The pharmacokinetics of cyclosporin A (CS‐A) were studied in 10 patients with primary biliary cirrhosis (PBC) after oral administration in steady state. Mean values for area under the blood concentration‐ time curve (AUC), time to maximal blood concentration (tmax), maximal blood concentration (Cmax) and elimination half‐life (t1/2,z) were similar to results of previous studies in transplant patients. The variation between patients was large. No significant correlations of pharmacokinetic data with biochemical or histological parameters were found. Because of the high variability of pharmacokinetic parameters, patients with PBC treated with CS‐A need to be regularly controlled for nephrotoxicity by estimation of serum creatinine and bioavailability (trough blood levels).
Although a number of clinical risk factors for deep vein thrombosis (DVT) and embolism are recognised, the precise pathogenetic mechanism operating in the majority of cases is never established. Whilst it is important to recognise congenital deficiencies of naturally occurring anticoagulant proteins, their incidence is often unknown in any given hospitalized population. To examine this controversy, a case controlled study was undertaken to correlate venous thromboembolism at our institution with laboratory tests of haemostasis and to define those having predictive value for this event. Patients with the clinical diagnosis of DVT were divided into those having venographic confirmation (Group 1; n = 106) and a matching series where these studies were negative (Group 2: n = 74). The most frequent associations with DVT were the confirmed diagnosis of severe pulmonary tuberculosis (n = 30), carcinoma (n = 13) and surgery (n = 6); no proven case of a congenital factor deficiency was documented. Comparison of laboratory data from groups 1 and 2 showed, respectively, higher levels of fibrinogen, being 4.6 ± 0.8 g/L versus 3.16 ± 1.12 g/L (p < 0.05), fibrin(ogen) degradation products (FDP) of 11.5 ± 8.3 μg/ml versus 1.4 ± 1.63 (p < 0.01), and tissue plasminogen activator antigen (tPA) 26.5 ± 14.5 versus 12.1 ± 11.2 (p < 0.01). Decreased levels of several coagulation inhibitory proteins were seen only in association with clinical and haematologic evidence of multisystem disease with coagulopathy. No isolated deficiencies of these proteins were observed, even in the small group of idiopathic recurrent venous thrombosis in this series. Increased plasma fibrinogen, FDP, and plasminogen activator antigen levels may indicate the presence of DVT in individuals at risk, and in the case of pulmonary tuberculosis may be associated with a potential hypercoagulable state.
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