Irritant contact dermatitis = التهاب الجلد التخريشي بالتماس |
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Irritant Contact Dermatitis
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This inflammatory reaction occurs after exposure to an irritant, a toxic compound that causes a reaction in most individuals who come into contact with it. Common irritants include alkalis, such as soaps, detergents, lye, and ammonia-containing compounds. The irritant response is determined by the type of chemical, its concentration, the mode of exposure, the body site, the barrier function locally, and the age of the patient. Atopy is a predisposing factor. The clinical morphology varies. Sometimes it is indistinguishable from allergic contact dermatitis.
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Chemical bums, usually caused by strong alkalis and acids, lead to immediate painful erythema progressing to vesiculation, necrosis, and, if severe, ulceration. Acute irritant reactions produce a monomorphic picture with scaling, redness, vesicles, pustules, or erosions and are caused by such mild irritants as detergents and water with additives. Agents producing this pattem include tretinoin, benzalkonium chloride, dithranol, adhesive tapes, and cosmetics. Dryness, chapping, and absence of vesicles characterize chronic irritant contact dermatitis. This reaction pattern is produced by repetitive contact to water, detergent, and solvents.
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Histopathology.
The histologic picture varies from extensive ulceration to simply diffuse hyperkeratosis or parakeratosis with congestion and ectasia to a spongiotic pattern essentially identical to allergic contact dermatitis. The variable features reflect the protean factors discussed above. Some correlations are worthy of note. In some instances, there is significant necrosis with nuclear karyorrhexis and cytoplasmic pallor. In severe reactions, the necrosis may extend into the dermis. Some irritants such as cantharidin and trichloroethylene produce acantholysis and neutrophilic infiltration in the epidermis . Other contactants may specifically target vascular endothelium. However, some reactions may be entirely spongiotic, such as those due to weak irritants, strong irritants in low concentration, and those in the "irritable skin syndrome." Because of these observations and those made in positive patch test sites, routine histopathologic changes do not reliably separate irritant from allergic contact reactions, although necrosis, neutrophilic infiltration, and acantholysis are more frequent in the former. In the recovery phase of irritant dermatitis, mild epidermal hyperplasia, sometimes psoriasiform, is often present. Psoriasiform hyperplasia may develop in chronic irritant reactions. In other words, most common irritants lead to subacute and chronic spongiotic dermatitis-histologic features that are identical to those of allergic contact reactions. Some contact reactions may manifest as only hypekeratosis and minimal spongiosis.
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Pathogenesis.
The pathogenesis at the cellular and molecular level of irritant contact dermatitis is not completely understood. Mechanisms of damage are variable with different irritants; these include keratin denaturation, damage of the permeability barrier through removal of surface lipid and water-holding substances, disruption of cell membranes, and direct cytotoxic effects. Recent studies indicate that very complex reaction patterns involving immunologic components occur in the irritant response. There are surprisingly more similarities than differences between irritant contact dermatitis and allergic contact dermatitis in morphology, clinical manifestation, chemokine expression, and involvement of T cells .
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