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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.
� 2010 Japanese Dermatological Association 595
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
596 � 2010 Japanese Dermatological Association
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
� 2010 Japanese Dermatological Association 597
Hand dermatitis ⁄ eczema
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.
598 � 2010 Japanese Dermatological Association
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.
� 2010 Japanese Dermatological Association 599
Hand dermatitis ⁄ eczema
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.
600 � 2010 Japanese Dermatological Association
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.
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Hand dermatitis ⁄ eczema
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.
602 � 2010 Japanese Dermatological Association
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).
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Hand dermatitis ⁄ eczema
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
604 � 2010 Japanese Dermatological Association
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
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Hand dermatitis ⁄ eczema
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.
606 � 2010 Japanese Dermatological Association
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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