Professional Documents
Culture Documents
220 C
CHAPTER
In patients with seborrheic dermatitis, the skin is sensitive to irrita-
tion, and exposure to sun or heat, febrile illnesses and overly aggressive 13
topical therapy may precipitate flares and dissemination. Irritated seb-
Pathology
Acute seborrheic dermatitis displays spongiosis with a superficial
perivascular and perifollicular lymphocytic infiltrate composed mainly Fig. 13.3 Seborrheic-like dermatitis due to dermatomyositis. This patient
of lymphocytes. Older lesions show irregular acanthosis and focal para presented with severe pruritus of the scalp. In addition to the scalp
keratosis. The latter may appear similar to psoriasis, but exocytosis of involvement, she had Gottrons papules and a photodistributed poikiloderma.
neutrophils, Munros microabscesses and confluent parakeratotic Courtesy, Jeffrey P Callen, MD.
horny layers are absent.
History
Asteatosis as the cause of nummular eczema was first mentioned by
Gross21 in the late 1940s.
Epidemiology
Dry skin probably occurs in everyone over the age of 60 years, but its A
severity is strongly linked to the exogenous factors mentioned above.
Pathogenesis
Xerosis of aging skin is not caused by deficient sebum production, but
by a complex dysfunction of the stratum corneum (see Ch. 124)22.
There is a decrease of intercellular lipids with a deficiency of all key
stratum corneum lipids23 and an altered ratio of fatty acids esterified
to ceramide 124, persistence of corneodesmosomes25, and premature
expression of involucrin and formation of the cornified envelope26,
resulting in corneocyte retention and marked impairment of barrier
recovery23. The water-binding capacity of the stratum corneum layer is
reduced owing to decreased synthesis of natural moisturizing factor
(NMF) which contains urea and degradation products of filaggrin27.
Consequently, the stratum corneum desiccates, loses its pliability and
forms small cracks, which render the skin surface dull, rough and scaly.
Mild xerosis is asymptomatic, but if more pronounced, the skin
conveys unpleasant sensations such as itching and stinging. Inflamma-
tion is enhanced by the release of proinflammatory cytokines secondary B
to barrier perturbation, mechanical factors (scratching, rubbing), and
the application of irritative or sensitizing substances in topical prepara- Fig. 13.4 Asteatotic eczema (eczema craquel). A The distal lower extremity
tions and skin care products. has obvious inflammation and xerosis with adherent white scales (pseudo-
ichthyosis) as well as a criss-cross pattern of superficial cracks and fissures said
Clinical Features to resemble a dried riverbed. B When widespread, there can be involvement of
the trunk and proximal extremities. Along with the distal lower extremity, the
Xerosis first arises on the shins. Later it may spread to the thighs, posterior axillary line is a common site for asteatotic eczema. A, Courtesy, Louis A
proximal extremities and trunk, but spares the face and neck as well Fragola, Jr, MD; B, Courtesy, Thomas Schwarz, MD.
as the palms and soles. It develops insidiously over many years, whereas
asteatotic eczema often has a more subacute to acute onset.
Xerotic skin is dry, dull, with fine bran-like scales which may be the care of xerosis in order to avoid relapses: regular use of emollients,
released as powdery clouds when patients take off their stockings. If including petrolatum-, urea-, ceramide- or lactic acid-containing prepa-
more advanced, the skin exhibits a criss-cross pattern of superficial rations, use of bath oils, and the elimination of factors that aggravate
cracks and fissures of the horny layer (crazy-paving, eczema craquel, dry skin (see above). Topical calcineurin inhibitors have also been used.
dried riverbed) and appears pink to light red in color (Fig. 13.4). The Coexisting stasis dermatitis should be treated as well (see below).
skin becomes rough, and may develop an appearance similar to ich-
thyosis vulgaris (pseudo-ichthyosis). In more advanced stages of astea
totic eczema, there is a dull erythema as well as oozing, crusting and
STASIS DERMATITIS
abundant excoriations; disseminated nummular lesions are frequently
seen. Vesiculation and lichenification are not regular features except Synonyms: Gravitational dermatitis Varicose eczema
when irritant or allergic contact dermatitis is superimposed. Congestion eczema
Pathology
Histologically, xerotic skin appears rather normal except for a compact Key features
and slightly irregular stratum corneum. Asteatotic eczema in addition Often associated with other signs of venous hypertension
exhibits mild focal spongiosis, parakeratosis and a lymphocytic infil- Can be complicated by allergic contact dermatitis
trate with neutrophils in the superficial dermis.
