The G1691A Mutation of the Factor V Gene (Factor V Leiden) and the G20210A Mutation of the Prothrombin Gene

contrast to the well-established role in the context of venous thrombotic events, the impact of both muta-tions for the onset of thrombotic events in the arterial vasculature is still controversially discussed. In support, some authors reported on an increased rate of arterial thrombotic complications in defined subgroups of patients, for example, an increased prevalence of stroke2,3 and myocardial infarction.4,5 The potential pathogenetic relevance of the FVL and prothrombin mutations for the manifestation of thrombotic microangiopathies has not yet been investigated in detail. Thrombotic microangiopathies represent a distinct group within the spectrum of thrombotic disorders, clinically characterized by schis-tocytic hemolytic anemia, low platelet count, and signs of organ dysfunction. Depending on the pattern of organ involvement, hemolytic-uremic syndrome (HUS) with predominant renal dysfunction, throm-botic-thrombocytopenic purpura (TTP) with pre-dominant neurological deficiency, and intermediat