398 Inflammation & Allergy - Drug Targets, 2009, 8, 398-404

Atopic Dermatitis in the Elderly

Ryoji Tanei*

Department of Dermatology, Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Sakaecho 35-2,
Itabashi-ku, Tokyo 173-0015, Japan

Abstract: Though atopic dermatitis (AD) is relatively uncommon in the elderly, elderly patients with AD are gradually
increasing in industrialized countries associated with an aging society. Therefore, the clinical features of senile AD are
becoming more apparent in some aspects. Three patterns of onset—senile onset, recurrence of AD with a history of
classic childhood AD, and recurrence or continuation of adult AD—are associated with AD in the elderly. A male
predominance in elderly AD may be a characteristic feature that differs from adult AD. Localized lichenifications in the
folds of elbows and knees that are typical of classic AD are uncommon. Similar to AD in the other age groups, both
extrinsic and intrinsic forms of AD exist in the elderly, and the major environmental allergens in the extrinsic form are
house dust mite, followed by pollens and foods. In addition to the clinical features, this review focuses on the
pathogenesis, diagnosis, management and future directions of this new subgroup of AD.
Keywords: Atopic dermatitis, the elderly, clinical feature, IgE, etiology, diagnosis, management.

INTRODUCTION observed. In the childhood phase (from 2 to 12 years), atopic

Atopic dermatitis (AD, also known as atopic eczema) is a
chronic relapsing inflammatory skin disorder, characterized
by IgE-mediated allergy and skin barrier defects in its
pathogenesis [1, 2]. AD was added to the group of atopic
disorders in 1930s based on its association with bronchial
asthma and allergic rhinitis [3]. Until the 1960-70s, AD was
considered to be a pediatric disease with a good prognosis—
known as classic childhood AD—as the first signs of AD
mostly appeared in the infantile phase and resolution of AD
occurred with an increase in age until puberty in typical
cases. With an increase in the incidence of the childhood AD
from the 1980s, cases in which clinical manifestations
persisted or first appeared during adolescence and adulthood
have increased in industrialized countries, known as adult
AD. It has had a significant impact on the quality-of-life of
patients and influenced public health policies worldwide. In
Japan, adult AD that are resistant to conventional therapy
became a major problem in the 1990s with the
commercialization and use of atopy-related goods and folk
medicine that did not have a scientific basis [4]. The
prevalence of AD has increased two- to threefold during past
few decades in industrialized countries. Nowadays, AD has
become a common and problematic condition, affecting up
to 20% of children and 1-3% of adults in the developed
world [5].
The characteristic symptoms of AD are: chronic course
of the disorder, dry skin, itching and age-specific
morphology and distribution of skin lesions. AD has been
divided into 3 phases based on its characteristics at different
stages in life. In the infantile phase (up to 2 years),
erythematous and papulovesicular eruptions on the face,
scalp and extensor surfaces of the extremities are often
*Address correspondence to this author at the Department of Dermatology,
Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology,
Sakaecho 35-2, Itabashi-ku, Tokyo 173-0015, Japan; Tel: 03-3964-1141;
Fax: 03-3964-1982; E-mail: rtanei@aol.com
dry skin and lichenified flexural eczema of the extremities
become more prominent. In the adolescent/adult phases
(from puberty to adulthood), chronic lichenified eczema on
the face, neck and trunk predominate [3-6].
It has been considered that AD usually resolves by the
fourth decade [7]. However, elderly patients with AD are
gradually increasing in Japan [8] and in other industrialized
countries [9-10] associated with an aging society. Therefore,
clinical features of senile AD are becoming more apparent in
some aspects [11].
This review focuses on the features of this new subgroup
of elderly AD.
CLINICAL FEATURES OF SENILE AD
The characteristics of senile AD with regards to its
epidemiology, onset, manifestations and IgE reactivity are
summarized in Table 1.
Epidemiology
Dermatitis is a common skin disorder among elderly
people. It can be classified into several types according to the
etiology, such as AD, contact dermatitis, seborrheic
dermatitis and asteatotic dermatitis. However, the incidence
of AD in elderly patients is markedly lower than other forms
of dermatitis. The estimated incidence of dermatitis in the
elderly (age 65 years and over) in our geriatric hospital in
Tokyo, Japan, in the past 10 years was as follows: AD
0.39%, contact dermatitis (both allergic and irritant types)
20%, seborrheic dermatitis 20% and asteatotic dermatitis
33% [11, 12].
The prevalence of AD in the senile phase, which was
reported as point and/or 1-year prevalence, was 0.6% in
Mexico (age 60 years and over) [13] and 2.6% in Japan (age
60 years and over) [14]. The prevalence of AD in the elderly
was lower than those in children and young adults: 10.1% in
Mexico (age 6-10 years) [15] and 11.2% and 9.8% in the age
groups 6-12 years [16] and the twentieth decade [17] in