One of the most common causes of disseminated eczema
Differential Diagnosis (autosensitization dermatitis)
Conditions that need to be distinguished from asteatotic eczema
include stasis dermatitis, adult atopic dermatitis (which may overlap Introduction
with asteatotic eczema), allergic contact dermatitis, nummular derma-
Stasis dermatitis is a common component of the clinical spectrum of
titis and scabies.
chronic venous insufficiency of the lower extremities (see Ch. 105). It
may arise as an early sign of chronic venous insufficiency, but can
Treatment persist or recur throughout all stages and is often most prominent when
222 Asteatotic eczema usually clears within a few days of the application ulcers are present. There is little doubt that chronic venous hyperten-
of topical corticosteroid ointment. Proper attention must be given to sion per se is the initial trigger for stasis dermatitis. Over time,
CHAPTER
additional etiological factors may act in concert, most importantly
contact sensitization to ingredients of topical therapies. Stasis derma-
therefore frequently found, most notably to topical antibiotics,
lanolin derivatives, emulsifiers, antiseptics (iodine), preservatives 13
titis is one of the most common causes of secondary dissemination of (parabens), balsam of Peru, fragrances, chemicals of plant origin,
term gravitation dermatitis by Belisario29. are present, draining exudates macerate the surrounding skin and
increase inflammation. They also favor colonization with resident
Epidemiology and transient skin flora bacteria which play an additional proin-
flammatory role (microbial eczema).
The prevalence of chronic venous insufficiency is variable among dif-
ferent ethnic groups and societies. In Central Europe, approximately
15% of the adult population has symptoms of chronic venous insuffi- Clinical Features
ciency and about 1% suffers from venous ulcers. Prevalence rates clearly The first sign of chronic venous insufficiency is usually a cushion-like
rise with age. pitting edema of the medial aspects of the shin and calf around and
proximal to the ankle, corresponding to the location of the major com-
Pathogenesis municating veins. Edema is more pronounced in the evening and
Chronic venous insufficiency and the microvasculature resolves overnight. Bouts of stasis purpura lead to spotty hemosiderin
deposits. At this stage, stasis dermatitis is mild or absent; the skin may
Venous hypertension of the lower limbs is linked to the upright position be dry and itchy. Later, the edema extends to the distal third of the calf
and is caused by multiple factors, most importantly valvular incompe- and subfascial edema arises, often accompanied by inflammation which
tence of the deep leg veins. Venous hypertension slows the blood flow may mimic cellulitis (pseudoerysipelas; acute lipodermatosclerosis).
in the microvasculature, distends the capillaries and damages the capil- Over a period of years, the skin, subcutaneous adipose tissue and deep
lary permeability barrier, allowing the passage of fluid and plasma fascia become progressively indurated and mutually adherent (chronic
proteins into the tissue (edema) and extravasation of erythrocytes lipodermatosclerosis; see Ch. 100). A firm circular cuff is formed
(stasis purpura and hemosiderin deposition). These processes lead to which appears to strangle the distal calf, creating an inverted wine
microangiopathy, with serious consequences30. bottle appearance. The skin may show intense hemosiderin pigmenta-
Proteins (particularly fibrin) are deposited around the vessels as tion and atrophie blanche. In this setting, venous ulcers develop spon-
hyaline cuffs; these may, together with interstitial edema, inhibit taneously or are triggered by scratching or other trauma. They arise
oxygen diffusion and metabolic exchange. most often in the supramalleolar region, but may later expand.
