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1/79. Photosensitivity due to alprazolam with positive oral photochallenge test after 17 days administration.

    We describe a 65-year-old male patient with photosensitivity due to alprazolam. A photopatch test was negative. An oral photochallenge test after taking alprazolam for 17 days with UVA irradiation was positive. alprazolam, a lipid-soluble drug, may require long duration of administration to cause photosensitivity.
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2/79. A newly identified patient with clinical xeroderma pigmentosum phenotype has a non-sense mutation in the DDB2 gene and incomplete repair in (6-4) photoproducts.

    We report here a patient (Ops1) with clinical photosensitivity, including pigmented or depigmented macules and patches, and multiple skin neoplasias (malignant melanomas, basal cell carcinomas, and squamous cell carcinomas in situ) in sun-exposed areas. These clinical features are reminiscent of xeroderma pigmentosum. As cells from Ops1 showed normal levels in dna repair synthesis in vivo (unscheduled DNA synthesis and recovery of rna synthesis after ultraviolet irradiation), we performed a postreplication repair assay and recovery of replicative DNA synthesis after ultraviolet irradiation to investigate if Ops1 cells belonged to a xeroderma pigmentosum variant pattern. Ops1 cells were normal, but there was an incomplete pattern repair in (6-4) photoproducts in contrast to a normal pattern repair in cis-syn cyclobutane pyrimidine dimers by repair kinetics using the enzyme-linked immunosorbent assay. Moreover, Ops1 cells were defective in a damage-specific DNA binding protein and carried a non-sense mutation in the DDB2 gene. These results suggest that (i) the DDB2 gene is somewhat related to skin carcinogenesis, photoaging skin, and the removal of (6-4) photoproducts; (ii) although it is believed that cyclobutane pyrimidine dimers are the principal mutagenic lesion and (6-4) photoproducts are less likely to contribute to ultraviolet-induced mutations in mammals, Ops1 is one of the ultraviolet-induced mutagenic models induced by (6-4) photoproducts.
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3/79. 4 cases of photocontact dermatitis due to ketoprofen.

    We report 4 cases of photocontact dermatitis due to ketoprofen, a non-steroidal anti-inflammatory drug derived from propionic acid. We carried out a skin biopsy to examine the amount of ketoprofen in the eruptive skin. We investigated the cross-reactions between tiaprofenic acid, suprofen and ketoprofen by patch and photopatch testing. In case no. 1, 17 days after the discontinuance of Mohrus poultice (containing ketoprofen as an active ingredient), we detected ketoprofen 312.5 ng/g in the area of skin where the poultice was applied. All 4 cases reacted positively to the causative medicaments containing ketoprofen and ketoprofen 1% pet. 3 out of 4 cases reacted positively to tiaprofenic acid 1% pet. Only 1 case out of the ketoprofen and tiaprofenic acid positive cases reacted positively to suprofen 1% pet. Vehicles of patients' medicaments were negative in all 4 cases. We suspected that the key structure of the cross-reaction between ketoprofen and tiaprofenic acid and suprofen was the benzoyl radical.
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4/79. Photosensitivity associated with treatment with triflusal.

    BACKGROUND: Triflusal is a fluorinated aspirin derivative with antiplatelet properties, which is used in spain for the management and prevention of thromboembolic disease. CASE REPORT: A 91-year-old female developed a systemic photosensitivity reaction 15 days after beginning triflusal preventive treatment (300 mg/12 h) for prior transient ischaemic attack. Photobiological study showed an abnormal response to light in areas exposed to ultraviolet B and A radiation, with a photopatch test positive to both triflusal and its main metabolite. These observations suggested a causal relation between triflusal and the clinical findings, as described in previous reports. CONCLUSIONS: The few cases reported to date and the clinicopathological features of this case suggested an immunological response as the most likely cause of the reaction.
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5/79. pyridoxine-induced photosensitivity and hypophosphatasia.

    We describe a case of photosensitivity due to pyridoxine hydrochloride (vitamin B(6)) in a heterozygote of hypophosphatasia. Photopatch tests using pyridoxine hydrochloride and pyridoxal 5'-phosphate, compounds referred to as vitamin B(6), with ultraviolet light A irradiation were positive. Laboratory examination showed low serum alkaline phosphatase. Tissue-nonspecific alkaline phosphatase exon amplification from DNA of the patient's lymphocytes detected deletion 1154-1156 hypophosphatasia mutation, indicating that this patient was diagnosed to be a heterozygote of hypophosphatasia. The seric pyridoxal 5'-phosphate level of this patient with hypophosphatasia was higher than in normals. Furthermore, after oral administration of vitamin B(6) this level increased greatly and long-lastingly, and this might be related to the low level of alkaline phosphatase in this patient. Photosensitivity in this patient may have been caused by abnormal metabolism of vitamin B(6) under the hypophosphatic condition.
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6/79. dapsone-induced photodermatitis in a patient with linear IgA dermatosis.

    dapsone (4, 4' diaminodiphenylsulfone) is an efficient antiinflammatory agent. Its therapeutic use may result in a variety of adverse effects. The most frequent unwanted reactions are hemolytic anemia and methemoglobinemia. By oral route dapsone is mainly metabolized to monoacetyldapsone (MADDS) and hydroxylamine dapsone (DDS-NOH). We report a 76-year-old female patient with linear IgA dermatosis who developed a dapsone-induced photosensitivity 8 weeks after initiation of sulfone therapy. She showed a widespread erythematous eruption in UV-exposed skin area. After clearing of skin lesions the photopatch test revealed positive reactions to dapsone, MADDS and DDS-NOH. dapsone-induced photosensitivity to date has been described only in leprosy patients. We demonstrate for the first time that this adverse reaction is not restricted to leprosy and that dapsone metabolites may also contribute to the mechanism of photosensitivity like the parent sulfone. dapsone-induced photosensitivity is a rare, not dose-related adverse effect of the sulfone and can also occur in patients with inflammatory skin disorders.
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7/79. piroxicam-induced photodermatitis. Cross-reactivity among oxicams. A case report.

