Cases reported "Skin Diseases"

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1/192. skin eruption with gabapentin in a patient with repeated AED-induced Stevens-Johnson's syndrome.

    skin eruptions have been reported with the use of all antiepileptic drugs and there is a significant risk of cross-reactivity between these agents in causing serious eruptions such as Stevens-Johnson's syndrome. Gabepentin is usually considered a safe agent for patients with a previous history of drug allergies and there have been no cases of skin eruption reported to the gabapentin post marketing surveillance. We report a patient who had severe Stevens-Johnson's syndrome induced by phenytoin and later by carbamazepine. Subsequent use of gabapentin also resulted in a skin eruption which was limited to the lower extremities but without systemic or mucosal involvement. This case suggests that patients with a strong history of drug-induced idiosyncratic reactions may experience such reactions to gabapentin as well.
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2/192. Anticoagulant-induced skin necrosis in a patient with hereditary deficiency of protein s.

    skin necrosis is a rare but debilitating complication of treatment with vitamin k antagonist anticoagulants such as warfarin. A clinically similar syndrome has been reported less frequently with heparin therapy. We recently managed a thirty-year-old female patient who developed skin necrosis on her left lower extremity while on warfarin for postpartum DVT. The lesions started to develop 48 hr after stopping heparin therapy. Discontinuation of warfarin and reinstitution of heparin was complicated by a rapid decrease in platelet count consistent with heparin-induced thrombocytopenia (HIT) and its associated risk of platelet activation and thrombosis. The diagnosis was supported by the identification of antibodies against heparin/platelet factor 4 complexes in the patient's serum. The platelet count recovered and the patient improved after switching to therapy with the heparinoid danaparoid. Evaluation for a hypercoagulable state revealed a partial deficiency of protein s, a condition that previously was identified in two of her family members. It is not clear if this patient suffered from warfarin-induced skin necrosis, a manifestation of heparin-mediated platelet activation, or a complex condition in which both drugs contributed. HIT may affect 1-3% of patients who receive unfractionated heparin, and this case raises the possibility that heparin may contribute to, or cause, some episodes of skin necrosis attributed to warfarin. Because many patients who develop warfarin-induced skin necrosis have been treated initially with heparin, it would seem prudent to consider HIT in these situations.
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3/192. Treatment of reticular erythematous mucinosis with a large dose of ultraviolet B radiation and steroid impregnated tape.

    To date, there are no successful treatments for reticular erythematous mucinosis (REM) other than antimalarial drugs such as chloroquine; these have many adverse side effects and are prohibited for use in japan. We report a case of REM improved by a large dose of ultraviolet B (UVB) radiation and a steroid impregnated tape. The large dose of UVB radiation improved the erythema after 5 weeks. Application of steroid impregnated tape to a lesion where a large dose of UVB had been given produced an additive clinical effect. UVB radiation and steroid impregnated tape are considered to be effective treatments for REM.
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4/192. Ichthyosiform sarcoidosis.

    Ichthyosiform sarcoidosis is a rare specific cutaneous manifestation of sarcoidosis; it clinically and microscopically appears as acquired ichthyosis. We report a 68-year-old black man with a 10-year history of chronic obstructive pulmonary disease who presented with a 2-month history of acquired ichthyosis. His skin biopsy specimen showed both noncaseating granulomas in the dermis, consistent with sarcoidosis, and ichthyosis vulgaris. Ichthyosiform sarcoidosis is an uncommon presentation of cutaneous sarcoidosis that has been previously described in 19 nonwhite patients whose lesions were located on the legs. The skin lesions appeared either concurrently with or preceded the diagnosis of systemic sarcoidosis in 76% of patients; 95% of the patients eventually developed systemic involvement of their sarcoidosis. The onset of acquired ichthyosis should prompt evaluation for an associated malignancy, connective tissue disease, endocrine abnormality, nutritional deficiency, drug reaction, or sarcoidosis. A skin biopsy specimen consistent with acquired ichthyosis may point to the presence of cutaneous sarcoidosis.
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5/192. Two cases of gigantic dystrophic calcinosis cutis caused by subcutaneous and/or intramuscular injections.

    We describe two female patients with gigantic dystrophic calcinosis cutis caused by a large number of subcutaneous and/or intramuscular injections which they received when they were much younger. Laboratory data and physical examinations were generally within normal limits, and we detected no disease which might induce cutaneous calcification. There are many reports of dystrophic calcinosis cutis caused by injection of several kinds of drugs. However, we found no previous report describing a patient with calcinosis cutis induced by local tissue injury from a large number of injections and with extraordinarily widespread calcification at the injection sites. Because we do not know the exact drugs injected, it is difficult to say if a specific ingredient in the injections was related to this condition. We do know that a large number of subcutaneous or intramuscular injections were frequently administered to patients who had difficulty in maintaining venous infusions in the past, so there may be similar cases of dystrophic calcinosis cutis which have not been reported.
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6/192. lichen planus associated with milia.

