Allergic contact dermatitis is an inflammatory process induced by direct contact of the skin of a sensitized individual to an allergen. Within hours, red macules or patches develop that usually evolve rapidly, sometimes through an intermediate stage of urticarial papules or plaques, into vesicles that may become bullae. Because the lesions, i.e., macules, papules, vesicles, and bullae, are not in themselves specific, diagnosis clinically is made by virtue of distinctive distribution that reflects the manner in which a particular allergen was contacted.
Examples of common allergic contactants are Rhus toxicodendron (“poison ivy”), nickel, thiurames in rubber, parabens in ointments, and chemicals in fragrances, whereas agents commonly responsible for irritant contact dermatitis are acids, alkaloids, machine oils, organic solvents, and oxidants.
Adjunctive Diagnostic Test
The most effective method for diagnosis with surety of allergic contact dermatitis is the patch test. Red macules, papules, or tense vesicles that arise at a site where the suspected causative agent has been applied confirm the diagnosis of allergic contact dermatitis.
Within hours after the skin of a sensitized person has come into contact with a particular allergen, red macules or patches develop that usually evolve rapidly, sometimes through an intermediate stage of urticarial papules or plaques, into vesicles that may become bullae. Sometimes, however, allergic contact dermatitis may present itself only as reddish papules or papulovesicles, but more often as tense vesicles as well. Episodically, depending on the patient’s degree of hypersensitivity, bullae may come into being. If the offending agent is removed, lesions of allergic contact dermatitis, no matter how widespread or severe, resolve, even without therapy, in a matter of weeks at most. If, however, the allergen continues to come into contact with the skin, the process may persist for years. In that latter situation, annoying pruritus leads to persistent rubbing, which causes lichen simplex chronicus to be imposed on the effects of longstanding allergic contact dermatitis.
The same general principles that apply to allergic contact dermatitis apply equally to irritant contact dermatitis, the earliest stage being red macules or patches that very soon are surmounted by vesicles or bullae, or both. In the case of irritant-induced blisters, however, the roof of the lesions often has a gray cast, a consequence of the epidermis having become necrotic secondary to the effects of the irritant. Although both allergic contact dermatitis and irritant contact dermatitis result from direct contact of the skin with an offending agent, the two mechanisms are completely different; allergic contact dermatitis results from immunologic mechanisms, whereas irritant contact dermatitis does not.
Integration: Unifying Concept
What has been written about clinical diagnosis of allergic contact dermatitis applies in principle to irritant contact dermatitis. Distribution, in addition to character of individual lesions, is decisive.
Irritant contact dermatitis is unrelated to hypersensitivity and is inducible in every human being by virtue of the intrinsically damaging character of an irritant, the earliest stage being red macules or patches that very soon are surmounted by vesicles, bullae, or both.
All of the morphologic expressions of allergic contact dermatitis and of irritant contact dermatitis are a consequence of a basic pathologic process, to wit, delayed hypersensitivity for the former and nonhypersensitivity, irritation, often with necrotizing effects, for the latter. In short, papules, vesicles, and bullae that develop in response to contact allergens and contact irritants are a reflection of an inflammatory process that involves the dermis and epidermis, the dermis first for allergic contact dermatitis in regard to where changes pathologic are witnessed initially and the epidermis first for irritant contact dermatitis. Conceptually, the epidermis is the first affected in allergic contact dermatitis, that being the site where a haptene forms without which the immunologic process could not commence. Spongiosis with little if any ballooning or necrosis is present in the case of allergic contact dermatitis, and ballooning accompanied by necrosis and little if any spongiosis is manifest that of irritant contact dermatitis.
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Edema, erythema, papules, pustules, and crusts. The bridge of the nose and paranasal folds have been spared.
Lichenification and hyperpigmentation of eyelids. The allergic contactant was sulfa in eye drops.
Scales, erosions, and discrete and confluent erythematous papules. The cause was nickel in the belt buckle.
A rectangular zone of erythema is artificial indicating external cause, a plaster containing an herb.
A line of erythematous macules, papules, and scales induced by sensitivity to nickel in a bracelet.
Extensive edema of the entire face, including eyelids, cheeks, lips, and ear, with oozing and scale-crusts.
Erythematous macules and urticarial papules and plaques called forth by a sensitizer in a hair dye.
Scales and erosions on an erythematous base secondary to an allergen in fingernail polish.
Erythematous papules, some excoriated, and others lichenified secondary to vigorous rubbing.
Slightly erythematous papules, some of them lichenified, verrucous keratoses, scales, and erosions.
New! Additional Images
Allergic contact dermatitis: Papules have become confluent to form a plaque on which is situated vesicles and bullae.
Allergic contact dermatitis: Papules, papulovesicles, and vesicles in linear array consequent to the effects of Rhus toxicodendron.
Allergic contact dermatitis: Papules and plaques, the latter resulting from confluence of papules.