Infective endocarditis is frequently complicated by thrombocytopenia. These patients are also at risk for septic emboli manifesting as thrombotic or hemorrhagic stroke, myocardial infarction, renal infarction, or even acute limb ischemia (de Gennes et al., 1990). Thus, the profile of macrovascular thrombosis and thrombocy-topenia characteristic of HIT can be mimicked, especially as heparin is often used to anticoagulate patients with septic endocarditis (Delahaye et al., 1990). Micro-embolization leading to multiple small infarcts or microabscesses, in such organs as muscles, adrenal glands, and spleen, is an additional feature of endocarditis (Ting et al., 1990) that is not seen in HIT. When endocarditis-associated thrombocytope-nia is unusually severe, potential explanations include platelet-reactive autoantibo-dies (Arnold et al., 2004) or procoagulant monocyte-stimulating factors secreted by microorganisms from within large vegetations (Selleng et al., 2006).
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