[Rheumatoid purpura in adults and mycoplasma infection].
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Biomedical subjects
Publications and source records attributed to M C Machet.
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Carpal tunnel syndrome (CTS) was observed in 4 cases of a consecutive series of 16 patients admitted for the initial diagnosis or follow-up of systemic scleroderma from 1986 to 1990. We also observed one case of ulnar nerve compression. Neurological involvement was confirmed by electromyogram, and motor and sensory nerve conduction studies. The neurological signs appeared at the beginning of the disease in two cases and preceded the discovery of scleroderma in two. CTS is not rare in scleroderma and must be carefully sought, both clinically and electrophysiologically. Patients with 'idiopathic' CTS might need clinical follow-up for early diagnosis of scleroderma.
Schnitzler's syndrome, first described in 1974, is defined by chronic non-pruritic urticaria, osteocondentation, and a monoclonal IgM dysproteinemia, but without criteria of lymphoproliferative disease. We report a patient with chronic urticaria and macroglobulinemia. In addition, he had double monoconal dysproteinemia IgM kappa (31.3 g/l) and IgA lambda, osteocondensation, and some cutaneous lesions of pseudoxanthoma elasticum. Only 20 cases of Schnitzler's syndrome have been reported hitherto. This is the first case associated with pseudoxanthoma elasticum, which was localized and discovered at the same time as Schnitzler's syndrome. We discuss the possible role of monoclonal immunoglobulin in the occurrence of localized elastorrexhis.
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BACKGROUND: Hepatitis C virus (HCV) frequently causes leucocytoclastic vasculitis as a result of type II or III cryoglobulinemia. HCV-associated vasculitis without cryoglobulinemia is less common. PATIENTS AND METHODS: A 33-year-old woman consulted for infiltrative necrotic purpura of the lower limbs, responsible for leg ulcers measuring less than 1 cm. Histopathological examination revealed vasculitis affecting the hypodermic arterioles and caused by periarteritis nodosa. No extracutaneous involvement was observed. The patient had presented asymptomatic untreated HVC infection (genotype 3) for two years. Antiviral treatment resulted in elimination of the patient's viremia and no relapse of skin lesions was observed two years after the end of treatment. COMMENTS: This patient presented vasculitis due to cutaneous nodular periarteritis associated with HVC without cryoglobulinemia. Hepatic impairment was mild and did not require any antiviral treatment. No further skin involvement was seen after treatment with colchicine and because the patient's viral genotype was favorable, we decided to initiate antiviral therapy. This therapeutic approach should be considered by dermatologists, but it is nevertheless important to assess the risk of interferon-induced aggravation of vasculitis.
INTRODUCTION: Cutaneous lesions are rarely inaugural in Churg and Strauss syndrome. We report the case of a patient in whom recurrent papular lesions of the penis revealed a Churg-Strauss granulomatous angeitis. OBSERVATION: A 54 year-old man consulted for recurrent non-infiltrated and painless erythematous papules of the penis over the past 4 years. His past history revealed severe asthma, which had appeared at the same time, nasal polyposis and chronic sinusitis. Other than the genital organs, the clinical examination was normal. Histological exploration of a cutaneous biopsy of the penis showed a necrotic granulomatous vasculitis. The usual biological examinations were normal. Research for proteinuria, hematuria and measurement of polynuclear anticytoplasm antibodies were negative. Pulmonary X-ray revealed a bilateral interstitial syndrome with micronodules. The broncho-alveolar wash revealed moderate granulocyte alveolitis with numerous eosinophilic polynuclears. The electromyogram showed a reduction in the sensitive potential of the nerves explored in the 4 limbs. Churg-Strauss granulomatous angeitis was diagnosed. Treatment with 0.8 mg/kg/day of prednisone was initiated. The cutaneous lesions disappeared rapidly. Since three months later there had been no relapse, corticosteroid therapy was slowly and progressively reduced. Nine months later, the patient exhibited new papular lesions of the glans penis and progressive relapse of asthma. Treatment with cyclophosphamide (Endoxan(R)) combined with systemic corticosteroids was initiated. DISCUSSION: In view of the concomitance of necrotic granulomatous vasculitis in the cutaneous biopsies, severe, recent corticosteroid-dependent asthma, eosinophil-rich pulmonary infiltrate, allergic rhinitis, chronic sinusitis and the onset of a neuropathy, the diagnosis of Churg-Strauss syndrome was retained. The absence of hypereosinophilia in the blood during diagnosis can be explained by the oral corticosteroid therapy at low doses because of the asthma and sinusitis. However, hypereosinophil blood levels had been reported in several prior hemograms. Damage to the genital organ is exceptional during Churg-Strauss syndrome and is usually of granulomatous prostatitis form. Only one other case has been reported. Our observation is original in that it was isolated to the genital skin, which led to the diagnosis of Churg and Strauss granulomatous angeitis with systemic involvement.
We report the fourth case of low-grade gastric MALT lymphoma associated to Helicobacter heilmannii. This spiral organism may be present in the gastric mucosa of animals where it is non pathogenic while, in humans, its presence is always associated with chronic gastritis. In this case, Helicobacter heilmannii was observed in the absence of Helicobacter pylori. Regression of endoscopic and histological lesions after Helicobacter heilmannii eradication suggests its role in gastric lymphoma. This observation underlines the need for searching for Helicobacter heilmannii by careful histological examination, in the absence of Helicobacter pylori, and the importance of its eradication in the treatment of gastric lymphoma.