A presentation of eczema

1. Eczema/Dermatitis
Prepared by DR Ghamdan Albaddai. IBB University

2. Eczema and dermatitis are synonyms.
The term eczema is derived from the
Greek word that means “to boil out or
over.” denoting a polymorphic
inflammatory reaction pattern involving
the epidermis and dermis.

3. Definition
• Non-infective inflammatory skin
condition that shows itching,
redness, and scaling.

4. AETIOLOGICAL CLACIFICATION
Contact dermatitis

5. CLINICAL CLACIFICATION
Acute
Chronic
Acute dermatitis: is characterized by ill-defined
inflamed edematous, erythematous patches of
epidermis with papulovesicular eruptions and
exudation of serum.
Subacute dermatitis: is characterized by presence of
Redness that can be less intense than the acute
stage, visible scales and crusts.
Chronic dermatitis: characterized by thickened
hyperpigimented plaques of skin with accentuated
skin markings (lichenification).

6. Atopic Dermatitis
Contact Dermatitis
Lichen Simplex Chronicus
Seborrheic Dermatitis
01
02
04
05
TABLE OF CONTENTS
03
06
Essential Dermatitis
Stasis Dermatitis
07 Uncommon Eczematous Appearing Diseases

7. ATOPIC DERMATITIS
1. Itching is prominent
2. The antecubital and popliteal fossae are typically affected
3. Chronic waxing and waning course
01

8. INTRODUCTION ..
Atopic eczema is predominantly a disease of childhood that gives rise to
poorly demarcated chronic pruritic papular inflammation of the skin.
Uncontrollable scratching is prominent. Most cases improve with age,
although approximately 50% of children retain evidence of the condition
into adult life.
It is often associated with a personal or family history of other atopic
disorders, such as asthma and allergic rhinoconjunctivitis.

9. INTRODUCTION ..
 Common 5-20% of children worldwide.
 The condition usually starts within the first 6 months of life. Two-thirds
have a family history of atopy. Remission occurs within 10–20 years in 40–
60%, although some relapse later.
 Atopy’ defines those with an inherited tendency to develop asthma,
allergic rhinitis, conjunctivitis or atopic eczema and is present in 15–25%
of the population. Atopics produce high levels of circulating
immunoglobulin (Ig) E antibodies commonly to inhalant allergens
(e.g.house dust mite)

10. INFLUENCING FACTORS
■ Genetic factors: positive family history of allergic triad
dermatitis, asthma, allergic rhinitis
■ Immunological factors: it is considered T-helper 2 disease,
elevated serum level of immunoglobulin E in 80% of cases
■ Environmental factors: dust, pollution

11. ATEIOPATHOGENESIS
■ Skin barrier:
Individuals with atopic eczema have an impaired skin barrier which
allows excess water loss through the skin (drying effect) and an
increased potential for exogenous irritants and allergens to penetrate
(inducing inflammation). Discovery of a strong association between
loss-of-function mutations in the gene encoding filaggrin, which is a
skin barrier protein expressed in the outer layers of the epidermis,
and individuals with atopic eczema has shown how critical epidermal
function is to development of atopic eczema.

12. ATEIOPATHOGENESIS
■ Immunology :
Individuals with atopic eczema make aberrant immune responses to
environmental allergens which become skewed towards Th2 responses
(p. 10),inducing allergen-specific IgE production. The basic cause of
these immune defects is still unclear. However, the serum IgE is
normal in 20% of atopic eczema subjects.

13. CLINICAL PICTURE
The appearance of atopic eczema differs
depending on the age of the patient.
1- infantile phase:
o Age: 2 months - 2 years
o lesion: intensely pruritic papules and
vesicles on erythematous base,
associated with excoriations, vesicles,
and serous exudate
o Site: face and extensors

14. CLINICAL PICTURE
2- childhood phase :
o Age: 2 years to 12 years
o lesion: Erythematous, excoriated, scaling
papules
o Site: flexural areas mainly antecubital
fossa, popliteal fossa and the neck

15. CLINICAL PICTURE
3- adult phase :
o Age: >12 years
o lesion: dryness and lichenification
o Site: flexural areas

16. DIAGNOSIS

17. 1 – Question?
Where is the site of lesion during infantile phase?
2 – Question?
What are the influencing factors for atopic eczema?
3 – Question?
Mention three finding suggestive of atopic eczema?