    BACKGROUND: there is a group of patients with contact allergy to thimerosal (thiosalicylic acid and ethylmercuric chloride), thiosalicylic acid sensitized, who develop photodermatitis to piroxicam. We present a case which we have investigated cross-reactivity among different oxicams. methods AND RESULTS: a 44-year-old man with contact allergy to thimerosal. A few hours after the intake of Feldene (piroxicam) while running outside, developed a papuloerithematosus exanthema in the neck, knees and forearms, and microvesicles on the finger webs, that became descamative a few days later. Oclusive patch tests with thiosalicylic acid, mercury, piroxicam, tenoxicam, droxicam and meloxicam and photopatch test with the oxicams were performed. patch tests with thiosalicylic acid and piroxicam were positive and negative with the others. All the oxicams photopatch tests were positive. CONCLUSIONS: we present a case of photodermatitis and dermatitis to piroxicam, in a patient with contact allergy to the thiosalicylic moiety of thimerosal, in which cross-reactivity with the other oxicams have been demonstrated. In cases of oxicams-induced photodermatitis, all oxicams should be avoided, to elude posible cross-reactions.
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8/79. Photopatch testing in seven cases of photosensitive drug eruptions.

    OBJECTIVE: The most important goal in the management of photosensitive drug eruptions, as in other types of drug eruptions is identification of the causative drugs to prevent reexposure to them. CASE SUMMARIES: Seven patients whose lesions were mainly distributed on sun-exposed areas underwent laboratory tests, phototests, and photopatch tests with suspected drugs. Phototests were done with ultraviolet A (UVA), UVB, and visible light. Drugs used in the photopatch tests were usually prepared as 10% concentrations in petroleum base, which did not produce reactions in 10 control subjects, followed by irradiation of suberythema doses of UVA. Systemic provocation by oral administration of small doses of causative drugs with irradiation of suberythema doses of UVA was performed to confirm the results of skin tests in four patients. Two patients were not rechallenged with the causative drugs. None of the patients had systemic lupus erythematosus, porphyria, or pellagra. All showed positive reactions to photopatch testing. Systemic provocation confirmed the results of photopatch tests in four patients. The two patients who were not rechallenged had no recurrence of lesions. One patient ingested only one drug at the time of eruptions, and provocation or avoidance was not attempted. A photoallergic mechanism was considered in five cases. CONCLUSIONS: Although there is no information about the appropriate concentrations or vehicles for suspected drugs, photopatch testing could be reliable for identification of causes of photosensitive drug eruptions. Besides piroxicam (a well-known photosensitizer) and carbamazepine, isoniazid and triflusal were identified as the causes of the reactions.
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9/79. Parthenium dermatitis presenting as photosensitive lichenoid eruption. A new clinical variant.

    Parthenium hysterophorus is the commonest cause of airborne contact dermatitis (ABCD) in india. The disease usually manifests as itchy erythematous, papular, papulovesicular and plaque lesions on exposed areas of the body. Rarely, however, the disease may present as actinic reticuloid or photocontact dermatitis. We have observed a different clinical variant of this disease where certain patients with Parthenium dermatitis have presented with discrete, flat, violaceous papules and plaques on exposed areas of the body closely simulating photosensitive lichenoid eruption. We had 8 patients, 6 males and 2 females between 30 and 62 years of age, with itchy, violaceous, papules and plaques on the face, neck, ears, upper chest and dorsa of the hands for 6 months to 6.5 years. Four of these patients had a history of improvement of the lesions up to 30% in winter and aggravation of lesions on exposure to sunlight. There was no personal or family history of atopy. Cutaneous examination in all patients revealed multiple flat, violaceous, mildly erythematous papules and plaques on the forehead, sides and nape of neck, ears, 'V' area of the chest, and extensor aspects of the forearms and hands. Skin biopsies from these lesions showed features of chronic non-specific dermatitis. Patch testing with standardized plant antigens showed a positive patch test reaction to Parthenium hysterophorus in all patients, with a titre of contact hypersensitivity (TCH) varying from undiluted to 1 : 100. We conclude that Parthenium dermatitis may occasionally present with lesions very similar to the lesions of photosensitive lichenoid eruption in morphology and distribution. This clinical presentation of Parthenium dermatitis needs to be recognized to avoid misdiagnosis.
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10/79. Chronic actinic dermatitis treated with cyclosporine-A.

    Chronic actinic dermatitis (CAD) groups together all chronic photodermatosis with light photosensitivity. We report the case of a 69-year-old man who, for over one year, had presented a reddish-brown erythema and shedding, with thickened and hypo-elastic skin on the face, scalp, neck and on the back of the hands and forearms. patch tests were positive to isoeugenolo 1% and photo-patch tests showed a positivity to phenotiazine 2%. After a short and ineffective treatment with beta-carotene and photo-protectors, the clinical picture was resolved with the administration of oral steroids but with a relapse of the dermatitis once the dosage was lowered. We therefore started treatment with cyclosporine-A (4.5 mg/kg/die), which resulted in a rapid improvement of the clinical picture, but with a reappearance of the manifestations when the dosage was lowered. The treatment was resumed and we observed that the dose of 1.5/mg/kg/die resulted morbus-static. The patient is still being treated with this drug at this dosage. The result is that the disease is under control and no side effects are present. As we consider CAD an invalidating disease it seems to us that Cy-A could be taken into consideration as an alternative to traditional treatments.
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