 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 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 5q  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 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.