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Biomedical subjects

M Hanss

Publications and source records attributed to M Hanss.

60 records · Page 4Linked to original sources

[Treatment by lepirudin and acenocoumarol of heparin induced thrombocytopenia after valvular surgery: a word of caution].

The diagnosis and treatment of type II heparin-induced thrombocytopenia (HIT) after valvular surgery raise difficult issues due to the substitution of heparin by other anticoagulants. A 50-year-old man with hepatic cirrhosis and acute infective endocarditis underwent aortic valve replacement. On the 4th postoperative day platelet count decreased to 50 g/l. Platelet aggregation was demonstrated in vitro with unfractioned and low molecular weigh heparins and danaparoid sodium. As serum creatinine was 94 micromol/l, lepirudine (r-hirudin) was administered at recommended doses. However, six hours later hirudinaemia estimated by ecarin-clotting time was 3 mg/l and lepirudine dose had to be divided by 15 in order to reach therapeutic levels. Similarly, INR increased up to 6,7 on the 11th postoperative day after acenocoumarol 1 mg daily was administered. Despite the presence of oesophageal, gastric and duodenal lesions at risk of haemorrhage no bleeding was detected. The reasons for overdosage are discussed. The necessity of measurement or calculation of creatinine clearance before lepirudine prescription and frequent hirudinaemia during treatment is emphasized.

Acenocoumarol↗

Spontaneous intracerebral hemorrhage revealing Addison's disease.

We report a case of spontaneous intracerebral hemorrhage occurring in a young woman and revealing Addison's disease. This autoimmune primary adrenocortical insufficiency was associated with premature ovarian failure. Exhaustive research for nonhypertensive causes of intracerebral hemorrhage was negative. Initial coagulation studies disclosed severe hypofibrinogenemia and prolonged prothrombin time related to vitamin K-dependent coagulation factor deficit. Clotting abnormalities cleared at 4 months under treatment with hydrocortisone. Glucocorticoids are potent regulators of fibrinogen biosynthesis, increasing fibrinogen secretion. We conclude that primary adrenocortical insufficiency induced this hemorrhagic diathesis leading to spontaneous intracerebral hemorrhage. This latter has never been reported in Addison's disease. Primary adrenocortical insufficiency should be considered as a rare potential cause of nonhypertensive intracerebral hemorrhage.

Addison Disease↗