Abstract
Increased plasma levels of prothrombin fragment 1 + 2 (F1 + 2) found in patients with sickle-cell disease reflect enhanced endogenous thrombin generation. We postulate that hypercoagulability contributes to vaso-occlusion. The intensity of acenocoumarol treatment required to reduce the F1 + 2 level to 50% of pretreatment level was investigated in seven patients with symptomatic sickle-cell anaemia during steady-state disease for a period of 2 months. All patients had increased levels of F1 + 2 compared with an age-matched control group. Normalization of the F1 + 2 was achieved at a median INR of 1.64 (range 1.18-2.2). It is concluded that low-intensity oral anticoagulation normalizes the hypercoagulability in sickle-cell disease.
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