[Side-effects of anti-TNF alpha agents].
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Biomedical subjects
Publications and source records attributed to J-L Schmutz.
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INTRODUCTION: Transcutaneous electric nerve stimulation (TENS) is useful for many chronic pains. It induces few serious side effects, but skin reactions are not rare. We report on two cases of contact dermatitis due to TENS electrodes by sensitization to the acrylate in TENS conductive gel. CASE REPORTS: A 50 year-old man suffered from post-traumatic lumbar pair. He developed eczematous lesions on the sites where the TENS electrodes were applied. Patch tests were positive with the TENS gel, with ethylene glycol dimethylacrylate (2 p. 100 petrolatum) and ethyl-acrylate (2 p. 100 petrolatum) on day 2 and 4 readings. A 54 Year-old man had a paralysis of the foot elevator following rupture of an aneurysm. After 2 months, he had an eczema on the sites where the TENS electrodes were applied. Patch tests were negative with the TENS electrodes but positive with 2-hydroxyethyl acrylate (0.1 p. 100 petrolatum), triethyleneglycol diacrylate (0.1 p. 100 petrolatum), 2-hydroxyethyl methacrylate (2 p. 100 petrolatum) and 2-hydroxypropyl methacrylate (2 p. 100 petrolatum) on day 2 and 4 readings. DISCUSSION: TENS transmits small electrical currents through the skin that induce the depolarization of the affected sensory nerve endings. They have few serious side effects but skin reactions such as irritation, burns or allergy to propylene glycol in the electrode gel, to the rubber of the electrodes (mercaptobenzothiazole) or to the metallic part of the electrodes, i.e. nickel, are not uncommon. To our knowledge, only one case of an allergy to the polyacrylates of TENS electrode gel has been previously reported in the literature. We emphasize that acrylate could be the main sensitizer in the more recently commercialized TENS electrodes and will propose alternative ways of treating patients sensitized to acrylate and who require treatment with TENS.
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INTRODUCTION: Degos' disease or atrophic malignant papulosis is defined by porcelain white cutaneous lesions with atrophic scarring, often associated with severe and fatal systemic involvement (visceral and neurological). Benign forms are rare or under-reported and the familial forms are exceptional. It is a very rare disease, only two hundred cases have been reported in the literature with a sex ratio of 3M/1F. The pathogenesis of Degos' disease remains controversial. The exceptional observation of familial form raises the question of a genetic predisposition of this disease or an infectious aetiology with a low virus. OBSERVATION: A 41 year-old woman was known to have Degos' disease for 26 years with only cutaneous manifestations. One of her two sons developed atrophic cutaneous lesions at the age of 20. In both patients, no thrombotic or immunological abnormalities were found. The karyotype was performed with normal results. DISCUSSION: Degos' disease or malignant atrophic papulosis can have a long lasting benign evolution. Our patient, who had presented a benign form for 26 years, had the longest evolution ever documented in literature. We cannot be sure that her son will have a benign course of his Degos' disease because the diagnosis is recent and because the systemic involvement can appear after many years of evolution. In the familial forms, from our study and the 31 cases previously described in the literature, with ten different families, the course of the disease seems to be less severe than in sporadic forms. Among these familial forms of Degos' disease, only 4 patients presented a malignant form, which in one case did not prove a relationship between the death and the Degos' disease. Are the sporadic forms with only skin involvement less frequently reported? Has the familial form of Degos' disease the same course as a very severe common sporadic form?
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Delayed reactions to radio-contrast media (RCM) with positive skin tests are rare. We report the study of a series of 15 patients who presented delayed reactions to RCM, with an analysis of the clinical features and the results of standardized drug skin tests. Patch tests were performed with RCM and iodized antiseptics (IAs). If negative, prick tests were performed, followed by intradermal tests (IDTs), then intravenous administration under hospital surveillance. The main clinical features were maculopapular rashes or a macular rubella-like rashes. Patch tests were positive with RCM in 2 of 15 cases and with IAs in 4 of 15 cases. All the prick tests were negative. IDTs were positive at 24 h in 8 of 15 cases. 5 of 12 patients had a non-severe relapse of the rash upon receiving an RCM despite clearly negative skin tests with the readministered RCM. Visipaque cross-reacted with Iopamiron, Iomeron, Telebrix, Omnipaque, Xenetix and Hexabrix. Omnipaque cross-reacted with Hexabrix and Iopamiron. IDTs with delayed readings are of better value than patch tests in such patients. The readministration of RCM with negative IDTs must be performed with progressive amounts under hospital surveillance. Cross-reactions between various classes of RCM are frequent. The responsible epitopes are unknown. Iodine itself could be involved.
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BACKGROUND: We report a case of keratosis lichenoides chronica and prolonged exposure to a source of heat (infrared radiation). CASE REPORT: A 35 year-old man was examined for a symmetric and reticulate dermatosis on the abdomen, the interior of arms and lower extremities. The lesions had progressed over several months. They were characterized by hyperpigmentation, erythematous, bullous and squamous papules. These lesions were associated with those of the scalp, evoking seborrheic dermatitis. The patient was exposed to a source of heat with an electric radiator on his bare chest everyday. The skin biopsy showed a lichenoid reaction. All these elements allowed to put the diagnosis of keratosis lichenoides chronica, probably actived by the infrared light. DISCUSSION: Keratosis lichenoides chronica is a rare acquired dermatosis of the young adult. Its physiopathology remains elusive. This dermatosis is characterized by keratosic violaceous lichenoid papules distributed symmetrically. The eruption is usually asymptomatic. The histological examination indicates a lichenoid reaction. The progression is chronic and the disease is very resistant to therapy. Keratosis lichenoides chronica has never been described as being able to be induced by Koebner's phenomenon. In the literature, two cases of erythema ab igne were associated with lichen planus. For some authors, keratosis lichenoides chronica is an entity itself, for others it would be related to lichen planus. These arguments enabled us to diagnose keratosis lichenoides chronica probably activated by the infrared light.
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