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Eczemas. by Dr Mahesh Mathur, MD,DCP. Eczema (ekzein=to boil forth ) *543 AD. Definition. Inflammatory skin reaction characterized - Histologically by spongiosis Varying degrees of acanthosis , Superficial perivascular lympho-histiocytic infiltrate.
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Eczemas by Dr Mahesh Mathur,MD,DCP
Eczema (ekzein=to boil forth ) • *543 AD
Definition • Inflammatory skin reaction characterized -Histologically by • spongiosis • Varying degrees of acanthosis, • Superficial perivascularlympho-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
Eczema • 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
Types of Eczema • Endogenous Atopic Seborrheic Discoid/nummular Pompholyx Venous/Stasis Asteatotic • Exogenous Allergic Contact Irritant Photosensitive
Atopic Dermatitis • common, often associated with other atopic disorders, such as allergicrhinitis and asthma.1 • The clinical manifestations AD vary with age three stages can oftenbe identified. • In infancy, the first eczematous lesions usuallyemerge on the cheeks and the scalp. Scratching causes crusted erosions. • During childhood,lesions involve flexures, nape, the dorsal aspects ofthe limbs. • In adolescence and adulthood, lichenified plaquesaffect the flexures, head, and neck.
In each stage, itchingthat continues throughout the day and worsens at night causessleep loss and substantially impairs the patient's quality oflife. • increased immunoglobulin E [IgE] production & eosinophils increase in blood & Tissues • Cause of great morbidity, Hamper child mental & physical development
Epidemiology • Atopic dermatitis (AD) frequently startsin early infancy • 45% of all cases of AD begin withinthe first 6 months of life • 60% begin during the first year, • 85% begin before 5 years of age. • Up to 70% of these childrenhave a spontaneous remission before adolescence. • The diseasecan also start in adults • The lower prevalence of AD in rural as compared with urban areas suggests alink to the "hygiene hypothesis," which postulates that theabsence of early childhood exposure to infectious agents increasessusceptibility to allergic diseases.
Genetics of Atopic Dermatitis • High concordance rate among monozygotictwins (77%) verses dizygotic twins (15%). • Genomewide scans have highlighted several possible atopicdermatitis–related loci on chromosomes 3q21,1q21, 16q,17q25, 20p,and 3p26. chromosome 5q31-33. • All of them encode cytokinesinvolved in the regulation of IgE synthesis:- IL-4,5,12, 13, and GMCSF. • Type 2 helperT cells (Th2) produce interleukin-4,5and interleukin-13, cytokines up-regulate the productionof IgE.. • In persons with atopic dermatitis, a geneticallydetermined dominance of Th2 cytokines affects the maturationof B cells and a genomic rearrangement in these cells that favorsisotype class switching from IgM to IgE.
Pathogenesis • 1.One holds that the primary defect residesin an immunologic disturbance that causes IgE-mediated sensitization,with epithelial-barrier dysfunction regarded as a consequenceof the local inflammation. • 2. Proposes that an intrinsicdefect in the epithelial cells leads to the barrier dysfunction.
Modified clinical Features • 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
Lab Studies • 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
Treatment • General Measures • Emollients • Topical Steroid • Topical Immunomodulators • Sedating sytemic Antihistaminics • Systemic Antibiotics
Seborrhoeic dermatitis 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.
Epidemiology • 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%
Pathogenesis • 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,
clinically • 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 marginatederythema and greasy scaling. • Occasionally, seborrhoeic dermatitis may become generalized, resulting in erythroderma.
CONTACT DERMATITIS • 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.
Epidemiology • 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.
Pathophysiology • 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.
Clinical Picture • 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 • otitisexterna,pruritusani 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.
Clinical Picture • 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. • Lichenifiedpruritic 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.
