Showing papers by "M. den Heijer published in 2000"

Recurrent venous thrombosis and markers of inflammation.

Abstract: Inflammatory processes may play a key role in venous thrombosis, by inducing a procoagulant state through the action of cytokines and chemokines on monocytes and endothelial cells. Plasma concentrations of three inflammatory mediators, interleukin 6 (IL-6), interleukin 8 (IL-8) and monocyte chemotactic protein 1 (MCP-1), that mediate the cross-talk between inflammation and coagulation, were measured in 182 subjects with recurrent venous thrombosis and 350 healthy subjects recruited through a general practice. Elevated levels of IL-6 (>90th percentile of the control group) were detected in 25.8% of the patients with venous thrombosis in comparison with 10% (by definition) of the controls [odds ratio 2.4 (95%CI 1.5-3.8)]. In 21.5% of the patients elevated plasma levels of IL-8 (>90th percentile) were determined [odds ratio 2.0 (95%CI 1.2-3.5)]. Elevated levels of MCP-1 (>90th percentile) were detected in 24.1% of the patients [odds ratio 1.9 (95%CI 1.2-3.2)]. This is the first large clinical study showing that an increase in inflammatory mediators is associated with venous thrombosis. Future prospective studies are necessary to clarify the causal nature of the inflammatory process with respect to venous thrombosis.

Thrombosis prophylaxis in hospitalised medical patients: does prophylaxis in all patients make sense?

Abstract: Background: Most studies on thrombosis prophylaxis focus on postoperative venous thrombosis. In medical wards thrombosis prophylaxis is generally restricted to patients who are immobilised. Our primary aim was to investigate the incidence of venous thrombosis in a general internal ward, to assess whether more rigorous prophylaxis would be feasible. Methods: We investigated the incidence of venous thrombosis in patients hospitalised from 1992 to 1996 and related our findings to literature reports. Results: The incidence of symptomatic venous thrombosis in internal patients during hospitalisation was 39/6332 (0.6%). Among these 39 patients, 24 had a malignancy, whereas 876 out of all 6332 patients had a known malignancy. So, the incidence in this group with cancer was 2.7% compared with 0.3% (15/5456) in the non-cancer group (relative risk for venous thrombosis due to malignancy was 10.0 (95%C.I. 5.3–18.9). Conclusion: The incidence of venous thrombosis during hospitalisation in a department of general internal medicine is low and does not justify prophylaxis in all internal patients. Cancer is a strong risk factor for hospital-acquired thrombosis in the medical ward. Further studies may answer the question as to whether thrombosis prophylaxis in this subgroup is feasible.