcient numbers of T-lymphocytes to cause contact dermatitis. On subsequent exposure, antigen-presenting cells and specic T cells meet locally, leading to cytokine production within the skin, thus leading to development of an erythematous reaction, which reaches a maximum in 1848 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 classication of HD has already been described (vide supra). However, no single classication of hand eczema is completely satisfactory. A simple method is to classify it according to the stage of eczema: 1 Acute: clinical features range from erythema, chapping to a orid dermatitis with edema, inammation, vesiculation, pain, exudation, bullae formation and tissue necrosis. 2 Subacute: milder, characterized by erythema, papules and crusting. 3 Chronic: lichenication characterized by thickening of the skin, exaggerated skin marking, scaling and pigmentation. The preceding classication is easy to comprehend and facilitates treatment approach. However, an anatomical classication is useful in dening the etiology of HD. A morphological classication 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.

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Pompholyx Pompholyx is a frequent deep-seated vesicular eruption 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 (cheiropompholyx) (Figs 2,3) and of the soles (podopompholyx). It accounts for 520% of all cases of hand eczema.20,32 The role of sweat glands is disputed, although distribution of lesions corresponds to emotionally activated palmoplantar sweating and hot weather. However, hyperhidrosis is not a constant feature. Role of atopy may be signicant. Lodi et al.58 found personal and family history of atopy in 50% of their patients as compared to 12% controls. Primary irritants may cause pompholyx, for example in metal workers exposed to soluble oils.59 Contact allergens
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Figure 3. Hand dermatitis eczema: pompholyx keratotic scaly lesions of the hands.

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known to cause pompholyx are primin, isopropyl para phenylene diamine, benzisothiazol ones, dichromates, perfumes, fragrances, balsam and even nickel sulfate. It was found that many nickel-sensitive patients presented with this pattern of hand eczema and produced ares 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 characterized by sudden onset of crops of clear vesicles, which appear deep-seated and sago-like. There is no erythema, but a sensation of heat and prickling of the palms may precede the attacks. Vesicles may become conuent and present as large bullae. Resolution with desquamation occurs in 23 weeks. Rubbing and inappropriate treatment may produce secondary eczematous changes. Nails can be involved. The attacks can occur at intervals of 34 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 supercial, white

Figure 2. (a,b) Hand dermatitis eczema: pompholyx showing multiple vesicles on the thenar eminence of the palms extending to dorsa of the hands.

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desquamation on the sides of ngers and on palms or on feet, mainly during summer months. There are usually no vesicles, but some patients may subsequently develop true pompholyx. The condition is relatively asymptomatic. Hyperkeratotic palmer/tylotic eczema Hyperkeratotic palmer tylotic eczema is a distinct form with highly irritable, scaly ssured, hyperkeratotic patches on the palms and palmer surfaces of ngers (Fig. 4), seen frequently in men of middle age. Etiology is unknown, and patch tests are usually negative. 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, plastic, fertilizers and drugs.62 Ring eczema In ring eczema, an irritable patch of eczema begins under a ring and typically spreads to involve the adjacent side of the middle nger 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 concentrations of soap and detergents beneath rings, with

micro-trauma or friction also playing a role. Ring dermatitis has also been described as a clinical presentation of fragrance sensitization.63 The dermatitis remains conned 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 damaged, the skin over the palms becomes dry, appears crisscrossed with supercial cracks and loses its normal pliability. There may be associated dryness and chapping of skin over dorsa of knuckle joints. Exudation and weeping are not usually seen. The condition is usually bilateral (Fig. 5). Fingertip eczema As the name suggests, ngertip eczema is a condition that characteristically involves the palmer surface of the tips of some or all of the ngers. Skin is dry, cracked and glazed and breaks down into painful ssures (Fig. 6). It usually remains localized. Two clinical patterns have been described. The rst type involves most or all of the dominant hand, particularly thumb and forenger, and worsens in winter. It is most likely more of a cumulative irritant dermatitis due to degreasing agents and to trauma. The second pattern involves preferentially the thumb, forenger and the third nger 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 ngers. 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 ngers and the contiguous palmer skin over the metacarpophalangeal joints, thus resembling an apron. Rarely, it is caused by contact allergens, but may reect the effect of irritants. It is more common in women and is largely endogenous.64

Figure 4. Hand dermatitis eczema: hyperkeratotic palmer tylotic eczema and hyperkeratosis of the palms.

