The prothrombotic state in rheumatoid arthritis: an additive risk factor for adverse cardiovascular events.

Rheumatoid arthritis (RA) has been recognized to increase cardiovascular morbidity and mortality independent of established risk factors. The chronic inflammatory state, a hallmark of RA, is considered an autonomous risk factor, whereas components of innate and adaptive immunity are believed to contribute to the onset of acute cardiovascular events. Several studies have suggested that RA confers a prothrombotic state featured by abnormalities in coagulation and fibrinolytic systems together with an altered state of platelet reactivity.

Induction of IRAK-M is associated with lipopolysaccharide tolerance in a human endotoxemia model.

Recent in vitro and murine in vivo studies have identified several potential LPS tolerance factors. In this study, we describe the expression kinetics of these LPS tolerance factors in standardized human endotoxemia models using i.v.