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Atopic Dermatitis in the Elderly Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 399

Table 1. Clnical Features of Senile AD

Incidence & prevalence Incidence of AD in elderly patients is markedly lower than other forms of dermatitis

Prevalence of AD in the elderly is lower than that in children and young adults

Gender ratio Male predominance

Patterns of onset Three patterns are apparent:

a) Senile onset

b) Recurrence with a history of classic childhood AD

c) Recurrence and/or continuation of adult AD

Skin manifestations Generally similar to those in adult AD:

Chronic eczematous dermatitis on the face and neck and lichenification on the trunk and extremities

Other clinical stigma of AD (facial erythema and pallor, Hertoghe's sign, dirty neck and follicular lichenified papules)

Features of senile AD that differ from adult AD:

Classic sign of localized lichenifications in the folds of the elbows and knees is uncommon

Reverse sign of lichenification around the unaffected folds of elbows and knees is common

IgE reactivity Both extrinsic and intrinsic forms exist

Major extrinsic environmental allergens include house dust mites, pollens, and foods
AD, atopic dermatitis.

Japan, respectively. A recent research from Germany has
reported a lifetime prevalence of AD of 4.3% in the elderly
population (mean age 62 years, range 50-74 years) [18].
A gender difference in the prevalence of senile AD is
uncertain; however, a male predominance was found in
studies from Japan [14] and Australia [19]. In our clinical
study over a 9-year period [11], the male: female ratio of
senile AD was 3:1. In contrast, several studies of adult AD
have indicated that the prevalence in women is higher than
that of men, especially in young adults [10, 17, 19, 20].
Thus, a male predominance in senile AD may be a
characteristic that differs from adult AD.
Onset
Three patterns of onset—senile onset, recurrence with a
history of classic childhood AD and recurrence and/or
continuation of adult AD—may be associated with senile
AD [11]. A history of childhood and adult AD may also be
present.
In a study from Turkey, it was reported that cases of AD
with an onset after puberty (so-called adult-onset AD)
comprised of 73% young adults (age 18-29 years) and 1.6%
elderly patients (age in their 70s) [9]. In patients with a
history of childhood AD, the recurrence rate of AD in the
senile phase is still unknown. In a study from Sweden, AD
persisted in 59 to 68% of patients who had a history of AD
as young adults; this was noted after 25 to 41 years of
follow-up [10].
Manifestations
The characteristics of skin manifestations seen in senile
AD are basically similar to those in adult AD, if the
diagnosis of AD is based upon standardized diagnostic
criteria [4, 10-11]. Chronic eczematous dermatitis on the
face and neck, lichenified/exudative lesions on the trunk, and
lichenification with or without pruriginous papules and
nodules on the extremities are observed. Other stigma of AD
such as facial erythema and pallor, Hertoghe’s sign (loss of
the lateral eyebrows), dirty neck and follicular lichenified
papules may also be observed in senile AD. Because of these
variable features, skin manifestations tend to be diagnosed
provisionally as unclassified eczematous dermatitis and/or
erythrodermic eczematous rash [11].
A feature of senile AD that might distinguish it from
adult AD is the involvement of the folds of elbows and
knees. Localized lichenification in the antecubital and
popliteal fossae are typical signs of classic childhood AD
and adolescent/young adult AD (Fig. 1a), but are uncommon
in senile AD. In our study of 16 patients with senile AD, this
sign was observed only in one patient (6.25%). On the
contrary, eczematous dermatitis surrounding the fossae was
seen frequently in patients with senile AD (Fig. 1b). These
findings in the antecubital and popliteal areas were observed
in 12 patients (75%) and 10 patients (62.5%), respectively.
The reverse sign may be typical in senile AD, but are
observed in classic childhood AD and adult AD as atypical
features [11].
IgE Reactivity
One of the most important clinical features of AD is
cutaneous hyperreactivity to environmental allergens and
irritants that are innocuous to normal individuals. Recently,
two distinct subtypes of AD have been delineated based on
this hyperreactivity: an “extrinsic” form associated with IgE-
mediated sensitization to environmental allergens and an
“intrinsic” form without detectable IgE-mediated
sensitization. This classification is also relevant in asthma
and allergic rhinitis [21].
Recent studies have indicated that the frequency of
extrinsic and intrinsic AD is 70-80% and 20-30%,