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Figure 5. (a,b) Hand dermatitis eczema: housewives dermatitis. (c) Skin over the palms is dry, criss-crossed and has supercial cracks.
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Figure 6. (a,b) Hand dermatitis eczema: ngertip dermatitis. Dry, cracked, glazed skin, breaking down into painful erosions, affecting the palmer surface of the ngers.

edge and normal intervening skin. The plaques usually 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 specic 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 metals as the common allergens.67 In an Indian study on 50 patients with discoid eczema, patch testing analysis showed a positive reaction to allergens in 56%, with potassium dichromate as the most common allergen (20%), followed by nickel (16%), cobalt chloride 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 ngers. 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, ngers 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 clearing 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

Discoid eczema Discoid eczema is characterized by circular and or oval plaques of eczema with a clearly demarcated

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the hands and the feet. It is associated with grossly elevated immunoglobulin (Ig)E levels without any personal 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 ngers and spreads to the sides. Each episode may be mild and may clear spontaneously but recurs at regular intervals. This specically 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 occurring on both hands, usually asymmetrically. The degree of activity and distribution of lesions varies.

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OCCUPATIONAL DERMATITIS/ECZEMA
This is by far the most frequently reported occupational hazard. Of all the occupational diseases, dermatoses comprise 2070% in different countries of the globe, and contact dermatitis alone contributes 2090%. 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 occurrence. 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 nonoccupational 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 diamine, epoxy and resins. However, if subjects with irritant occupational contact dermatitis (IOCD) are compared with those with allergic occupational contact 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

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

Denmark claimed a higher prevalence of occupational 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 prevalence of occupational irritant dermatitis in both sexes.69,70 Hands are the most common site affected and are involved in 7080% cases of OCD. In a study in Sweden, 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, construction, manufacturing, laundering, food handling,

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gardening, automobile repairs and domestic work. Various irritants and sensitizers implicated are rubber, metals, cutting uids, chemicals, resins, soldering uxes, solvents, soaps, detergents, foodstuffs and plants. The Indian studies found housewives involved in domestic work to be the most commonly affected.8,23 A study from Singapore found the construction 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 antigens (22.6%), nickel (22.6%) and shampoos, ammonium thioglycolate and ammonium persulfate73 were the usual incriminating allergens. A study on hairdressers 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 commencing 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 dermatitis, 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 bakers hands that is further scratched and excoriated.77 A study of 246 shoemakers showed contact dermatitis in 36 individuals with hyperkeratosis of the ngers as the primary morphological presentation. Most common allergens seen were p-tert-butylphenolformaldehyde and mercaptobenzothiazole.78 Flower bulb growers (gardeners) had contact irritation with many skin irritants like hyacinth sap, bulbs and pesticides. Skin of the hands was often damaged, characterized by redness, itching, callous formation and ssures.41

DIAGNOSIS
The diagnosis of ACD of the hands depends upon the history, examination of the skin surface and laboratory 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 patients hobbies, work prole, occupational and home environment, habits and use of medicaments is necessary to consider various exogenous factors involved in the etiopathogenesis. Another signicant 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 specic pattern to grade the severity of eczema. Any simultaneous 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 nonspecic 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 contact dermatitis. It may either be primary or secondary 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 difcult 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 secondary bacterial infection and infectious eczematoid dermatoses (IED).

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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 considered the only systematic proof of ACD.11 Patch testing is based on the observation that primed antigen-specic 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 rst 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 modied 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 dened 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 occlusion 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 modied way using gauze strips patches impregnated with proper concentrations of the allergen. Later, lter 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 development of this method.76 In this, lter paper discs of 1 cm diameter are attached to polythene-coated aluminum 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 acrylicbased 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 aluminum.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 advantage of exact dosage, thin surface spread, equal distribution 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 TAKEN WHILE 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 antigens 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 dermatitis. 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 erythematous and inltrated, commonly with minute papules or

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vesicles, which in severe reactions coalesce to form bullae. This is accompanied by a thickening of the dermis due to inltration. The results are recorded as recommended by the international contact dermatitis research group. Reasons for false-positive reactions include adhesive tape reactions, improper concentration of the antigen or improper vehicle (as these can act as irritants), acute phase of dermatitis, dermatitis near a test site and recent patch testing at same site. Another cause is angry back85 or excited skin syndrome, 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 insufcient 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 anaphylactic reactions, are-up of pre-existing dermatitis and risk of sensitizing the tested individual. Rare sideeffects include secondary infection at test site, hyperpigmentation and depigmentation, pseudolymphoma and keloid reactions.13 Open test This test is applied while testing poorly dened 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 preparation again routinely as before in order to detect sensitivity. It is useful in detecting allergy to cosmetics.