18. COMPLICATIONS
Patients with atopic dermatitis are frequently troubled by skin
infections :
■ Bacterial infections (mostly staphylococcus aureus) : pustules,
impetigo
■ cellulitis may develop giving rise to fever and systemic upset
■ viral infections : Viral warts, molluscum contagiosum or herpes
simplex

19. INVESTIGATIONS
■ Skin biopsy of an acute eczematous lesion reveals spongiosis,
epidermal thickening, parakeratosis and an inflammatory cell
infiltrate (mostly lymphocytes), oedema, and vasodilatation in the
dermis.
■ Prick tests or the allergen-specific IgE tests to inhalant and
(sometimes) food allergens are frequently popositive.
■ Total serum IgE levels are raised in 80% of patients.
■ Swabs for bacterial and viral culture may be helpful during an
exacerbation.

20. TREATMENT
Prophylactic treatment :
■ Try to reduce exposure to allergens
■ Wool, polyester and nylon clothes irirritat, so should be avoided
and replaced by cotton clothes.
■ Soap and ‘bubbly’ products should be completely avoided.

21. TREATMENT
Topical treatment:
■ Emollients
■ Topical steroids: 1% hydrocortisone ointment applied twice a day is usually
adequate, Moderate potency steroid may be used for a short time in children with
resistant eczema, and for more prolonged periods in adults.
■ Calcineurin inhibitors: Tacrolimus ointment (0.03% children, 0.1% adults) or
pimecrolimus are alternatives to steroids, especially in facial and hand eczema.
■ Topical antibiotics may used for secondary infection.

22. TREATMENT
Systemic therapy:
■ Sedative antihistamines, given at night, are helpful principally
through the sedative effect.
■ Infected exacerbations frequently require the intermittent use of
an oral antistaphylococcal antibiotic.
■ Eczema herpeticum should be assessed urgently and treated with
aciclovir.
■ Patients with severe and resistant forms of atopic eczema may be
treated with narrow-band UVB, azathioprine or ciclosporin.

23. CONTACT
DERMATITIS
1. Irritant or allergic etiology
2. Distribution conforms to areas of contact
3. Avoidance of the contactant results in cure
02

24. DEFINITION
TYPES OF CONTACT DERMATITIS
Dermatitis caused by exposure to an exogenous agent.
Contact dermatitis may be caused by direct toxic action of a substance on the skin,
so-called primary irritant dermatitis, or by a substance inducing a delayed
hypersensitivity reaction, allergic contact dermatitis.
Irritant contact dermatitis/eczema is more common than allergic contact
dermatitis

25. PRIMARY IRRITANT DERMATITIS
a non-specific inflammatory rash that results from direct contact with toxic
‘irritating’ materials. The degree and the severity of damage are dependent
on both the concentration of the toxic material, duration of contact as well
as the condition of the skin at the time of contact.
DEFINITION
The most important irritants are:
• water and other fluids
• abrasives, i.e. frictional irritancy
ETIOLOGY
• chemicals, e.g. acids and alkalis
• solvents, soaps and detergents.

26. PRIMARY IRRITANT DERMATITIS
It may be acute, subacute or chronic.
Acute irritant dermatitis : It is seen after
single, usually accidental, exposure to a
strong skin irritant such as acid, alkali...
Etc. Lesions appear rapidly, usually within
4-12 hours of contact, exactly at the sites
of contact and are painful and itchy. The
affected skin becomes reddish-brown and
vesicles develop (chemical bum)
CLINICAL TYPES

27. PRIMARY IRRITANT DERMATITIS
Subacute irritant dermatitis : It results from
repeated exposure of a small area as in
napkin dermatitis due to prolonged repeated
exposure of the napkin skin to urine and stool.
The napkin area shows erythema, blistering
and crusting.
Chronic irritant dermatitis : It results from
repeated exposures (cumulative exposure) to a
mild cutaneous irritant, as continual contact
with detergents. In washer woman's hands
which look dry, fissured and itchy.
CLINICAL TYPES

28. DIFFERENTIAL DIAGNOSIS
The condition must be distinguished from allergic contact dermatitis by a carefully
taken history and patch testing.
Psoriasis of the palms may resemble contact dermatitis, but the areas affected are
better marginated and nearer to the wrist and are usually accompanied by signs of
psoriasis elsewhere.
Ringworm usually affects one palm only and is marked by diffuse erythema and
silvery scaling. If there is any doubt, scales should be examined for fungal
mycelium under the microscope.