400 Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5
respectively, depending on the country and defining criteria
[22]. A German study showed that the proportion of intrinsic
AD in adult AD was 5.4% [23]. Similar to other age groups,
both extrinsic and intrinsic forms of AD exist in senile AD.
In our study, the frequency of intrinsic AD in senile AD was
6.25 % (one out of 16 patients). If the “mixed” type of AD
associated with intrinsic asthma (and/or rhinitis) is
considered, as opposed to the “pure” type of intrinsic AD
without associated respiratory diseases, the frequency was
12.5% (two out of 16 patients) [11, 21 and 24].
Fig. (1a). The classic sign of localized lichenification in the elbow
fold of a young adult with AD.
Fig. (1b). The reverse sign of lichenification around the elbow fold
in a patient with senile AD.
As in adult AD, the major environmental allergens in the
extrinsic form of senile AD are house dust mite, pollens and
foods. In our study of 14 patient who demonstrated a mean
total serum IgE level of approximately 10000 IU/mL, high
serum titers of specific IgE to Dermatophagoides, Timothy
grass, sweet vernal grass, milk and cheese were detected in
12 (85.7%), 9 (64.3%), 8 (57.1%), 7 (50%), and 7 (50%) of
the patients with senile extrinsic AD, respectively. Specific
IgE to Dermatophagoides were also detected as the principal
antibodies in 8 patients (57.1%), and the titers in 5 patients
(35.7%) exceeded the highest limit. Although a history
and/or complication of asthma and allergic rhinitis were
noted in 4 of the 14 patients (28.6%), the total IgE levels and
the specific IgE titers of the patients with senile extrinsic AD
Ryoji Tanei
seemed to be unaffected by the presence or absence of
allergic respiratory disorders [11].
GENERAL REMARKS IN THE PATHOGENESIS OF
AD AND ITS RELATION TO SENILE AD
In general, AD is the result of a complex interaction of
susceptibility genes, the host environment, epithelial barrier
dysfunction and a dysregulated immunologic response (22).
This concept is applicable to senile AD.
Susceptibility Genes
Many different candidate genes have been identified
which are theoretically associated with the etiology of AD: a
clustered family of T helper (Th) 2 cytokines including
interleukin (IL)-4 and IL-13 genes on chromosome 5q31-33,
serine protease inhibitor Kazal type 5 (SPINK5) gene on
chromosome 5q31, IL-4 receptor gene on chromosome
16p12.1-11.2, mast cell chymase gene on chromosome
14q11.2, and filaggrin gene on chromosome 1q21 [25].
Especially, the gene mutation of filaggrin—a protein with a
key role in epidermal barrier function by retaining water and
increasing flexibility of the cornified layer—is now thought
to be the most widely reproducible genetic risk for AD and
other forms of dermatitis. Decreased expression of filaggrin
has been observed both in AD lesional skin and unaffected
atopic dry skin [26]. However, these genetically analyses
have not been performed on elderly patients with AD.
The Host Environment
Environmental exposures to allergens (e.g. house dust
mite, pollens, molds and foods), irritants (e.g. inappropriate
clothing, sweat) and pathogens (e.g. Staphylococcus aureus)
have been implicated in the pathogenesis of AD. For
instance, Dermatophagoides species of house dust mites
have been found at tenfold concentration in the homes of
atopic individuals when compared to those of controls.
Avoidance and removal of mite allergens have been shown
to improve AD symptoms [27, 28]. In senile AD, a decrease
in the activities of daily living (ADL) especially in those 75
years and over may develop a higher risk of environmental
exposure to allergens, irritants and pathogens. Longevity
might also increase the risk of sensitization to environmental
allergens among older people.
Epithelial Barrier Dysfunction
Epithelial barrier defects, not only in the skin but also in
the digestive canal, are involved in the pathogenesis of AD.
The immature function of the digestive canal could
predispose atopic infants to IgE reactivity directed against
various foods, especially egg, milk, soy and wheat. Food
allergens induce skin rashes in nearly 40% of children with
moderate to severe AD [5, 29]. However, most patients
outgrow food allergy after the age of 3 [22], as the result of
immune tolerance caused by the maturation of the epithelial
barrier function of the digestive canal.
Dry skin conditions are common in infants and children
as a part of normal skin physiology before puberty, although
a genetic predisposition (e.g. filaggrin) seem to influence
severe disease. Barrier impairment in dry skin conditions
that allows the entry of allergens, irritants and pathogens, is
thought to be a major contributor to the development of
infantile and childhood AD.

