Key result
Management of acute elevations of fibrinogen using ancrod, a thrombin-like enzyme, can safely deplete fibrinogen to achieve clinical benefit when carefully controlled.
Ancrod, a thrombin-like enzyme, is discussed as a potential therapeutic option to safely deplete fibrinogen and manage its acute elevations in the context of atherosclerosis and vascular occlusive disease.
Should not yet change practice for fibrinogen management; leaves open ancrod's role pending randomized trials.
Elevated plasma fibrinogen is an independent risk factor for generalized atherosclerosis. Markers of elevated fibrinogen include cigarette smoking, diabetes, hypertension and a sedentary life-style; all are associated with vascular occlusive disease. A variety of molecular mechanisms have been proposed by which fibrinogen could directly influence the vessel wall [1]. In addition, fibrinogen degradation products stimulate macrophages to produce a variety of factors including interleukin 6, an important mediator of inflammation. For this reason, atherosclerosis could be described as a low-grade, generalized inflammatory condition of the arterial wall. As illustrated in figure 1, the exact role of fibrinogen in these processes is complex and multifocal. This discussion will focus on the management of acute elevations of fibrinogen using ancrod, a thrombin-like enzyme, that triggers a cascade of normal reactions. When these are carefully controlled, fibrinogen can be safely depleted to achieve clinical benefit.
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C W Cole (1998) conducted a review in Acute elevation of plasma fibrinogen / Atherosclerosis. Ancrod was evaluated. Management of acute elevations of fibrinogen using ancrod, a thrombin-like enzyme, can safely deplete fibrinogen to achieve clinical benefit when carefully controlled.
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