    The formation of milia is well recognized in both bullous and inflammatory dermatoses. There are several reports of milia developing in a rare variant of lichen planus pilaris known as lichen planus follicularis tumidus (LPFT), but the association of milia with other types of lichen planus (LP) has not been documented in the literature. We report five patients who developed milia during the course of either drug-induced or idiopathic LP and one in whom milia developed in a lichenoid tattoo reaction. Milia were noted to occur transiently during the resolving phase of LP. Most cases were severe enough to warrant treatment with systemic steroids. The association of milia with LP is not restricted to the rare clinical variant LPFT. We speculate that a severe lichenoid reaction with basal layer degeneration may precipitate the formation of milia in some cases of LP.
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7/192. Fixed drug eruption due to atenolol: a case report.

    We report a case of (generalized) fixed drug eruption induced by atenolol, a beta adrenoreceptor blocking agent. atenolol has been shown to be effective treatment for hypertension, angina pectoris and cardiac arrhythmia. However, adverse skin reactions are very rare. We present a case of (generalized) fixed drug eruption due to atenolol and review the cutaneous reaction to the drug.
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8/192. The use of a posterior-based tongue flap for the closure of a pharyngocutaneous fistula.

    The closure of a pharyngocutaneous fistula by the use of a posteriorly based tongue flap is described. The use of such a flap for this purpose has not been previously recorded in the literature.
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ranking = 0.22608618602512
keywords = closure
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9/192. paronychia with pyogenic granuloma in a child treated with indinavir: the retinoid-mediated side effect theory revisited.

    BACKGROUND: The introduction of hiv-1 protease inhibitors into the treatment of patients infected with hiv-1 has had a major influence on clinical practice. However, the use of protease inhibitors is frequently associated with the development of resistance and several side effects and interactions with other drugs have been reported. OBSERVATIONS: We present the first pediatric patient with paronychia with pyogenic granuloma associated with the administration of the protease inhibitor indinavir. Clinical findings are discussed in view of a possible interference of indinavir with endogenous retinoid metabolism. CONCLUSION: Considerable evidence advocates the mediation of indinavir side effects by impaired oxidative metabolism of retinoic acid through the inhibition of cytochromes P450 3A by indinavir rather than by impaired formation of 9-cis-retinoic acid. copyright (R) 2000 S. Karger AG, Basel
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10/192. Troglitazone improves psoriasis and normalizes models of proliferative skin disease: ligands for peroxisome proliferator-activated receptor-gamma inhibit keratinocyte proliferation.

    BACKGROUND: psoriasis is often treated with agents that activate nuclear hormone receptors for glucocorticoids, retinoids, and vitamin d. The peroxisome proliferator-activated receptor-gamma (PPARgamma) is a related nuclear hormone receptor that can be activated by its ligands, including the thiazolidinediones. OBJECTIVE: To assess whether treatment with troglitazone, a currently available thiazolidinedione used to treat diabetes mellitus, has an effect on psoriasis in normoglycemic patients and whether ligands for PPARgamma have an effect on models of psoriasis. DESIGN: Open-label administration of troglitazone in patients with psoriasis and evaluation of drug actions in cellular, organ, and transplant models of psoriasis. SETTING: University and community hospital outpatient departments and university laboratories. patients: patients with chronic, stable plaque psoriasis and control subjects. Five patients with psoriasis received troglitazone (none withdrew); 10 different untreated patients and 10 controls provided tissue samples. INTERVENTIONS: Oral troglitazone therapy at various dosages in patients with psoriasis; also, use of troglitazone, ciglitazone, and 15-deoxy-delta-12,14-prostaglandinJ2 in psoriasis models. MAIN OUTCOME MEASURES: Investigator-determined clinical results in patients and cell counts and histological evidence in models. RESULTS: All patients' psoriasis improved substantially during troglitazone therapy. Peroxisome proliferator-activated receptor-gamma was expressed in human keratinocytes; ligands for PPARgamma inhibited the proliferation of normal and psoriatic human keratinocytes in culture. Troglitazone treatment normalized the histological features of psoriatic skin in organ culture and reduced the epidermal hyperplasia of psoriasis in the severe combined immunodeficient mouse and human skin transplant model of psoriasis (P<.05 compared with untreated controls). CONCLUSIONS: Peroxisome proliferator-activated receptor-gamma might be a useful intracellular target for the treatment of psoriasis; further study is needed to assess the clinical value of ligands for PPARgamma, including troglitazone.
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