Atopic Dermatitis in the Elderly
These findings suggest that natural resolution of classic
childhood AD occur with the development of epithelial
barrier function in the skin and digestive canal during
growth. Therefore, the decline of those epithelial barrier
functions associated with aging may induce a collapse of
tolerance to food allergens, and increase susceptibility to the
environmental allergens, irritants and pathogens, which can
lead to systemic sensitization [30] in senile AD. In fact,
decreased immunohistochemical expression of filaggrin has
also been observed in senile xerosis [31] and a possible role
of xerosis in sensitization to the environmental allergens in
the elderly with nummular dermatitis has been suggested
[32].
Dysregulated Immunologic Responses
Phenotypic analyses of the peripheral blood of patients
with extrinsic or intrinsic AD have found elevated numbers
of Th2 and decreased numbers of Th1 cells. An increased
frequency of allergen-specific Th2 cells producing IL-4, IL-5
and IL-13, but little of Th1 cells producing interferon (IFN)-

in the peripheral blood has also been observed in patients
with extrinsic AD. These findings suggest a systemic Th2
predominance, characterized by abnormal IgE production,
peripheral eosinophilia, mast cell activation and induction of
Th2 cytokines i.e. IL-4 and IL-13 in patients with AD [21].
However, in the lesional skin of AD, activation of both
Th1 and Th2 cells have been shown. In the acute phase, Th2
cells expressing mRNA of IL-4, IL-5 and IL-13 significantly
increased, while in chronic phase, Th1 cells expressing IFN-