29. NATURAL HISTORY AND DIAGNOSIS
■ An ‘irritant’ substance will injure anyone’s skin if there is sufficient
contact. The duration of the contact is as important as is its intimacy.
■ Occlusion enhances the penetration of irritants and so worsens
dermatitis. The simultaneous application of more than one irritant will
often compound an irritant reaction synergistically. However, some
individuals are more prone to develop primary irritant contact dermatitis
– especially atopic subjects.

30. NATURAL HISTORY AND DIAGNOSIS
■ The disorder is seen particularly often in manual workers (occupational
dermatitis) and housewives (housewives’ dermatitis).
■ Builders, mechanics, hairdressers, cooks, and laundry workers are some of
the groups that are frequently affected.
■ The condition causes considerable economic loss due to loss of work.
Contact with alkalis, organic solvents, detergent substances, cement, and
particulate waste is often responsible.

31. ALLERGIC CONTACT DERMATITIS
Dermatitis caused by contact with an agent to which delayed (cellular)
hypersensitivity has developed.
DEFINITION
First exposure to allergen stimulates cell mediated immunity with formation of
memory cells (sensitization). Re-exposure to the same allergen stimulates the
memory cells that initiate immunological reaction results in skin inflammation.
Sensitization may develop after many years of daily contact with the allergen,
the patient may be unaware that he is reacting to this particular substance.
PATHOGENESIS

32. Many number of substances are
capable of causing allergic contact
dermatitis.
Nickel dermatitis is the commonest
allergic contact dermatitis
ETIOLOGY

33. CLINICAL PICTURE
Symptoms: itching
Sings:
 Dermatitis occur at the sites of skin contact with the ‘allergen’ but occasionally
spreads to distant areas where no obvious contact occurs.For example, an eczema on
the wrist of a woman with a history of reacting to cheap earrings suggests a nickel
allergic response to a watchstrap buckle
 Early lesions include papules and vesicles. Continued exposure leads of the lesions
wii-lichenificatioin which undergo acute or subacute every now and then.

34. Rash from nickel allergy (nickel in earrings)

35. Nickel allergic contact dermatitis

36. allergic contact dermatitis

37. allergic contact dermatitis due to eye
liner along the eyelid margin
allergic contact dermatitis due to hair dye on the
scalp, forehead ,upper eyelids and other areas

38. Contact dermatitis at the root of the
nose due to eye glass frame
C.d. due to the plastic spectacle frame
Dermatitis above and behind the external ear

39. Question ?

40. DIFFERENCES BETWEEN
PRIMARY IRRITANT AND
ALLERGIC CONTACT
DERMATITS
Primary irritant Allergic contact
Susceptibility Everyone Only some
persons
Prior exposure Not required,
lesions
develops at first
exposure
Essential, no
lesions at first
exposure
Onset Rapid 4-12
hours after
contact
Gradual 24
hours or longer
Affected sites Sites with direct
contact
Sites of contact
and distant
sites

41. DIAGNOSIS
Accurate history taking and careful clinical examination to identify all involved
areas are very important.
The definitive technique for diagnosing allergic contact hypersensitivity is
patch testing. In this test, possible allergens are placed in occlusive contact
with the skin for 48-hour periods, and the area is inspected 48–72 hours after
removal of the patch. A positive test is revealed by the development of an
eczematous patch with erythema, swelling, and vesicles at the site of
application.
In practice, low concentrations of allergen are applied to avoid false-positive
primary irritant reactions. In most cases, a battery of the commonest allergens
causing allergic contact dermatitis in that community is applied in appropriate
concentrations

42. TREATMENT
It is very important to identify the etiological agent and prevent further
contact with it. Eczema will subside rapidly in most cases after removal
from the antigen
■ Prophylactic treatment :
Avoiding contact with the etiological agent
Protective measures e.g. Occlusive gloves with underneath cotton gloves
:
■ Topical treatment:
The use of weak or moderately potent topical corticosteroids and emollients will
speed the resolution

