[An epidemic in a hospital caused by a methicillin-resistant strain of Staphylococcus aureus].
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Biomedical subjects
Publications and source records attributed to H G Schipper.
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This study was designed to examine the effect of selective correction of antithrombin III activity on the increased turnover of fibrinogen, which occurs in patients with liver cirrhosis supposedly due to disseminated intravascular coagulation. Human antithrombin III concentrates were therefore transfused in seven patients with cirrhosis and antithrombin III deficiency (less than 80%). Fibrinogen half-life and the fractional catabolic rate constant were calculated from the turnover of 125I-fibrinogen which was represented by a two-compartment model. Prior to antithrombin III transfusion, 125I-fibrinogen half-life was 76.7 +/- 15.2 h and the fractional catabolic rate constant was 0.33 +/- 0.11 of the plasma fibrinogen pool per day. In six healthy adult controls these values were significantly different: 109.4 +/- 8.8 h and 0.19 +/- 0.01 respectively. Correction of antithrombin III activity with human antithrombin III concentrate reduced the increased turnover of radiolabelled fibrinogen to normal. The 125I-fibrinogen half-life became 108.4 +/- 17.6 h and the fractional catabolic rate constant decreased to 0.23 +/- 0.06. These observations indicate that decreased antithrombin III activity contributes in an important way to the increased 125I-fibrinogen turnover in patients with cirrhosis and this might reflect intravascular coagulation.
Three patients with a severe bleeding disorder and disseminated intravascular coagulation were effectively treated with human antithrombin-III concentrates. This treatment, followed by administration of prothrombin complex and platelet suspensions, resulted in a normal haemostasis, which was maintained during clinical investigations and surgery.
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The low bioavailability of albendazole affects the therapeutic response in patients with echinococcosis. Cimetidine co-administration is reported to improve bioavailability. To analyze the assumed dose-dependent bioavailability of albendazole, we administered 5 to 30 mg/kg albendazole to 6 male volunteers in a randomized cross-over study. To assess the effect of cimetidine (10 mg/kg twice daily), the drug was given with albendazole (20 mg/kg). A dose-dependent bioavailability was not observed. This was due to inter-individual variability of the maximal concentration (Cmax 38%-72%) of albendazole sulphoxide (ABZSX), the active metabolite of albendazole. Cmax was 0.21+/-0.14 mg/L after 5 mg/kg and 0.39+/-0.19 mg/L after 30 mg/kg albendazole (P = 0.217). Cimetidine tended to decrease Cmax by 52% (P = 0.109) and significantly inhibited ABZSX breakdown as indicated by the prolongation of ABZSX elimination half-life from 7.4+/-3.3 hr to 19.0+/-11.7 hr (P = 0.028). Remarkably, the inter-individual variability of Cmax was significantly lower during cimetidine co-administration: 14% versus 72%.