Efavirenz-induced photoallergic dermatitis in HIV.
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A 52-year-old man developed contact and photoallergic dermatitis caused by diphenhydramine hydrochloride as well as contact dermatitis from paraphenylenediamine. The diphenhydramine photoallergy was elicited by long-wave ultraviolet light. The action spectrum differs from that noted in a recent report in which wavelengths shorter than 320 nm were responsible for eliciting diphenhydramine photoallergy. To the best of my knowledge, this is the third case of diphenhydramine photosensitivity reported in the English literature. The combination of both contact and photosensitivity to diphenhydramine has not previously been described.
Photoallergic contact dermatitis developed in a patient who had used deodorant soaps containing tribromsalan. He persistently reacted to light, since the dermatitis persisted long after cessation of contact with the causative chemical. During this period, he experienced generalized, eczematous dermatitis on several occasions. On testing, the patient showed extremely severe photosensitivity extending through the ultraviolet to the visible spectrum. At that time, a skin biopsy specimen showed the microscopic findings of eczematous dermatitis. A diagnosis of actinic reticuloid was first made histologically nine years after the initial examinations, when the patient was 56 years old. This long-term follow-up study may support the view that photoallergic contact dermatitis, persistent light reaction, and actinic reticuloid could constitute various phases of a single disease.
A 36 year old woman with psoriasis vulgaris developed generalized photoallergic dermatitis to 8-methoxypsoralen after 16 uneventful treatments with 8-methoxypsoralen und UVA (PUVA). The diagnosis of photoallergy was confirmed by re-exposure to oral 8-methoxypsoralen and total body UVA irradiation; phototests using topical and oral 8-methoxypsoralen with a high intensity monochromator or with a new high intensity light apparatus for the delivery of UVA; and histological studies. Photoallergy occurred only with UVA, but not with UVB or UVC. There was no photoallergy following trimethylpsoralen.
The case of a 51 year old woman, working in the field of agriculture, is reported; she developed a photoallergic dermatitis and a fulminant hepatitis after the use of the herbicide phenmedipham (Betanal). Photopatch-testing revealed sensitization to phenmedipham and, additionally, to maprotiline hydrochloride (Ludiomil), an antidepressant taken by the patient at about the same time. The possible relationship of these reactions with the clinical symptoms are discussed.
There is little literature regarding conventional patch tests and photopatch tests to oxybenzone resulting in both immediate- and delayed-type hypersensitivity reactions. A patient was patch-tested and photopatch-tested to various sunscreen chemicals. Both immediate- and delayed-type hypersensitivity reactions were observed with oxybenzone. The positive patch tests were also photoaccentuated. Oxybenzone, a common sunscreen allergen, can result in both contact urticaria and delayed-type hypersensitivity on both conventional patch testing and photopatch testing. Allergic contact dermatitis to sunscreen chemicals has traditionally included contact urticaria, allergic contact dermatitis, and photoallergic contact dermatitis. Due to the recognition of p-aminobenzoic acid (PABA) and its esters as sensitizers, the presence of benzophenones in "PABA-free" sunscreens has become more prevalent, especially in sunscreens with a sun protection factor (SPF) greater than 8. In our patient, immediate- and delayed-type hypersensitivity reactions were seen to oxybenzone (2-hydroxy-4-methoxybenzophenone, 2-benzoyl-5-methoxyphenol, benzophenone-3, Eusolex 4360, Escalol 567, EUSORB 228, Spectra-Sorb UV-9, Uvinul M-40) upon conventional patch testing and photopatch testing.
The most common "allergic" photodermatoses are reported in this review: (a) systemic and topical exogenous photosensitizations with phototoxic and photoallergic reactions and the most frequently chemicals photosensitizers incriminated. (b) idiopathic photodermatoses including benign summer eruption, polymorphous light eruption and solar urticaria. Clinical recognition patterns are stressed as well as differential diagnosis. Photobiological exploration is also detailed.
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BACKGROUND: The panel of patch test allergens used for the evaluation of patients with suspected photoallergy typically does not include plant and pesticide allergens. The prevalence of allergic contact dermatitis and photoallergic contact dermatitis to plant and pesticide allergens was determined for this subgroup of patients. OBSERVATION: Positive reactions were detected in 12 of 26 patients who were tested with our photoallergen series: 5 with allergic contact dermatitis, 5 with photoallergic contact dermatitis, and 2 with both. Four of the 12 patients had positive patch and photo-patch test reactions to plant allergens, pesticide allergens, or both. The positive patch test reactions were to the plants Taraxacum officinale (dandelion) and Tanacetum vulgare (tansy) and to the pesticides folpet and captafol. Positive photo-patch test reactions were to the pesticides folpet and captan. The histories of the patients suggested that 2 or 3 of the 4 patients had clinically relevant reactions. In the other 8 patients, positive reactions to the patch and photo-patch tests included fragrances, sunscreens, and antibacterial agents. CONCLUSION: Plant and pesticide allergens should be included in the patch and photo-patch test series used for the evaluation of patients with suspected photoallergy.
Photoallergic and allergic contact dermatitis are examples of type IV hypersensitivity reactions that involve T cell-mediated immune responses against haptens that come into contact with the skin. These two types of allergies differ in that for routine contact allergens, the hapten is usually a chemically reactive species that readily couples to host proteins; for photoallergic reactions, UV light (320 - 400 nm) is necessary to generate ("photoactivate") the chemically reactive hapten. From this point on, both photoallergic and allergic contact dermatitis are likely to proceed along the same pathways. For both types of cutaneous delayed-type hypersensitivity, there are naturally occurring mechanisms that terminate this type of T cell-mediated inflammation (tolerance induction). An important tolerance mechanism in the skin involves the induction of T-cell clonal anergy by "amateur" antigen-presenting cells such as keratinocytes. Advances in the understanding of the molecular pathways of T-cell activation and inactivation by antigen-presenting cells have identified critical signaling molecules such as B7/BB-1 antigen. The overexpression of these signaling molecules by the keratinocytes of transgenic mice disrupts the normal kinetics of resolution of murine contact hypersensitivity. These animals have prolonged contact hypersensitivity reactions that resemble some chronic dermatologic conditions in humans. This animal model may be a useful tool to better understand chronic allergic and photoallergic contact dermatitis.
PURPOSE: To determine whether photoallergic contact dermatitis is as uncommon as it is usually considered to be and to review the associated clinical features. METHODS: We reviewed the literature on photoallergic reactions induced by the topical contact of the skin with a chemical in the presence of, or followed by, exposure to UV or visible light. Some of the more recently observed photo-allergens and those presenting special clinical features are discussed. RESULTS: The literature cites several topical substances that give rise to photoallergic contact dermatitis, some of them only exceptionally but others quite frequently. The clinical features are not always those of a eczematous eruption, and several parts of the body may be affected. CONCLUSIONS: Many topical photoallergic culprits have been reported in the literature, the most important of which are sunscreen agents and, recently, non-steroidal anti-inflammatory agents (NSAIDs). Not at all exceptional is the occurrence of photoaggravation and recurrent transient or even persistent light reactions on previously exposed as well as non-exposed areas (often sparing the original application site), particularly with the NSAID ketoprofen. Moreover, cross-reactions with chemically-related as well as non-chemically related molecules are common. The potentially misleading clinical features observed in some cases, the diversity of the casual substances identified, and the low frequency with which photopatch testing is carried out in general indicate that the occurrence of photoallergic contact dermatitis might well be underestimated.
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