Venous thromboemboliс complications and tuberculosis: is there an interaction?

Abstract

Venous thromboembolic complications (VTEC) haven’t lost their status as an important medical and social problem for many decades. There are about 300 thousand people die from VTEC in Russia every year. Another significant problem for our country is tuberculosis. Tuberculosis is one of the most common severe infections in the world, most often occurs as a chronic disease and can induce VTEC due to a variety of synergistically acting factors. Previously published studies examined the interaction between tuberculosis and VTEC, but they were based on the data obtained from countries with a high incidence of tuberculosis and a low prevalence of venous thrombosis. An analysis of the literature has shown that tuberculous inflammation determines all three interrelated components of the Virchow’s triad: endothelium inflammatory damage, venous stasis and hypercoagulability. In addition, treatment regimens for the disease with the inclusion of rifampicin also contribute to the development of VTEC due to the pronounced procoagulant properties of the drug. Another equally important agent that potentiates hypercoagulation is the HIV virus, which affects the endothelium and immunocompetent cells. Currently available epidemiological data indicate that HIV infection is associated with an increased risk of VTEC in 2-10 times compared to the general population of the same age. In this context, tuberculosis and HIV/TB co-infection can be considered as a large reversible risk factor for the development of VTEC and included in the prognostic risk assessment scales for acute venous thrombosis and embolism.