Slow blood flow induces upregulation of ICAM-1 and VCAM-1 on At the latest stage, stasis dermatitis appears when lipodermatoscle-
endothelia31, expression of L-selectin on neutrophils32, and rosis develops. Erythema and scaling are most pronounced around the
activation of neutrophils and macrophages33. Neutrophils are inner malleoli, but may extend to involve the entire distal lower extrem-
attracted into and trapped within affected areas (notably the ity. It is severely pruritic, as evidenced by multiple scratch marks, which
medial supramalleolar region)34. lead to oozing and crusting. Episodes of vesiculation occur infrequently,
Release of inflammatory mediators, free radicals and proteases by always raising the suspicion of superimposed contact sensitization.
neutrophils leads to pericapillary inflammation. Free iron ions Chronic lesions of stasis dermatitis invariably exhibit considerable
released from hemosiderin deposits create a proinflammatory lichenification. Once ulcers are formed, stasis dermatitis often becomes
vicious cycle by increasing free radical production and lipid highly irritated, oozing and erosive.
peroxidation and activating matrix metalloproteinases35. Platelets Contact sensitization often leads to secondary dissemination. Patches
accumulate in the microvasculature and may trigger focal of eczema arise in a strikingly symmetric distribution pattern, particu-
thrombosis. larly on the anterior aspect of the contralateral leg, the anterior thighs
The subsequent imbalance in the capillary network can produce and the extensor surface of the upper extremities (Fig. 13.5); lesions
fibrosis and tissue remodeling, lipodermatosclerosis (i.e. dermal may generalize to involve the trunk and face.
sclerosis and septal sclerosis that present as sclerosing panniculi-
tis), dysfunction of the lymphatics, and stellate sclerotic areas
Fig. 13.5
depleted of capillaries with the formation of peripheral giant Autosensitization
capillaries (atrophie blanche). These same processes may later dermatitis in a patient
result in the formation of venous ulcers. with venous ulceration.
Of note, patients with stasis dermatitis (with or without ulceration) Note the involvement of
the extensor surfaces of
have elevated plasma levels of homocysteine, when compared to a
the upper extremities in
control population36, and hyperhomocysteinemia is associated with an this patient with an
increased risk of thromboses. allergic contact
dermatitis to neomycin,
Pathogenesis of stasis dermatitis as well as stasis
Chronic inflammation and microangiopathy are likely to be responsible dermatitis and venous
for stasis dermatitis. Stasis dermatitis typically occurs in the same (i.e. ulceration. Courtesy, Jean L
the medial supramalleolar) regions where microangiopathy is most Bolognia, MD.
intense, and the patches of dermatitis arise preferentially over dilated
varicose veins. Also, dermal inflammation is known to induce epider-
mal dysfunction (e.g. barrier impairment).
Sometimes, patients report intense pruritus that even becomes mani-
fest before the eczema. Pruritus may be caused both by repeated conges-
tion and decongestion, and by the release of inflammatory mediators
within the dermis. Scratching or rubbing worsens and perpetuates the
dermatitis.
Key features
Secondary lesions of eczema distant from the primary site of
exposure or involvement
Symmetric distribution pattern
Most often associated with allergic contact dermatitis and stasis
dermatitis
Introduction
Dermatitis caused by exogenous agents initially arises at the site of
contact. Not infrequently, additional patches of eczema develop at
Pathology distant sites. This phenomenon, termed secondary dissemination, has
puzzled dermatologists for decades. It is most often observed in allergic
The histologic features of eczema, including stasis dermatitis, vary
contact dermatitis, particularly if associated with stasis dermatitis (see
according to the stage of the lesion. In acute eczematous eruptions,
Fig. 13.5), but may occur with uncomplicated stasis dermatitis, other
intraepithelial edema predominates, with fluid accumulation as micro-
forms of eczema, and, occasionally, severe tinea pedis.
