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Abstract
A hypercoagulable state has been previously described in sickle cell (SC) patients, possibly related to a decrease of the physiological coagulation inhibitors.A range of laboratory tests have provided solid evidence for the existence of a chronic hypercoagulable state in SCD .
The presence of a persistent hypercoagulable state combined with the infrequent occurrence of significant thrombotic events suggest that thrombosis is largely a subclinical process in SCD and has been associated with autopsy findings of platelet and fibrin thrombi in the microvasculature in the lungs and the brain.
Several etiologic factors may play a role in the pathogenesis of the hypercoagulable state in SCD . The specific changes in the lipid membrane composition of the abnormal RBCs and the hemosiderosis may contribute to the activation of the coagulation process and the activation of other blood cells, including the platelets, monocytes, and granulocytes, alone or together, and may induce activation of the vascular endothelium, which further contributes to the thrombotic process.
Venous thrombosis is more prevalent in SCD patients who are not receiving regular transfusions and those who have undergone splenectomy. These patients may be more susceptible to thromboembolism because they have more circulating damaged RBCs and increased platelet counts.
The present study was intended to evaluate the effect of urinary 11-dehydrothromboxane B2 as a marker of hypercoagulable state in sickle cell disease. This study was carried out at Hematology out patient clinic and clinical pathology department during the period from October 2009 to april 2010.