predominated [3, 5]. Eosinophils, together with infiltrating
dendritic cells, are thought to be responsible for the Th2-to-
Th1 switch by secreting IL-12 [33]. A possible role of IL-17-
producing T helper cells (Th17 cells) in influencing the
severity and cutaneous remodeling in AD has also been
reported [33, 34]. It has been elucidated that IgE-dependent
immediate hypersensitivity reactions, IgE-mediated late
phase reactions, and T cell-mediated delayed-type hypers-
ensitivity reactions can contribute to the immunopatho-
genesis of the inflammation [35-37].
In senile AD, the aging of the immune system that
involves thymic involution in the elderly might play an
important role in its pathogenesis. The acquired (specific)
immune system—in which T cells play a central role—is
immature and do not function well in the early stages after
birth. The thymus is the key organ in the development of T
cells; therefore, the establishment and decline in T cell
function and T cell-dependent immune responses are
preceded by thymic preservation and involution. Thymic
involution is generally known to occur after puberty, but
early signs of involution may be observed as early as 5 years
old. Indeed, the age-related decline of T cell numbers begins
during childhood or after puberty [38]. Thus, it can be
speculated that in addition to epithelial barrier functions, the
maturation and subsequent mildly decreased stability of the
function of T cells and the acquired immune system
influences the course of infantile and childhood AD, and also
the improvement and/or resolution of adolescent and adult
AD.
Aging is associated with a progressive decline in T cell-
mediated immune responses; therefore, it has been regarded
as a sort of immune deficiency condition. After the age of 40
Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5 401
to 50 years old, virtually the entire T cell supply is generated
from existing naïve and memory T cells, rather than from the
involuted thymus [39]. The number of T cells is significantly
decreased after the 7th decade of the life in healthy
individuals. Naïve T cells are reduced more dramatically
with CD8 than CD4 cells; however, memory T cells are
concomitantly increased. A decline in T cell-dependent
immune responses (e.g. antibody formation, cytolytic T cell
activity, and delayed-type hypersensitivity including the
tuberculin skin test) first occurs after the age of 50 and
accelerates after the ages of 65 to 70 [38, 39]. In senile AD,
this progressive decline of function and phenotypic changes
in T cells and acquired immune system in the aged may be
involved in its immunopathogenesis. This hypothesis is
supported by the observation that primary T cell immuno-
deficiency disorders frequently have raised concentrations of
serum IgE and cause AD-like eczematous dermatitis [5]. A
functional imbalance between helper/effector T cells and
regulatory/suppressor T cells with aging, with a relative
deficit of the latter, may induce an activation of
hypersensitivity reactions and a collapse of immune
tolerance to environmental allergens in elderly patients with
an atopic diathesis. Immunosuppressive T cells including
allergen-specific inducible T regulatory cells, allergen-
specific IL-10-secreting T regulatory type 1 cells [40] and
allergen-specific CD8+ suppressor T cells [41] might be
decreased in senile AD, whilst naturally occurring
CD4+CD25high regulatory T cells increase with aging [42]. In
fact, in the peripheral blood of patients with severe AD, a
significant decrease of CD8+ T cells including suppressor
cells have been observed, and a positive correlation with
high levels of serum IgE is seen [43]. A tendency of the
systemic Th1/Th2 balance to shift towards Th2 cytokine
responses with aging [44] might also be associated with the
etiology of senile AD.
DIAGNOSIS OF SENILE AD
In older patients, senile AD often coexists with other
medical conditions, such as hypertension, gastrointestinal
disorders, cardiac/cerebral vascular diseases, and diabetes
mellitus. This may complicate the diagnosis of AD since
itching and pruritic skin disorders may be due to other
disorders and/or side effects of medications Furthermore,
clinical findings of senile AD seem to be more variable than
those in other age groups, probably due to individual
differences in immune function, epithelial barrier function
and environmental factors among elderly people associated
with aging. Therefore, the diagnosis of senile AD requires a
follow-up of the clinical course of the skin manifestations
and analyses of atopic diathesis.
Diagnostic Problems
At present, no single clinical, laboratory or
histopathologic marker exists that will definitively diagnose
AD [27]. Until more specific, objective markers are
identified, AD is defined as a clinical syndrome
characterized by a spectrum of symptoms and signs,
diagnosed by a standardized criteria including the Hanifin
and Rajka’s diagnostic criteria [45], the United Kingdom
(U.K.) Working Party’s diagnostic criteria [46], and the
Japanese Dermatology Association criteria [47]. For clinical
diagnosis of senile AD, the Hanifin and Rajka’s criteria may
402 Inflammation & Allergy - Drug Targets, 2009, Vol. 8, No. 5
be the most suitable. It might be more practical that
clinicians substitute a blood test for detecting specific IgE
instead of a skin reactivity test to environmental allergens in
regards to the minor features of the criteria [45]. This is
because the results of the two tests are largely consistent
with each other [36] and a large number of the elderly
patients take medicines like oral antihistamines that suppress
the skin reactivity test at the first medical examination for
their chronic eczematous dermatitis. The Japanese
Dermatology Association criteria are useful for the initial
screening of senile AD. The U.K. diagnostic criteria that