or macrovesicles, accompanied by lymphocytes in a perivascular array
Disseminated eczema appears later than the primary lesions by a few
in the superficial dermis and exocytosis of lymphocytes into the epi-
days to weeks, tends to follow a strikingly symmetric distribution
dermis. In the subacute phase, spongiosis is still evident, but may be
pattern, and shows a predilection for analogous body sites (e.g. extensor
subtle; vesicle formation is absent. The epidermis thickens variably and
aspects of the lower and upper extremities, palms and soles). It may
parakeratosis may develop. Lymphocytes persist in the dermis and
even arise in the absence of and without a preceding primary eczema,
epidermis, but in fewer numbers.
e.g. in nummular dermatitis (see below). Disseminated eczema must
In the chronic phase, thickening of the epidermis is more pronounced
be distinguished from atopic dermatitis, which a priori arises in a dis-
and it occurs in a regular, psoriasiform pattern or has a more irregular
seminated fashion.
profile. Inflammation and spongiosis are mild to absent. Change in the
granular layer is variable, from thickening, simulating lichen simplex
chronicus, to thinning, when the pattern more closely approaches pso- History and Pathogenesis
riasis; the latter changes are seen more often in nummular eczema (see The phenomenon of secondary dissemination of eczemas was first
below). Ascribing a specific cause of the dermatitis based upon this described by Whitfield39, but its pathogenesis is still not fully eluci-
constellation of histologic findings is impossible, although individually dated. The orderly and symmetric distribution pattern may reflect
necrotic keratinocytes suggest the diagnosis of an irritant dermatitis. systemic (hematogenous) dissemination and argues against simple
In stasis dermatitis, biopsy specimens display the histologic features spread of contact irritants or allergens on the body surface. It is unclear,
just outlined, as well as signs of venous hypertension: dilated capillaries however, what exactly is disseminated via the bloodstream. It could be
surrounded by cuffs of fibrin, hemosiderin deposits, and hyperplastic allergens; for example, the ingestion of allergens such as nickel has been
(and at times thrombotic) venules (Fig. 13.6). In later stages, there is shown to elicit disseminated eczema in sensitized individuals40,41.
fibrosis of the dermal connective tissue and sclerosis of the adipose Hematogenous dissemination of microbial products leading to a
tissue (see Ch. 100). variety of (non-infectious) manifestations distant from the site of infec-
tion, such as tuberculids and bacterids, was an accepted pathogenic
model in the first half of the twentieth century and was extrapolated
Differential Diagnosis to the phenomenon of disseminated eczema. Dyshidrotic eczema of the
Stasis dermatitis is a straightforward diagnosis if the cutaneous signs soles, for example, was interpreted as an id reaction associated with
of venous hypertension are present. Difficulties may arise in differen- tinea pedis, and nummular eczema as an id reaction caused by focal
tiating the individual etiologic components, such as asteatotic eczema infections of the tonsils. Because disseminated eczema could hardly be
and irritant or allergic contact dermatitis. Patch testing is required to attributed to infections as a whole, attention shifted to an autosensi-
exclude the latter. Plaques of stasis dermatitis may be mistaken for tization to epidermal antigens mediated by cytotoxic autoantibodies.
nummular eczema, psoriasis or even mycosis fungoides. This hypothesis, however, was never verified.
Instead, it became clear both from animal experiments42 and from
routine patch testing (excited skin syndrome, angry back)43,44 that
Treatment inflammatory processes of the skin, both allergic and irritant or caused
The major aim of therapy is the management of venous hypertension by infections, lower the irritancy threshold of distant skin and thus
a complex goal which is reviewed in Chapter 105. Basic measures facilitate the development of an eczematous reaction. Obviously, circu-
include the regular use of adequate compression bandages or stockings lating activated memory T cells may play an additional role in dis-
to improve venous return, lifestyle changes, and exercise of the calf seminated eczema associated with allergic contact dermatitis, including
muscles. If indicated, surgical strategies are undertaken (see Ch. 155). that seen with poison ivy dermatitis following a short, rapid taper of
224 However, these surgical approaches do not replace the need for ongoing systemic corticosteroids. It remains to be determined which factors
compression therapy. Topical treatment is the same as for other types regulate the symmetric distribution of disseminated eczema.
