Cases reported "Dermatitis, Photoallergic"

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1/19. Photosensitivity with sulfasalazopyridine hypersensitivity syndrome.

    Five weeks after the start of treatment with an association of sulfasalazopyridine and piroxicam, a 30-year-old woman presented with an eczematous eruption in light-exposed areas, hepatomegaly and fever (38 degrees C). Laboratory studies showed leukocytosis, eosinophilia and hepatic cytolysis. Treatment consisted of withdrawing the two drugs and topical steroids. The clinical signs regressed in 6 days. An increase in eosinophilia and hepatic cytolysis was observed until the tenth day, after which the trend reversed. Laboratory parameters were normal on the twentieth day. One month later, photopatch testing was performed. A patch test with sulfanilamide irradiated with UVA was positive. Clinical and laboratory findings were highly suggestive of drug hypersensitivity syndrome. The positive result from the UVA photopatch test with sulfanilamide suggests that sulfasalazopyridine was involved in the occurrence of hypersensitivity syndrome in our patient. We conclude that photodistributed eruptions can be observed in drug hypersensitivity syndrome with photosensitizing drugs.
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2/19. Prolonged photosensitivity following contact photoallergy to ketoprofen.

    We report the third case of prolonged photosensitivity secondary to contact photoallergy to topical ketoprofen, a 2-arylpropionic acid derivative. The patient suffered from persistent photosensitivity for more than 1 year after the withdrawal of ketoprofen with recurrent eruptions on sun-exposed skin areas. This photosensitivity was associated with a persistent decrease in polychromatic and UVA minimal erythemal doses. Photobiological testing revealed cross-reactivity with fenofibrate and benzophenones. Photoallergy to ketoprofen is due to the benzophenone structure or to the very similar thiophene phenylketone of tiaprofenic acid, but not to the arylpropionic function. Thus, fenofibrate, tiaprofenic acid and benzophenones should be avoided by patients with a positive history of photocontact dermatitis to ketoprofen.
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3/19. Thiazide-induced lichenoid photosensitivity.

    We report the case of a 77-year-old male who developed a florid photosensitive eruption while taking thiazide diuretics for heart failure. The lesions were lichenoid in appearance and this was confirmed histologically. The eruption cleared on withdrawal of the drug. Although thiazide-induced photosensitivity is a well-documented phenomenon, there have been no histologically proven cases of a lichenoid eruption in light exposed areas in the recent literature.
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4/19. Polymorphous light eruption in african americans: pinpoint papular variant.

    BACKGROUND: Polymorphous light eruption (PMLE) is the most common chronic idiopathic photodermatosis usually manifesting as a papular eruption (3-6 mm), with several other morphological variants described. methods: Between June 1998 and August 2001, nine patients presented with complaints of a pruritic pinpoint papular eruption associated with sun exposure. A detailed history and complete skin examination were performed along with a skin biopsy if active lesions were present. Phototesting to ultraviolet-A (UV-A), ultraviolet-B (UV-B) and visible light was performed in four patients. Antinuclear antibody (ANA) testing was performed in three patients. The diagnosis of PMLE was made based on the history, morphology of the lesions, results of phototesting and skin biopsy if available. RESULTS: In all patients, pinpoint papules (1-2 mm) were observed on sun-exposed areas, sparring the face and flexural surfaces. All patients were African American women with skin type IV-VI and a mean age of 39.3 years (range 21-52 years). Phototest results were normal in three patients; one patient, who was on glyburide, had a decreased minimal erythema dose to UV-A. ANA testing was negative. Two histopathologic patterns were observed: (i) focal lichenoid and perivascular lymphohistiocytic infiltrate with red blood cell extravasation in four specimens and (ii) superficial and deep interstitial lymphocytic infiltrate with papillary dermal edema in the remaining three specimens. All patients responded to topical corticosteroids, broad-spectrum sunscreens and antihistamines. CONCLUSION: Recognition of this pinpoint papular variant of PMLE in dark-skinned individuals is important in the evaluation and management of these patients.
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5/19. Celecoxib-induced photoallergic drug eruption.

    Photoallergic dermatitis is caused by a photosensitizing substance plus sunlight exposure in a sensitized person. If the photosensitizer is delivered internally, it is called a photoallergic drug reaction. Celecoxib is a new generation non-steroidal anti-inflammatory drug and sulfonamide derivative. We report a photoallergic drug eruption associated with the introduction of celecoxib. To our knowledge, this is the first report of photoallergic drug reaction associated with celecoxib.
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6/19. Topical dexketoprofen as a cause of photocontact dermatitis.