43. Question ?

44. ESSENTIAL
DERMATITIS
1. Idiopathic etiology
2. Diagnosis of exclusion
3. Treatment is symptomatic: suppress inflammation and itching
03

45. DEFINITION
Essential (nonspecific) dermatitis is an
epidermal eruption that may be acute or
chronic, and localized or generalized.
It is a diagnosis that is made by
exclusion when an underlying cause such
as an allergen or irritant cannot be found,
and its distribution is not typical of
defined eczematous eruptions such as
atopic or seborrheic dermatitis.
Acute
Chronic

46. PATHOGENESIS
The cause of essential dermatitis is unknown. Scratching results in
histamine release, which causes more itching, more dermatitis, and a
chronic, self-perpetuating eruption.

47. HISTORY
Itching is the chief complaint prompting patients to seek medical attention. It is often
severe enough to interfere with normal daily activities and to interrupt sleep. The itching
may be episodic or constant.
The patient frequently has a history of “sensitive skin” that is intolerant to topical
preparations such as moisturizers, soaps, and detergents and to irritating fabrics such wool.

48. PHYSICAL EXAMINATION
The varied appearance of essential dermatitis occurs because of its evolution from an acute to a
chronic process. Acutely, intercellular edema leads to vesiculation. Chronically, lichenification
occurs.
The polymorphism is manifest by vesicles, juicy papules, patches, and plaques.
Secondary changes include oozing, crusting, scaling, and fissuring.
Characteristic of essential dermatitis is the indistinct border between normal and abnormal skin.

49. TYPES OF IDIOPATHIC ECZEMA
■ Dyshidrotic – hands and feet
■ Autosensitization – generalized
■ Xerotic – dry skin
■ Nummular – oval patches

50. DYSHIDROTIC ECZEMA
Dyshidrotic eczema is characterized by deepseated vesicles (which resemble the pearls in
tapioca pudding) involving the hands (palms), feet (soles), and sides of the digits. It occurs
bilaterally and symmetrically.
AUTOSENSITIZATION
Autosensitization or id eruption is a generalized subacute dermatitis that follows a localized
acute dermatitis, usually of the feet or hands. It is thought to be a hypersensitivity reaction
to a substance produced by the acute dermatitis.

51. XEROTIC ECZEMA
Xerotic eczema is the result of low
humidity and dry skin. It occurs in the
winter and is manifest by dry fissured
skin of the trunk and extremities. It
particularly affects the elderly and
the lower legs of all age groups.

52. NUMMULAR ECZEMA
Nummular eczema is characterized by
oval, weeping patches with crusted
papulovesicles. It occurs on the trunk
and extremities.

53. BIOPSY
The histologic hallmark of dermatitis is intercellular
edema of the epidermis leading to widening of
intercellular spaces with a sponge-like appearance of
the epidermis (spongiosis).
When the process is acute and severe, it results in
intraepidermal vesicle formation. When it is chronic,
the epidermis becomes hyperkeratotic and thickened
(acanthotic).
Spongiosis is the histologic hallmark of dermatitis.
Acute
Chronic

54. THERAPY FOR ESSENTIAL DERMATITIS
■ Topical Steroids – Cream, Ointment, Solution
● Hydrocortisone 1% (lowest potency)
● Triamcinolone 0.1% (medium potency)
● Fluocinonide 0.05% (high potency)
● Clobetasol 0.05% (super potent)
■ Antihistamines
Initial

55. THERAPY FOR ESSENTIAL DERMATITIS
■ Intralesional Steroid
■ Systemic Steroid
■ Macrolide Immunosuppressants
■ Baths and Compresses
■ Antibiotics if secondary infection
■ Antipruritic
■ Ultraviolet light
Alternative

56. Avoid the use of long-term systemic
steroids because of systemic side-effects.

57. DIFFERENTIAL DIAGNOSIS
Acute
■ Contact dermatitis
■ Dermatophyte infection
■ Herpes simplex virus
■ Herpes varicella-zoster
■ Impetigo
Chronic
■ Contact dermatitis
■ Psoriasis
■ Drug eruption
■ Dermatophyte
■ Dermatitis herpetiformis

