Transcript Eczema - Dr. Raj Kumar Sharma

 Eczema
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*543 AD
(ekzein=to boil forth )
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Inflammatory skin reaction characterized Histologically by
spongiosis
Varying degrees of acanthosis,
Superficial perivascular lympho-histiocytic
infiltrate.
Clinical features of eczema include
itching, redness, scaling and clustered &
papulo-vesicles.
The condition may be induced by a wide
range of external and internal factors acting
singly or in combination
Characterized into two groups.
 The first, exogenous eczemas related to
clearly defined external trigger factors in
which inherited tendencies play a minor
role.
 The Endogenous eczema is mediated
by processes originating within the body.
 In some conditions, however, there are
both external and internal
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Endogenous
Atopic
Seborrheic
Discoid/nummular
Pompholyx
Venous/Stasis
Asteatotic
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Exogenous
Allergic Contact
Irritant
Photosensitive
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common, often associated with other
atopic disorders, such as allergic rhinitis and
asthma.1
The clinical manifestations AD vary with age
three stages can often be identified.
In infancy, the first eczematous lesions usually
emerge on the cheeks and the scalp.
Scratching causes crusted erosions.
During childhood, lesions involve flexures,
nape, the dorsal aspects of the limbs.
In adolescence and adulthood, lichenified
plaques affect the flexures, head, and neck.
In each stage, itching that continues
throughout the day and worsens at
night causes sleep loss and
substantially impairs the patient's
quality of life.
 increased immunoglobulin E [IgE]
production & eosinophils increase in
blood & Tissues
 Cause of great morbidity, Hamper
child mental & physical development
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Atopic dermatitis (AD) frequently starts in early
infancy
45% of all cases of AD begin within the first 6
months of life
60% begin during the first year,
85% begin before 5 years of age.
Up to 70% of these children have a
spontaneous remission before adolescence.
The disease can also start in adults
The lower prevalence of AD in rural as
compared with urban areas suggests a link to
the "hygiene hypothesis," which postulates that
the absence of early childhood exposure to
infectious agents increases susceptibility to
allergic diseases.
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Genetics of Atopic Dermatitis
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High concordance rate among monozygotic twins
(77%) verses dizygotic twins (15%).
Genomewide scans have highlighted several
possible atopic dermatitis–related loci on
chromosomes 3q21,1q21, 16q, 17q25, 20p,and
3p26. chromosome 5q31-33.
All of them encode cytokines involved in the
regulation of IgE synthesis:- IL-4, 5,12, 13, and
GMCSF.
Type 2 helper T cells (Th2) produce interleukin-4,5
and interleukin-13, cytokines up-regulate the
production of IgE..
In persons with atopic dermatitis, a genetically
determined dominance of Th2 cytokines affects
the maturation of B cells and a genomic
rearrangement in these cells that favors isotype
class switching from IgM to IgE.
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1.One holds that the primary defect
resides in an immunologic disturbance
that causes IgE-mediated sensitization,
with epithelial-barrier dysfunction
regarded as a consequence of the local
inflammation.
 2. Proposes that an intrinsic defect in the
epithelial cells leads to the barrier
dysfunction.
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 Major
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Features
Pruritus
Eczema –Typical morphology/Age specific/Chronic relapsing
 Important
Features
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Xerosis
IgE reactivety
Family/Personal History of Atopic Disease
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Associated Features
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Atypical Vascular response-White Dermographism
Facial Pallor,Anterior subcapsular cataract,Keratoconus
Pit.Alba, Dennie-Morgan infraorbital folds
Keratosis Pilaris
Cutaneous Infections
Laboratory testing is seldom necessary.
 Allergy and radioallergosorbent testing is
of little value.
 A platelet count for thrombocytopenia
helps exclude Wiskott-Aldrich syndrome,
and testing to rule out other
immunodeficiencies may be helpful.
 Scraping to exclude tinea corporis is
occasionally helpful
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General Measures
 Emollients
 Topical Steroid
 Topical Immunomodulators
 Sedating sytemic Antihistaminics
 Systemic Antibiotics
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Chronic dermatitis has a distinctive
morphology (red, sharply marginated
lesions covered with greasy-looking
scales)
Distinctive distribution in areas with a rich
supply of sebaceous glands, namely the
scalp, face and upper trunk.
In some cases the flexures are also
involved, but this is not an essential
diagnostic criterion.
The prevalence of SD is 1-3% in the
general population
 3-5% in young adults, although mild
degrees of dandruff are of course much
more then The figure
 this is much high in patients with human
immuno-deficiency virus (HIV) infection i
-36%
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The yeast Malassezia ovale (Malassezia
furfur) is increased in the scaly epidermis
of dandruff and seborrhoeic dermatitis
 seborrhoeic dermatitis is common in
(AIDS), these patients probably have an
increased susceptibility to yeast infection
 seborrhoeic dermatitis of infancy
 Seborrhoeic dermatitis may also be a
complication of Parkinsonism,
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Skin lesions commone in hairy skin,
 involve the scalp, face, presternal and
interscapular regions and the flexures.