CHAPTER
Epidemiology
An estimated two-thirds or more of patients with contact dermatitis
13
associated with stasis dermatitis develop episodes of disseminated
Clinical Features
Disseminated eczema in allergic contact dermatitis is characterized by
moderately to poorly demarcated patches of eczema, most often on the
extremities (Fig. 13.7A). Lesions are also found on the face, and less so
on the trunk (Fig. 13.7B). The areas of involvement vary greatly in size
and number and may consist of discrete papules which are often excori-
ated. Disseminated eczema in patients with seborrheic and asteatotic
eczema differs slightly in predilection sites and morphology (see above).
Pathology A
In biopsy specimens of disseminated eczema, the histologic findings
are those of an acute or subacute dermatitis (see previous section).
Differential Diagnosis
Conditions to be distinguished are those eczemas that can arise in a
widespread or disseminated fashion: atopic dermatitis, airborne contact
dermatitis, contact dermatitis caused by constituents of textiles, and
photoallergic dermatitis. Other conditions to be considered are mycosis
fungoides and Szary syndrome.
Treatment
Topical corticosteroids and systemic antihistamines are the mainstay
of therapy. Short courses of systemic corticosteroids may be required,
but aggressive topical treatment of the inciting dermatosis is necessary
to help prevent recurrences or a rebound flare.
NUMMULAR DERMATITIS
However, the search for focal infections is still part of the routine
evaluation in some institutions. Nummular lesions of dermatitis are
Introduction not infrequently associated with contact sensitization as well as with
Nummular dermatitis is an uncommon disseminated eczema charac- xerosis and venous hypertension. Nummular dermatitis of the dorsa of
terized by its coin-shaped lesions. Because such lesions can occur as a the hands may be a manifestation of chronic irritant or allergic derma-
feature of atopic dermatitis, asteatotic eczema and stasis dermatitis, titis. Clinical and laboratory signs of atopy are absent in true num-
the position of nummular dermatitis as an independent clinical entity mular dermatitis.
has been questioned.
Clinical Features
Epidemiology Nummular dermatitis is defined as an eruption of round (discoid)
Nummular lesions of eczema are not uncommon. However, in the eczematous patches almost exclusively of the extremities (Fig. 13.8),
literature there are widely discrepant data on the prevalence of num- often the lower legs in men and the forearms and dorsal aspects of the
mular dermatitis, ranging from 0.1% to 9.1%4. Some of this variability hands in women. The lesions are well demarcated and measure 13cm,
may reflect the degree to which a distinction is made between num- only occasionally being larger. They may be acutely inflamed with vesi-
mular dermatitis and coin-shaped lesions observed in patients with cles and weeping, but are more often lichenified and hyperkeratotic.
other forms of eczema. Men are affected slightly more often and at a Pruritus may be intense and excoriations are often prominent. Num-
later age than women (>50 vs <30 years, respectively). mular dermatitis usually takes a very chronic course. A particularly
therapy-resistant variety has been termed oid-oid disease (Sulzberger
Pathogenesis Garbe syndrome)45.
The pathogenesis has not been fully elucidated (see above). The tradi-
tional view of nummular dermatitis being microbial in origin, i.e. Pathology
either secondary to bacterial colonization or due indirectly to hematog- Histologically, the changes of subacute to chronic dermatitis are seen 225
enous dissemination of bacterial toxins, has not been corroborated. (see section Stasis dermatitis).
