[When sunscreens do not help: allergic contact dermatitis to UV filters]. / Wenn Sonnenschutzprodukte nicht mehr helfen: Allergisches Kontaktekzem auf UV-Filter.

Ultraviolet (UV) filters may cause allergic and more frequently photoallergic contact dermatitis. Therefore, a photopach test should always be performed in case of a suspected contact sensitivity to UV filters. We report a case of a 65-year-old woman with a recurrent erythema of the face and décolleté after sun exposure despite application of a sunscreen. The (photo)patch test revealed a contact sensitivity to the UV filter butyl-methoxybenzoylmethane. Treatment with a topical glucocorticoid and avoidance of the particular UV filter led to a rapid improvement.

Photoallergy.

Many--topically applied or systemically administered--substances may trigger photoallergic skin reactions following exposure to ultraviolet (UV) radiation. While most cases represent photoallergic contact dermatitis due to topically applied agents, systemically triggered photoallergy is considerably less common. The photopatch test--a UV-exposed variant of the conventional patch test--is the mainstay in the diagnosis of photoallergic or phototoxic reactions.

Facial Sweet syndrome mimicking photoallergic contact dermatitis.

Sweet syndrome (acute febrile neutrophilic dermatosis) usually presents with painful erythematous plaques, malaise, and fever. Histologically skin infiltration with neutrophils is characteristic. The etiology of the disease is unknown. Sweet syndrome can be subdivided into the classical form, which is usually idiopathic and is associated with some kind of inflammation, the paraneoplastic form and the drug-induced one. We present the unusual case of an 83-year-old woman who appeared to have facial photoallergic contact dermatitis but turned out to have facial Sweet syndrome.

Piroxicam has at least two epitopes for contact photoallergy.

We have demonstrated previously in guinea pigs that the induction of photocontact sensitivity to piroxicam (PXM) also induces a state of cross-reactive contact hypersensitivity to two compounds having structurally related elements, thimerosal (TMS) and thiosalicylate (TOS). The present study was conducted to determine whether oral administration of TOS would desensitize guinea pigs previously photosensitized with PXM. At the same time, the spectrum of reactivities against these compounds and against tenoxicam (TXM) which resembles only piroxicam was assessed by appropriate sensitizing and eliciting protocols. As expected, animals photosensitized to PXM developed reactivities against all four compounds, PXM and TXM (photosensitivity) and TMS and TOS (contact sensitivity). By contrast, photosensitization with TXM induced cross-reactivity only against PXM. Moreover, the induction of contact sensitivity against TMS or TOS induced photosensitive cross-reactivity to PXM, but not to TXM. Finally, the oral administration of TOS produced a transient desensitization only for TMS and TOS. These results suggest that photosensitization with PXM induces two distinct reactivities. The first reactivity cross-reacts with TMS and TOS and is suppressible with orally administered TOS. The second cross-reacts only with TXM and is not suppressible with oral TOS. We conclude that PXM acquires at least two distinct immunogenic epitopes when exposed to UVA irradiation.

Pemphigus vulgaris exacerbated by exposure to sunlight.

We report two cases of pemphigus vulgaris who showed exacerbation of their bullous skin lesions after exposure to sunlight. These cases indicate that ultraviolet light is an aggravating factor, not only for pemphigus foliaceus, but also for pemphigus vulgaris.

[Photoallergy].

Photoallergy is an entity of allergy in the dermatological field. Sunlight is involved in the pathophysiology of photoallergy. Photoallergy is classified into intrinsic and extrinsic diseases. As extrinsic diseases, photosensitivity due to drugs and photocontact dermatitis are important for physicians as well as dermatologists. Physicians should have accurate understanding of these disorders.

Photonucleophilic addition of the epsilon-amino group of lysine to a triflusal metabolite as a mechanistic key to photoallergy mediated by the parent drug.

A mechanism for triflusal-induced photoallergy involving complexation of 2-hydroxy-4-trifluoromethylbenzoic acid with site I of human serum albumin and subsequent formation of a covalent adduct by photoreaction between a metabolite and a neighboring lysine residue is proposed. This is supported by the observed photobinding to poly-L-lysine. Thereby, a photoantigen is generated, which is a likely trigger of the immune response.The goal of the work presented herein is to gain deeper insight into the molecular basis of photoallergy mediated by triflusal through its active metabolite, 2-hydroxy-4-trifluoromethylbenzoic acid (HTB). For this purpose, the interaction between HTB and human serum albumin (HSA) was investigated by fluorescence and laser flash photolysis to monitor inclusion into the protein binding sites through variation in the excited-state properties. A remarkable lengthening of HTB triplet lifetime in the presence of HSA was observed. The use of oleic acid as a displacement probe clearly suggests the preference for dark binding in site I. The mechanism of photobinding was studied by irradiation of HTB in the presence of amino acids, and, in the case of lysine, a photoadduct was detected that arises from nucleophilic attack by the epsilon-amino group to the trifluoromethyl substituent of HTB. Accordingly, photobinding of the metabolite to poly-L-lysine was also observed. Overall, these results are consistent with a mechanism for triflusal photoallergy involving complexation of HTB to site I of HSA and subsequent formation of a covalent photoadduct with one neighboring lysine residue.

Pelagra / Pellagra

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Solar urticaria in Singapore: an uncommon photodermatosis seen in a tertiary dermatology center over a 10-year period.

BACKGROUND: Solar urticaria is an uncommon photodermatosis, characterized by the appearance of pruritic wheals after sun exposure. In this study, we examine the photobiological characteristics of solar urticaria in the heterogeneous group of Singaporean patients. METHODS: The photobiological features of all patients treated for solar urticaria at a tertiary dermatology center in Singapore over a 10-year period were retrospectively examined. RESULTS: A total of 19 patients were diagnosed to have solar urticaria from 1993 to 2002. The mean age at diagnosis was 26 years, with a racial distribution of 17 (90%) Chinese, one (5%) Malay, and one (5%) Indian. Fifteen (79%) patients were males and four (21%) were females. The face/neck (47%) and arms/forearms (58%) were most often affected. Six (32%) patients had a history of atopy and two (11%) had dermographism. Fifteen (79%) patients had Fitzpatrick's skin type IV, three (16%) had skin type III and one (5%) patient had skin type V. The mean exposure time to wheal formation was 23 min. The action spectra of solar urticaria were visible light for 12 (63%) patients, ultraviolet (UV) A for one (5%), visible light and UVA for five (27%), and natural sunlight for one (5%) patient. All patients reported partial improvement with a combination of antihistamines and sunscreens as the main modality of treatment. CONCLUSIONS: Our data suggest that solar urticaria is an uncommon photodermatosis and a rare form of urticaria. Wheals were mostly elicited by visible light and/or UVA. A combination of antihistamines and sunscreens provided a useful form of therapy for patients with solar urticaria.

Successful treatment of recalcitrant chronic actinic dermatitis with tacrolimus.

Therapeutically, chronic actinic dermatitis is a problematic condition. Frequently applied sunscreen usually fails to mitigate the clinical symptoms, and steroids--while efficient--exert many undesired side-effects with prolonged usage. We present a case of chronic actinic dermatitis responding well to topically applied tacrolimus (Protopic) in combination with chemical and physical UV protection.