Eczema (ekzein=to boil forth )

*543 AD

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

Endogenous Atopic Seborrheic Discoid/nummular Pompholyx Venous/Stasis Asteatotic

Exogenous Allergic Contact Irritant Photosensitive

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

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.

Genetics of Atopic Dermatitis

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.

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.

Major Features Pruritus Eczema –Typical morphology/Age specific/Chronic relapsing

Important Features Xerosis IgE reactivety Family/Personal History of Atopic Disease

Associated Features 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

General Measures Emollients Topical Steroid Topical Immunomodulators Sedating sytemic Antihistaminics Systemic Antibiotics

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%

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,

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

Blepharitis

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.

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,

8.4 million outpatient visits to American physicians for contact dermatitis.

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.

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.

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. processing film using color-developing chemicals .

Medications: Self-prescribed and physician-prescribed medications are important causes of ACD.

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.

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.

Hair dyes: Individuals allergic to hair dyes typically develop the most severe dermatitis on the ears and adjoining face rather than on the scalp.