    We reported on the case of a patient who developed a cutaneous eruption in a photoexposed area 1 week after a continous topical treatment with dexketoprofen (Enangel). Photopatch tests were positive for dexketoprofen, ketoprofen and piketoprofen and patch test was positive for piketoprofen. Control photopatch testing with dexketoprofen in 15 healthy volunteers was negative. Dexketoprofen, ketoprofen and piketoprofen are non-steroidal anti-inflamatory drugs (arylpropionic acid derivatives) often used as topical anti-inflammatory agents. It appears that the benzophenone moiety of their chemical structure is the cause of their photosensitivity and cross-photoreaction.
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7/19. Pinpoint papular variant of polymorphous light eruption: clinical and pathological correlation.

    BACKGROUND: Polymorphous light eruption (PMLE) is the most common chronic idiopathic photodermatosis usually manifesting as a papular eruption along with several other morphological variants including a pinpoint papular variant. methods AND MATERIALS: Between June 1998 and August 2003, 10 PMLE patients presented to the Department of dermatology at Henry Ford Hospital with complaints of a pruritic pinpoint papular eruption associated with sun exposure. In six patients skin biopsies were performed along with a detailed history and complete skin examination. We correlated the histology with the clinical course of disease corresponding to acute and subacute disease presentation. We also performed immunohistochemistry on three cases to study the immunophenotype in PMLE. RESULTS: The clinical, histologic and immunostain findings are summarized. Acute: Clinically pinpoint papules and vesicles, some with erythematous base, were seen. histology showed focal vesicle formation, spongiosis, oedema, red blood cells extravasation, and superficial and deep perivascular and interstitial lymphocytic infiltrate with occasional eosinophils. Subacute: Clinically pinpoint papules with or without erythema were seen. histology of the pinpoint lesion showed a nodular collection of lymphocytes and histiocytes with claw-like extension of epidermal rete ridges at the lateral boundaries of the lesion. Overlying epidermal atrophy with adjacent spongiosis, exocytosis, oedema and a superficial perivascular lymphocytic infiltrate and parakeratosis was also observed. The histologic differential diagnosis included lichen nitidus. Immunohistochemical stains revealed the following results: CD8, CD68 positive, CD4 variable (strongly positive to negative) and S-100 negative. CONCLUSION: (i) Pinpoint papular variant of PMLE is a distinct entity, which shows characteristic histology corresponding to the clinical course of the disease (acute and subacute). (ii) The histologic and immunophenotypic differential diagnosis of this variant during the subacute phase includes lichen nitidus.
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ranking = 3.5
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8/19. Photoallergic contact dermatitis from topical diclofenac in Solaraze gel.

    Solaraze gel (Shire Deutschland GmbH & Co. KG, Cologne, germany) containing 3% diclofenac has been licensed in 2001 as a topical treatment for actinic keratoses. It is commonly used in dermatological practice. Undesirable effects are believed to be rare but include pruritus, paresthesia and application-site reactions (dry skin, rash, erythema, contact dermatitis and vesicobullous eruptions). Recently, a few cases of contact dermatitis due to three different allergens including diclofenac have been reported (1,2).
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9/19. Photoallergic contact dermatitis to oxybenzone.

    A 21-year-old woman developed an erythematous papulovesicular eruption of photo-exposed sites, following the use of an oxybenzone-containing sunscreen. Patch testing, photopatch testing, phototesting, and histology produced findings strongly suggestive of oxybenzone photoallergy. Photopatch testing with a monochromator source showed abnormal UVA responses, with evidence of immediate urticaria, and delayed-onset dermatitis. Sun-barrier use is associated with a risk of the development of contact or photocontact allergic reactions. The benzophenones are frequently used in high-protection factor sun-barrier preparations, and appear to have a particular ability to induce such responses.
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10/19. Phenofibrate-induced lichenoid photodermatitis.

    Phenofibrate is an hypolipemiant drug derived from fibric acid. Cutaneous side effects such as pruritus, rash, urticarial lesions and some rare cases of photosensitivity have been described (1-3). The reported photosensitivity cases are clinically described as eczematous (1-3); some have been reproduced by photopatch-testing (2, 3). We studied a patient with a clinical and histopathological lichenoid eruption over light-exposed areas clearly related to phenofibrate therapy for an essential hypercholesterolemia.
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