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Objectives: Raynaud's syndromes may be observed in HIV-infected patients, particularly those with Kaposi disease treated with bleomycin. This complication occurs in 10% of patients given bleomycin although only 7 cases have been reported in the literature. The aim of this study was to determine the frequency of certain biological abnormalities observed in HIV patients with Kaposi disease given bleomycin and who develop Raynaud's syndromes., Patients and Methods: A survey was conducted from 1989 to 1995 among 1074 patients infected with HIV-1. There were 121 patients with Kaposi disease and 73 of these were treated with bleomycin. The clinical features and laboratory results (cryoglobulinemia, free protein-S, protein-C, anticardiolipin antibodies, von Wille-brand factor (vWF.ag) endothelin-1) were obtained in 5 patients who developed biomycin-induced Raynaud's syndrome., Results: Amont the 73 patients with Kaposi disease treated with bleomycin (total mean dose = 227 mg (120-380 mg)), 5 patients (12.6%) developed a severe Raynaud's synchrome including two who suffered digital necrosis Withdrawal of bleomycin led to improved symptomatology (n = 2) or an aggravation (n = 1) in the 3 patients followed., Conclusion: Raynaud's syndromes are frequent (12.6%) in HIV patients with Kaposi disease treated with bleomycin. The vascular toxicity of bleomycin, demonstrated in animals, would appear to be the causal factor among others. Release of endothelial factors (vWF.ag endothelin-1) and perturbed hemostasis related to the HIV infection (protein-S deficiency, anti-cardiolipin antibodies) could be an expression of and aggravate the vascular toxicity of bleomycin.

Objective: Although portal obstruction is a complication in cirrhosis which is usually associated with hepatocellular carcinoma, its precise neoplastic or thrombotic nature is not easy to determine. Serum antiphospholipid antibodies could be involved in thrombosis-related portal obstruction., Patients and Methods: The presence of serum anticardiolipid antibodies was investigated by an immunoenzymatic technique in 129 patients with alcoholic cirrhosis, 47 patients with hepatocellular carcinoma with (n = 18) or without (n = 29) portal obstruction, and 82 patients without hepatocellular carcinoma or portal obstruction. Five control groups were included: patients with non alcoholic cirrhosis (n = 21), non cirrhotic alcoholic liver disease (n = 21), chronic viral hepatitis (n = 14), extra-hepatic cholestasis (n = 9), and hypergammaglobulinemia associated with human immunodeficiency virus infection without liver disease (n = 28)., Results: The prevalence of serum anticardiolipid antibodies was 57% in patients with alcoholic cirrhosis, which was significantly different from the prevalence in the control groups which ranged from 0 to 32%. Anticardiolipid antibodies were of IgA isotypes in 90.5% of the cases, mainly related to the degree of liver failure but not to hepatocellular carcinoma or portal obstruction., Conclusion: In alcoholic cirrhosis, serum anticardiolipid antibodies do not seem to be related to the pathogenesis of portal obstruction in patients with hepatocellular carcinoma. They could rather reflect liver lesions and immunological dysfunctions.

Protein S is the cofactor of activated protein C which, together with the antithrombin system, is a major regulator of coagulation. Congenital protein S deficiency is an important risk factor for venous thrombosis. In this study of 105 patients with protein S deficiency, 64 had one of several thromboembolic accidents, including 14 arterial thrombotic accidents involving the central nervous system or the myocardium. These accidents occurred in young subjects (mean age: 25 +/- 13 years) only one-third of whom had another risk factor. This high frequency of arterial thrombosis associated with protein S deficiency calls for a prospective study in young subject with cerebral vascular accident or myocardial infarction.

The authors have studied 21 patients with Crohn's disease and have looked for signs of platelet and blood coagulation activation, by measuring platelet factor 4, beta thromboglobulin and fibrinopeptide A: a fibrinolytic system study with tissue plasminogen activator assessment has also been made. Beta thromboglobulin, platelet factor 4 and fibrinopeptide A were increased in 80 per cent, 100 per cent and 60 per cent of cases respectively. Beta thromboglobulin was significantly correlated with the Van Hees activity index. Plasminogen before venous stasis was significantly decreased and 9 patients had a plasminogen release defect. The relationship between Crohn's disease and thrombosis might partially be explained by a release of inflammation mediators and/or endotoxins: these mediators might induce thrombosis by interfering with the antithrombogenic properties of the endothelial cell. In conclusion these data prove that active Crohn's disease is currently associated with a prethrombotic state, present biologic tests that might predict a venous or arterial thrombosis at short term are not available.