SECTION
3
Papulosquamous and eczematous dermatoses
Differential Diagnosis
Nummular dermatitis must be distinguished from nummular lesions
of atopic dermatitis and dissemination secondary to contact dermatitis and monocytes. HTLV-1 is transmitted primarily via sexual inter-
or stasis dermatitis. Other conditions to be considered are psoriasis, course, blood transfusions, needle sharing in intravenous drug users,
Bowens disease, mycosis fungoides and tinea corporis. and breastfeeding. It has been associated with adult T-cell leukemia/
lymphoma (ATLL), tropical spastic paraparesis, and infective dermati-
Treatment tis. The activity of HTLV-1 in infected subjects appears to be low
more than 90% of carriers remain asymptomatic47 and the majority of
Options comprise medium- to high-potency topical corticosteroid oint- disease symptoms (other than infective dermatitis) emerge during
ments, topical tacrolimus or pimecrolimus, and emollients. Tar prepa- adulthood. HTLV-1 induces spontaneous T-cell proliferation independ-
rations have also been used successfully. However, a number of patients ent of exogenous stimuli, followed by interleukin (IL)-2 receptor expres-
will require phototherapy to clear the lesions. sion (CD25), increased IL-2 secretion, and induction of interferon-,
IL-5 and IL-10. In symptomatic patients, levels of tumor necrosis
PITYRIASIS ALBA factor- and IL-6 are elevated48. Infected individuals are more suscep-
tible to a variety of infections and parasitoses such as scabies and
strongyloidiasis49.
Key features
Minor feature of atopic dermatitis Epidemiology
Ill-defined, hypopigmented patches, primarily on the face of Major endemic areas of HTLV-1 infection include Africa, northeastern
children and adolescents South America, the Caribbean basin, southern Japan, and Iran.
Infective dermatitis was first described in 1966 by Sweet50, preceding
More clinically evident in individuals with darkly pigmented skin the detection of HTLV-1 by almost 15 years. Walshe51, in 1967,
Spontaneous remission was the first to suggest an underlying immune defect because relapses
of the dermatitis frequently occurred, even after a prompt initial
response to antibiotic treatment. The probability of developing infec-
Pityriasis alba is a fairly common, low-grade, eczematous dermatosis tive dermatitis was estimated to be 2% amongst perinatally infected
characterized by ill-defined, patchy hypopigmentation (Fig. 13.9). It is children52.
regarded as a minor feature of atopic dermatitis (see Table 12.1). For
details, see Chapter 12. Clinical Features
Infective dermatitis presents as an exudative and crusty eczematous
dermatosis, affecting primarily the scalp, axillae and groin, ears,
INFECTIVE DERMATITIS paranasal skin, eyelid margins and/or neck47. A generalized fine papular
rash is occasionally observed. Complications include parasitic infesta-
tions, corneal opacities, and progression to more severe HTLV-1-asso-
Key features ciated disorders (e.g. ATLL). Infective dermatitis rarely persists until
Rare dermatologic disorder of childhood and adolescence adulthood. However, according to Bittencourt53, 44% of adult patients
Association with human T-cell lymphotropic virus type I (HTLV-1) in Bahia with HTLV-1-associated ATLL had a history of infective
Eczema of the scalp, axillae and groin; watery discharge of the dermatitis. Diagnosis is established by major and minor criteria
nose (Table 13.1)
Prompt response to antibiotics
Differential Diagnosis
The major entity in the differential diagnosis is atopic dermatitis. Apart
from serologic evidence of HTLV-1 infection, lesions of infective der-
Introduction and Pathogenesis matitis are more exuberant and obviously infected, but pruritus is less
Human T-cell lymphotropic virus type I (HTLV-1), also referred to as intense. Crusting of the nasal vestibule and blepharoconjunctivitis are
226 human T-cell leukemia virus type I and adult T-cell lymphoma virus more prominent than in atopic dermatitis. Other disorders to consider
type 1, was first detected in 198046, and it can infect T cells, B cells include seborrheic dermatitis and impetigo.
CHAPTER
Treatment
Oral antibiotics result in improvement of the skin lesions but do not
prevent relapses. Topical treatments include antibiotics (including
intranasal), corticosteroids, and bleach baths.
DYSHIDROTIC ECZEMA
Key features B
Firm, pruritic vesicles of the palms, soles, and lateral and medial
aspects of the fingers and toes Fig. 13.10 Dyshidrotic eczema. A Clinically, firm vesicles are seen along
Association with atopic dermatitis and contact dermatitis (allergic the side of the thumb and thenar eminence. Some of them are deep-seated.