 Dandruff / seborrhoea
 extend beyond the frontal hairline as the 'corona
seborrhoeica
 Behind the ears redness and greasy scaling, Both
sides of the pinna, the periauricular region, and the
sides of the neck may be involved.
 Otitis externa, accompany seborrhoeic dermatitis
in other sites, or may occur alone.
 SD- characteristically involves the medial part of
the eyebrows, the glabella, and the nasolabial
folds
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SD On the trunk,
The petaloid form (so-called because the
lesions are petal-shaped).
on the front of the chest,
in the interscapular region
Groins, the anogenital and submammary
regions, and the umbilicus,
SD presents as an intertrigo, with diffuse,
sharply marginated erythema and greasy
scaling.
Occasionally, seborrhoeic dermatitis may
become generalized, resulting in
erythroderma.
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Contact dermatitis is used incorrectly as a
synonym for allergic contact dermatitis
(ACD).
Contact dermatitis is inflammation induced
by chemicals
Directly damage the skin -Irritent Dermatitis
Specific sensitivity in the case of ACD.
ACD is inflammation of the skin manifested
by varying degrees of erythema, edema, &
vesiculation.
It is a delayed type of induced sensitivity
resulting from cutaneous contact with a
specific allergen to which the patient has
developed a specific sensitivity.
the prevalence of contact dermatitis is
13.6 cases per 1000 population
 No racial predilection exists for ACD.
 Sex -ACD is more common in women than
in men.
 Age- ACD may occur in neonates. In
elderly individuals,
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8.4 million outpatient visits to American
physicians for contact dermatitis.
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Most chemicals able to provoke ACD have molecules (<500 d).
3000 chemicals are well documented as specific causes of ACD.
chemical molecules responsible for ACD must bind to carrier
proteins on Langerhans cells,
compounds induces Langerhans cell migration and maturation.
In contrast, only allergenic compounds induce CD1a+ CD83+
Langerhans cell migration with partial maturation .
Cytokines also play an important role in ACD .-adhesion molecules,
such as intercellular adhesion molecule 1. Interleukin 8 cytokine
indicating ACD,
Sensitization to a chemical requires intact lymphatic pathways.
The initial sensitization typically takes 10-14 days from initial exposure
to a strong contact allergen such as poison ivy.
Some individuals develop specific sensitivity to allergens (eg,
chromate in cement) following years of chronic low-grade exposure
Once an individual is sensitized to a chemical, ACD develops within
hours to several days of exposure.
CD4+ CCR10+ memory T cells persist in the dermis after ACD clinically
resolves.
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Only history and questioning can determine
ACD.
A positive patch reaction may indicate
only a sensitivity and not the cause of
current dermatitis.
Preexisting skin diseases -Individuals with
stasis dermatitis are at high risk for
developing ACD ,e.g Neomycin
otitis externa,pruritus ani and pruritus vulvae
may be because of sensitized to
medications applied .
Atopic dermatitis -Patients with atopic
dermatitis are at increased risk for
developing nonspecific hand dermatitis
and irritant contact dermatitis.
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Occupational dermatitis: Contact dermatitis is 1 of
the 10 leading occupational illnesses.
ACD- may improve initially on weekends and
during holidays,
Irritant contact dermatitis is more likelyf multiple
workers are affected in the workplace.
Hobbies: Hobbies may be the source of ACD, e.g.
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processing film using color-developing chemicals .
Medications: Self-prescribed and physicianprescribed medications are important causes of
ACD.
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Dermatitis patients -who did not clear with
topical corticosteroid treatment should be
considered for patch testing with a corticosteroid.
 Clinical
picture
Acute ACD is characterized by pruritic papules and
vesicles on an erythematous base.
 Lichenified pruritic plaques may manifest chronic ACD.
Occasionally- erythroderma, exfoliative dermatitis.
 The initial site of dermatitis often provides the best clue
regarding the potential cause of ACD.
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Hands: Hands are an important site of ACD, eg. chemicals
in rubber gloves.
 Airborne ACD: Chemicals in the air may produce airborne
ACD. usually occurs maximally on the eyelids, but it may
affect other areas.
 Ophthalmologic: Allergy to chemicals in ophthalmologic
preparations may provoke dermatitis around the eyes.
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Hair dyes: Individuals allergic to hair dyes typically develop
the most severe dermatitis on the ears and adjoining face
rather than on the scalp.