58. LICHEN
SIMPLEX
CHRONICUS
1. Localized chronic dermatitis from scratching
2. Goal is to break itch–scratch–itch cycle
3. occluded steroids may help
04

59. DEFINITION
also called “neurodermatitis”. it is a chronic
eczematous eruption of the skin that is the result
of scratching.
Pruritus precedes the scratching and may be
precipitated by frustration, depression, and stress.
The scratching then causes the lichenification and
further itching, resulting in an “itch–scratch–itch”
cycle that perpetuates the process.

60. HISTORY
PHYSICAL EXAMINATION
Some patients have a history of emotional or psychiatric problems. However, for
most, it is simply a nervous habit. Preceding the eruption, the patient has a pruritic
area of skin that is scratched, producing a plaque of chronic dermatitis.
Itching typically precedes the rash of lichen simplex chronicus.
The patient may appear anxious and may talk with pressured speech. There may be
little insight into the cause of the eruption. The lichenified plaque always occurs
within reach of scratching fingers

61. LABORATORY
AND BIOPSY
The biopsy in lichen simplex
chronicus is nonspecific,
showing only chronic dermatitis

62. THERAPY FOR SEBORRHEIC DERMATITIS
■ Steroids
● Topical under occlusion
● Intralesional – triamcinolone suspension: 10 mg/mL
■ Emotional support
Initial
Alternative
■ Tranquilizers and antidepressants

63. TYPES OF PSYCHODERMAYOSES
■ Lichen simplex chronicus
■ Habitual (neurotic) excoriations
■ Factitious dermatitis
■ Delusions of parasitosis

64. HABITUAL EXCORIATIONS
Habitual (neurotic) excoriations are characterized
by linear, “dugout” lesions that typically spare
the upper mid back, where scratching fingers
cannot reach.
Patients are usually neurotic women.

65. FACITIOUS DERMATITIS
a self-inflicted injury of the skin that presents as a bizarre eruption (often ulcerated)
with linear and geometric outlines. The patient’s history is vague and unclear. The
diagnosis is made when the clinician has a high index of suspicion in a patient who
has apparent secondary gain from perpetuating the condition.
DELUSIONS OF PARASITOSIS
occur in disturbed or anxious eccentric individuals. This disorder begins as intractable
pruritus with a crawling sensation in the skin. The patients are convinced that they are
harboring parasites and usually bring “specimens” to prove infestation. These bits of
material or skin must be examined to rule out a true infestation.
More than half of these patients have no visible skin lesions. Those with active lesions
have excoriated, crusted papules secondary to picking. Illicit drug addiction should also
be ruled out.

66. SEBORRHEIC
DERMATITIS
1. Face and scalp most commonly involved
2. Treat with antiyeast and antiinflammatory agents
3. Check HIV status in severe cases
05

67. DEFINITION
INCIDENCE
a chronic, superficial, inflammatory process affecting the hairy regions of the body,
especially the scalp, eyebrows, and face. Its cause is thought to be an
inflammatory reaction to the Malassezia yeast.
a common problem affecting 3% to 5% of the healthy population.

68. PATHOGENESIS
Venous incompetence results in increased venous pressure of the lower legs.
This increased hydrostatic pressure results in swelling and edema.
Capillary proliferation and leakage of red blood cells and vascular fluids
result in inflammation.
If the condition is unchecked, fibrin deposition will occur around the
capillaries, resulting in tissue hypoxia, sclerosis, and necrosis with
ulceration.

69. HISTORY
The occurrence of seborrheic dermatitis parallels
the increased sebaceous gland activity occurring in
infancy and after puberty.
It has a waxing and waning course with a variable
amount of pruritus.
It has been associated with Parkinson’s disease and
acquired immune deficiency syndrome (AIDS).
Approximately one third of patients with AIDS and
AIDS-related complex have seborrheic dermatitis.

70. PHYSICAL EXAMINATION
Seborrheic dermatitis has a predilection for the
hairy regions of the skin, where sebaceous glands
are numerous.
The rash is bilateral and symmetrically distributed.
In its mildest form, dandruff, one sees fine, white
scale without erythema.
The patches and plaques of seborrheic dermatitis
are characterized by indistinct margins, mild to
moderate erythema, and yellowish, greasy scaling.