All the above tests also help in distinguishing irritant reactions from allergens and conrm 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 fascinating challenge for it is capable of remissions and exacerbation. Apparently, it is hard to avoid the allergens incriminated for the condition, more so in the underprivileged 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 calcineurinblocking, non-steroidal topical immunomodulators for effective management of eczema as a safer alternative95 is appreciated. Accordingly, local immunomodulator such as tacrolimus (calcineurin) and pimecrolimus are breakthrough advances. The formers 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 efcacy of topically applied tacrolimus ointment for the treatment of hand and or foot eczema, it was concluded that 0.1% tacrolimus ointment is a promising corticosteroid alternative.99 Furthermore, topical tacrolimus 0.1% was found to improve the induration
Table 1. Hand dermatitis eczema: acute
Acute Moist compresses Antiseptics Burrows solution Condys solution Oral antihistamines Oral antibiotics87 Systemic corticosteroids {pred. beta dexamethasone methylpred pulse8890 Use indication Soothing effect and removal of crusts and debris For control of secondary infection, softening of crust and debris Control of associated pruritus Control of superimposed bacterial infection Required for fulminant cases not controlled by topical corticosteroids

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

Sub-acute chronic Avoidance of allergen: use of gloves minimal, use of irritants like soaps detergents Topical therapy Emollients Bland With alpha hydroxy acids Topical steroids Low to medium strength Potent and highly potent i.d. triamcinolone92 Other applications like tar paste, salicylic acid, propylene glycol Topical immunomodulators Tacrolimus9395 Pimecrolimus9698 Topical Vitamin D3 derivatives100 Calcipotriol Maxa-calcitriol Bexarotene gel101 i.d. botulinum toxin102 Systemic therapy H1 blocker (oral antihistamines): hydroxyzine hydrochloride, cetirizine dihydrochloride H2 blocker: (cimetidine, ranitidine hydrochloride)103 Oral corticosteroids Oral immunosuppressants Cyclosporine105 Methotrexate98 Oral retinoids Chelating agents like disulram60,106 Phototherapy107 UV-B PUVA Oral Gel108 Bath109 Only UV-A110 Visible light111 Grenz rays112
PUVA, psoralen and ultraviolet A therapy; UV, ultraviolet.

Use indication In proven cases of allergic contact dermatitis to specic substances First-line of treatment to decrease itching and reduce dryness and scaling For thick scaly plaques Prolonged use in chronic cases Short-term; intermittent use91; hyperkeratotic eczema; refractory cases Recalcitrant localized patches of eczema Mainly as adjuvants to topical steroids For erythema, scaling, induration, ssuring, pruritus Used singly or in combination with topical steroids99 Recalcitrant hyperkeratotic eczema

Severe chronic cases Dyshidrotic eczema Alleviation of pruritus

Useful in atopic hand eczema. Suppressive effect on wheal, are, itching104 Rarely required; only in cases with acute exacerbation Refractory cases not responding to above treatment

Effective in recalcitrant hyperkeratotic hand eczema Useful in allergic contact dermatitis of hands to metals (nickel) Chronic stubborn cases not responding to treatment; dyshidrotic eczema

Tried in refractory cases

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 efcacious treatment option for chronic occupational HD. However, blinded and randomized controlled studies are necessary to conrm the results.114 In addition, efcacy and safety of tacrolimus ointment 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 efcacy of occlusive therapy with topical pimecrolimus in severe dyshidrosiform hand and foot eczema has also been claimed.116 Similarly, successful treatment 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 immunosuppressant, has been mooted in chronic recalcitrant HD.

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Accordingly, the efcacy of CyA was evaluated in seven patients of chronic HD. It was administrated at a daily dose of 2.5 mg kg in ve, 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 maintenance 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 216 weeks. In six of the seven patients, the dermatitis 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 ve patients with a starting dose of 2.5 mg kg per day, the daily CyA dose could be reduced to 1.252 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 conventional therapy. Similar, observations were made earlier.119 The efcacy and safety of oral alitretinoin (9-cisretinoic 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, prospective, 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. However, the preceding observation needs conrmation in the future studies on this invaluable addition to the therapy of chronic HD eczema.120

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