have shown high specificity but not uniform sensitivity for
diagnosis of AD [48], may be used to exclude mild cases,
such as nummular-type dermatitis of senile AD [9, 11].
Differential Diagnosis
For the diagnosis of senile AD, eczematous dermatitis
with lichenification in the flexural sites of the extremities is
the most important hallmark, although the folds of elbows
and knees tend to be spared. The presence of chronic
eczematous dermatitis on the face and neck and
lichenification on the trunk are also diagnostic features of
senile AD. A personal and/or family history of atopic
disorders and elevated serum levels of total IgE and allergen-
specific IgE antibodies would support the diagnosis [11].
Pruritic skin disorders necessitate differentiation from senile
AD; some disorders that have similar skin manifestations to
senile AD are as follows: asteatotic dermatitis, nummular
dermatitis [32], unclassified eczema [49] senile erythroderma
[50], pruritus senilis [51], urticaria, chronic prurigo,
papuloerythroderma [52], adverse drug reactions, scabies
and cutaneous T cell lymphoma. Nevertheless, certain
disorders including asteatotic dermatitis, nummular
dermatitis, unclassified eczema, senile erythroderma,
urticaria and chronic prurigo may be involved in the clinical
course of senile AD, and may trigger its development [8,
11]. Thus, it could be speculated that pruritic skin disorders
in the elderly have some etiological similarities to senile AD
in regards to the spectrum of symptoms and signs that
characterize the disorders.
MANAGEMENT OF SENILE AD
At present, there is no 100% life-long cure for AD.
Management comprises of treatment to protect the skin
barrier (e.g. moisturizer and emollients), anti-inflammatory
measurements (e.g. topical corticosteroids and oral
antihistamines), and the identification and avoidance of
trigger factors (e.g. environmental allergens) [53].
Management of senile AD should basically conform to this
concept.
Intermittent use of topical corticosteroids to treat AD,
along with regular application of moisturizers and emollients
such as urea and heparinoides, have been the standard
management of the disease. Topical calcineurin inhibitors
such as tacrolimus are useful for skin lesions in the face and
neck. Local adverse effects from the long term application of
topical corticosteroids in sensitive skin areas can cause
atopic red face, dirty neck and skin atrophy [4]; these are
rarely seen with long-term use of calcineurin inhibitors [53].
Antihistamines that inhibit release of chemical mediators
are the first choice in oral therapy. Additionally, oral
Ryoji Tanei
administration of suplatast tosilate (a Th2 cytokine inhibitor)
and disodium cromoglycate (an anti-allergic agent for food
sensitization) would be effective in patients with raised
serum IgE levels and/or positive results of specific IgE to
food allergens. Sedative effects of the antihistaminic drugs
could also effective for intense itching that causes sleep
disturbance, although precautions must be taken in the
elderly to avoid falls caused by sleepiness and
lightheadedness. It may be necessary to use a dose slightly
lower than the regular adult dose, considering the decline in
their ability to metabolize the drug due to aging.
In older patients, it is difficult to avoid trigger factors in
their environment and apply topical medication sufficiently,
because of their decreased ADL with aging and lifestyle.
Therefore, systemic corticosteroids may be used for
moderate to severe cases of senile AD, but require
appropriate monitoring of adverse events such as
hypertension, gastric ulcer, cataract, osteoporosis and
diabetes mellitus. Systemic immunosuppressants, including
cyclosporine are also useful for the treatment of severe cases
of senile AD, but may carry an increased risk of skin and
internal malignancy and organ toxicity in the elderly.
In recent research on AD treatment, systemic and topical
immunomodulators such as omalizumab (an anti-IgE
monoclonal antibody) [54] and signal transducers and
activators of transcription 6 (STAT6) decoy
oligodeoxynucleotides [55] have been reported.
FUTURE DIRECTIONS
The physical activity of healthy elderly has become more
youthful by approximately 7.5 to 10 years old during one
decade in urban areas of an aging society [56]. Meanwhile,
the prevalence of AD has increased two- to threefold during
past few decades in the industrialized countries [5]. The
number of young adult AD has continued to rise [4], and
persistence of AD after puberty of 40-60% has been reported
[57]. Therefore, the numbers of patients with senile AD will
increase in an aging society, and senile AD will become
more apparent in the near future. The natural lifetime course
of AD will become apparent in the coming decades, as the
current generation of the patients with a history of child AD
and/or adult AD became the elderly. In addition, great strides
in immunological, pharmacological and genetic research will
bring further insight into the pathogenesis and bring about
advancement in the diagnosis of AD. Research may also
result in preventive and/or a tailor-made medicine for AD in
the future, not only in patients with classic child and adult
AD, but also in patients with senile AD.
CONCLUSION
Taking together, it can be estimated that AD will increase
in the elderly population. Therefore, AD should be divided
into 4 phases: infantile, childhood, adolescent/adult, and
senile phases, based on the period of life and the age-specific
characteristics of this inflammatory and allergic skin disease.
ACKNOWLEDGEMENTS
The author wishes to express his thanks to Dr Kensei
Katsuoka (Professor and Chairman of the Department of
Dermatology, Kitasato University School of Medicine) and
his colleagues for their kind cooperation.
Atopic Dermatitis in the Elderly
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Accepted: September 16, 2009