71. LABORATORY
AND BIOPSY
Seborrheic dermatitis usually is not
examined by biopsy unless concern
exists about the possibility of
another disease such as Langerhans
cell histiocytosis.
The histopathologic changes are
those of dermatitis and therefore are
nondiagnostic with reference to
other eczematous conditions.

72. THERAPY FOR SEBORRHEIC DERMATITIS
■ Shampoos – two or three times per week
● zinc pyrithione 1%
● Selenium sulfide 1% or 2.5%
● Ketoconazole 1% or 2%
■ Hydrocortisone cream 1% or 2.5% b.i.d. as needed
Initial
Alternative
■ Tacrolimus ointment 0.1% or pimecrolimus cream

73. High-potency topical steroids should
be avoided in prolonged treatment
of seborrheic dermatitis, especially
the face and intertriginous skin.

74. COURSE AND COMPLICATIONS
In infants, seborrheic dermatitis can be expected to remit after 6 to 8
months. In adults, the course is chronic and unpredictable. However, it is
usually easily controlled with shampoos and topical hydrocortisone
preparations.
Rarely, it can cause widespread exfoliative dermatitis. In infants, the
association of a seborrhealike dermatitis with failure to thrive and diarrhea
is called Leiner’s disease.

75. DIFFERENTIAL DIAGNOSIS
■ Atopic dermatitis
■ Psoriasis
■ Tinea captitis
■ Langerhans cell histiocytosis
■ Lupus erythematosus
■ Rosacea
■ Perioral dermatitis
Seborrheic dermatitis is the most common cause of a “butterfly” rash.

76. STASIS DERMATITIS
1. Eczematous patches or plaques overlying lower leg edema
2. Chronic and itchy
3. Treat venous hypertension with compression stockings
06

77. DEFINITION
INCIDENCE
an eczematous eruption of the lower legs secondary to peripheral venous disease.
Venous incompetence causes increased hydrostatic pressure and capillary damage
with extravasation of red blood cells and serum.
a disease of adults, predominantly of middle and old age.

78. PATHOGENESIS
Venous incompetence results in increased venous pressure of the lower legs.
This increased hydrostatic pressure results in swelling and edema.
Capillary proliferation and leakage of red blood cells and vascular fluids
result in inflammation.
If the condition is unchecked, fibrin deposition will occur around the
capillaries, resulting in tissue hypoxia, sclerosis, and necrosis with
ulceration.

79. HISTORY
PHYSICAL EXAMINATION
Patients have a history of a chronic, pruritic eruption of the lower legs preceded by
edema and swelling. Patients with stasis dermatitis have often had
thrombophlebitis.
o Varicose veins are often prominent, as is pitting edema of the lower leg.
o The peripheral pulses are intact.
o The involved skin has brownish hyperpigmentation, dull erythema, petechiae,
thickened skin, scaling, or weeping.
o Any portion of the lower leg may be affected, but the predominant site is
above the medial malleolus.

80. CHARACTERISTICS OF
STASIS DERMATITIS
■ Edema
■ Brown pigmentation
■ Petechiae
■ Subacute and chronic dermatitis

81. LABORATORY
AND BIOPSY
The diagnosis of stasis
dermatitis is usually made
clinically.
The biopsy shows a subacute or
chronic dermatitis with
hemosiderin, fibrosis, and dilated
capillaries in the dermis
Vascular laboratory studies may
be used to assess for peripheral
vascular disease.

82. THERAPY FOR STASIS DERMATITIS
■ Support stocking (knee high, 20–30 mm Hg pressure)
■ Leg elevation
■ Topical steroids
■ Compresses if weeping
Initial
Alternative
■ unna boot
■ Surgery

83. Avoid the prolonged use of
topical antibiotics since allergic
contact dermatitis is frequent.

84. COURSE AND COMPLICATIONS
Stasis dermatitis is a chronic and slowly progressive disease unless treated.
Allergy to topical preparations may occur in 60% of patients with stasis
dermatitis. The compromised epidermal barrier from stasis allows
sensitization to occur more easily than in normal skin.
Contact dermatitis can easily be misdiagnosed as a flare-up of stasis
dermatitis.
Topical antibiotics are particularly prone to cause allergic contact
dermatitis.