B Histopathologically, spongiosis within the epidermis is accompanied by
and irritant)
macrovesicles; the thickened stratum corneum points to an acral location. A,
No disturbance of sweat gland function Courtesy, Louis A Fragola, Jr, MD; B, Courtesy, Lorenzo Cerroni, MD.
Juvenile plantar dermatosis was first reported by Mackie and Husain . 56 RECURRENT FOCAL PALMAR AND PLANTAR PEELING
Probably represents a mild form of dyshidrosis
Epidemiology Dry, circinate thin scales of palms and soles
Vesicles are absent
Juvenile plantar dermatosis occurs in prepubertal children, from the
age of 3 years and upwards (when shoes are worn for longer periods of PUSTULOSIS OF THE PALMS AND SOLES (SEE CH. 8)
time), and is only rarely seen in adults. There is seasonal variation A neutrophilic dermatosis, possibly related to pustular psoriasis
(worsening during the winter) and boys are affected slightly more often Chronic course with crops of non-pruritic, short-lived, superficial pustules,
than girls. particularly of the instep
Yellowbrown macules admixed with pustules
Pathogenesis SZARY SYNDROME (SEE CH. 120)
An atopic disposition is clearly a risk factor, but exogenous factors play Palms and soles are tender and exhibit scaling, which can be quite thick
an equally important role. Juvenile plantar dermatosis has been observed Associated with hypertrophic onychodystrophy and erythroderma
more often since impermeable materials such as plastic and rubber OTHER
have been used for sports shoes, which youngsters often wear all day
Atopic dermatitis
long. The humid environment leads to hydration of the horny layer, Irritant contact dermatitis (e.g. due to occlusive footwear)
which is then much less resistant to wear and tear. It is rubbed off by Pityriasis rubra pilaris
friction, leading to a characteristic glazed and thinned appearance of Acrokeratosis paraneoplastica
the skin. As involved areas become xerotic, cracks are formed. The Keratoderma blennorrhagicum
inherently dry skin of atopic individuals may be a predisposing factor. Inherited palmoplantar keratodermas (see Ch. 58)
Adults have a much thicker horny layer of their plantar skin and are Palmoplantar keratoderma associated with hypothyroidism
thus less at risk of developing the condition. Crusted scabies
Table 13.2 Differential diagnosis of dermatitis of the foot.
Clinical Features
The balls of the feet and the toe pads exhibit strikingly symmetrical
changes: fairly well demarcated shiny, reddish, tender, dry lesions with
some scaling (Fig. 13.11), and often with painful cracks and fissures. Differential Diagnosis
The dorsa of the feet, the interdigital spaces and the instep are typically Juvenile plantar dermatosis needs to be distinguished from allergic
spared. Similar lesions may be found on the hands. contact dermatitis to chemicals contained in leather (e.g. chromates,
dyes) or rubber. However, the latter is rare in children and, if present,
228
Pathology often involves the dorsa of the feet as well. Tinea pedis is equally
Histologically, the features of a chronic dermatitis are seen. uncommon in children, and the interdigital spaces are usually
CHAPTER
Fig. 13.11 Juvenile plantar dermatosis in a child. Erythema and scaling of the
plantar surface of the great toes and fifth toes as well as the ball of the foot
bilaterally. Note the glazed appearance of the skin of the left foot. Courtesy, Kalman
13
Watsky, MD.
Candidiasis Psoriasis
Intense erythema with Well-demarcated erythematous
desquamation/superficial plaques
erosions & peripheral Shiny in folds, scaly on convex
scale/collarettes surfaces
Satellite pustules Psoriasiform lesions elsewhere,
Favors folds, genitalia family history
Yeast/pseudohyphae on
KOH preparation
Recent antibiotic use,
thrush Other infections (e.g.
