Haemostatic Abnormalities in Patients with a Clinical Predisposition to Venous Thromboembolism

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.