85. DIFFERENTIAL DIAGNOSIS
■ Contact dermatitis
■ Superficial fungal infection
The history of application of a topical preparation to the skin and KOH testing will
help to differentiate the first two conditions from stasis dermatitis.
■ Bacterial cellulitis
Gramstaining and bacterial culture from bacterial cellulitis may be helpful, but often
are negative. An acute onset with fever particularly favors bacterial cellulitis.

86. Uncommon
Eczematous
Appearing Diseases
● Darier’s Disease
● Glucagonoma Syndrome
● Langerhans Cell Histiocytosis
● Lichen Sclerosus
● Pemphigus Foliaceus
● Wiskott–Aldrich Syndrome
● Zinc Deficiency
07

87. DARIER’S DISEASE
also known as keratosis follicularis, is a rare, autosomal
dominantly inherited genodermatosis. characterized by a
chronic, waxing and waning course beginning in childhood
and lasting a lifetime.
The eruption involves the scalp, face, neck, trunk, and
extremities with accentuation in the seborrheic areas.
It has tan, pink, brown, rough feeling papules that coalesce
into large plaques that can become secondarily infected,
resulting in crusting and weeping.
The skin biopsy is diagnostic, demonstrating epidermal
suprabasilar clefts with acantholytic keratinocytes.

88. a multisystem disorder characterized by migrating
erythematous, scaling, and crusted papules, patches, and
plaques along with the occasional vesicle and pustule.
The skin biopsy demonstrates characteristic superficial
epidermal necrosis. Hence, this condition is also known
by the descriptive name, necrolytic migratory erythema.
It is caused by a pancreatic tumor of the islet alpha cell,
which secretes raised plasma glucagon levels.
Besides the skin findings, patients with this syndrome
also have weight loss, anemia, diarrhea, and diabetes.
GLUCAGONOMA SYNDROME

89. LANGERHANS CELL
HISTIOCYTOSIS
a neoplasm of Langerhans cells that affects the skin and
extracutaneous organs. It can be acute and disseminated,
chronic and multifocal, and localized.
The acute, disseminated form typically presents in
infancy and involves the scalp, trunk, and intertriginous
areas (recalcitrant diaper dermatitis). There are tan, pink,
sometimes hemorrhagic, papules, and scaling, slightly
eroded, patches.
The skin biopsy demonstrates a proliferation of
Langerhans cells in the epidermis and dermis that stain
with S100 antibody, and are seen on electron microscopy
to contain Birbeck granules.

90. LICHEN SCLEROSUS
Lichen sclerosus can initially be confused
with a pruritic eczematous patch, especially
in the anogenital region of females.
On close inspection, or with time, the typical
ivory white papules and atrophic patches are
seen

91. PEMPHIGUS FOLIACEUS
This rare, milder form of pemphigus affects the superficial
epidermis, causing erythematous scaling with some
crusting, and a few flaccid bullae and erosions.
Like pemphigus vulgaris, a skin biopsy with
immunofluorescence is diagnostic. This reveals
subcorneal/granular layer acantholysis with intercellular
IgG staining.

92. a rare Xlinked recessive disorder that may appear like
atopic dermatitis.
Recurrent, severe infections suggest an
immunodeficiency that is characterized by increased
IgA and IgE levels, decreased IgM concentration, and
impaired cell mediated immunity.
Petechiae and bleeding episodes are a manifestation
of thrombocytopenia, as well as platelet dysfunction.
Infection, bleeding, and lymphoreticular malignancy
are causes of childhood death in these patients.
WISKOTT–ALDRICH SYNDROME

93. ZINC DEFICIENCY
an inherited (acrodermatitis enteropathica) or
acquired (parenteral nutrition) malady
characterized by perioral, genital, and acral
dermatitis plus diarrhea.
It usually begins in infancy, with the
diagnosis
confirmed by low serum zinc levels.
Essential fatty acid and biotin deficiencies
have a similar dermatitic appearance.

94. DO YOU HAVE ANY QUESTIONS?
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