Allergic contact dermatitis* congenital syphilis,
Consider if fails to respond to usual therapy dermatophytosis)
Holster distribution if reaction to rubber additives in diaper elastics
Seborrheic dermatitis May affect folds if reaction to components of baby wipes or topical
Well-demarcated, preparations
salmon-colored to red,
moist or scaly patches/
plaques Granular
Favors folds Atopic dermatitis (AD) parakeratosis
Involvement of other Excoriations, lichenification
flexural sites, scalp Favors skin at diaper margins and convex surfaces
Often relative sparing of the diaper area
Marked pruritus
Other pruritic eczematous lesions in usual sites of AD
Fig. 13.12 Differential diagnosis of diaper dermatitis. While the most common etiologies are irritant contact dermatitis, cutaneous candidiasis and seborrheic
dermatitis, patients often have a combination with one disorder superimposed on another. Discrete papules or nodules are seen in scabies, granuloma gluteale
infantum and perianal pseudoverrucous papules, whereas congenital syphilis often presents with erosions and even ulcerations. *Potential allergens include 229
sorbitan sesquioleate (an emulsifier in diaper balms), fragrances, disperse dyes, rubber additives (e.g. mercaptobenzothiazole), and preservatives in baby wipes
(e.g. iodopropynyl butylcarbamate). Inserts, Courtesy, Robert Hartman MD; Julie V Schaffer, MD.
SECTION
Treatment breast-fed infants: cow milk formulas are colonized by a greater number
Juvenile plantar dermatosis is a chronic but self-limiting condition. of urease-producing bacteria59.
Patients should be advised to avoid wearing impermeable socks and Prolonged use of diapers, dampness, and the factors detailed
shoes, and the application of emollients, keratolytics and/or paraffin- above lead to the breakdown of the horny layer barrier function. An
type ointments is beneficial. When shoes are removed, socks, if damp, alkaline pH also facilitates the development of secondary C. albicans
should also be removed and replaced by dry socks. infection.
As diaper dermatitis tends to be most prominent on the inner parts
of the thighs, genitalia and buttocks, friction between the skin and the
DIAPER DERMATITIS diaper material likely acts as a physical factor that leads to further irrita-
tion. In addition, chemical constituents of the diaper and/or topical
preparations and baby wipes may lead to contact sensitization.
Key features
Frequently, an irritant dermatitis of the diaper area due to
Clinical Features
occlusion and prolonged exposure to urine and feces Diaper dermatitis is strictly confined to the diaper area, presenting with
mild to pronounced erythema, erosions and scaling. In the common
Secondary infection with Candida albicans often occurs
form due to irritant contact dermatitis, genitocrural folds are typically
May be associated with seborrheic dermatitis and psoriasis spared. Depending on whether there is a secondary infection or an
underlying dermatosis (e.g. seborrheic dermatitis, psoriasis), the clini-
cal picture can vary (Fig. 13.12).
Epidemiology
Diaper dermatitis develops in at least 50% of infants, and it is respon- Differential Diagnosis
sible for a considerable percentage of dermatologic consultations in The differential diagnosis is outlined in Figure 13.12.
infants and toddlers. Seborrheic dermatitis is a predisposing factor.
Treatment
Pathogenesis In the acute phase, mild corticosteroid preparations are helpful. Topical
Diaper dermatitis is the cumulative result of several factors, in particu- imidazole creams are added for secondary infection with Candida spp.
lar dampness and exposure to urine and feces. In the past, ammonia The major goal of long-term management is avoidance of the causative
derived from the urea in urine was held as primarily responsible for factors. Frequent changing of highly absorbent disposable diapers is
diaper dermatitis. More recently, the blame has been placed on the associated with a lower incidence and severity of diaper dermatitis, and
(alkaline) pH of the urine and the role of fecal bacteria. Enzymes pro- it leads to a more physiologic pH.60 Emollients containing white paraf-
duced by fecal bacteria, as well as residual pancreatic proteases and fin (Vaseline) or soft zinc pastes provide both protective and soothing
lipase in the stool, act as irritants and these enzymes are also activated effects.
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CHAPTER
13
Asteatotic eczema
(eczema craquel). A The
distal lower extremity has
Adult seborrheic dermatitis of the face and scalp. Note the diffuse scaling of
the scalp in addition to erythema of the forehead.
231.e1