Chronic HIV disease and activation of the coagulation system

With current effective antiretroviral treatment, the spectrum of morbidity and mortality during chronic HIV disease has shifted away from AIDS defining clinical events. Persistent abnormalities in coagulation appear to contribute to excess risk for a broad spectrum of non-AIDS defining complications, including, but not limited to, venous and arterial thrombotic disease. Mechanisms specific to HIV disease, antiretroviral therapy, and lifestyle or behavioral factors contribute to a pro-coagulant state, in part, through increased tissue factor activity coupled with a paradoxical decline in the anti-coagulant response. Alterations in coagulation biology in the context of HIV disease appear to be largely a consequence of persistent systemic immune activation, micro- and macro-vascular disease, and, potentially, impaired hepatic synthesis of coagulation factors. The clinical consequences of HIV-related changes in coagulation biology, the degree to which they are unique to HIV disease, and whether they can be mitigated through adjunct treatments, remains a focus of current research.