Study of the pathophysiologic role of tissue factorpathway inhibitor in modulating thalassemia induced hypercoagulable state:relationship to oxidative stress

Document Type : Original Article

Authors

1 Physiology Department,Faculty of Medicine, University of Alexandria

2 Hematology Department, Medical Research Institute, University of Alexandria

3 Blood bank, Medical Research Institute, University of Alexandria

Abstract

In view of the improved care of thalassemic patients which resulted in doubling
of life expectancy, additional previously undescribed complications are now being
recognized.In particular, a chronic hypercoagulable state has been observed in these
patients, yet the actual mechanism of its production has not been fully elucidated. To
our knowledge, the tissue factor pathway and its inhibitor have not been studied in
thalassemics. The aim of the present work was to estimate tissue factor pathway
inhibitor (TFPI) relation to oxidative stress assessed by thiobarbituric acid reactive
substances (TBARS). Twenty patients with thalassemia major and ten healthy controls
were enrolled in the study. Complete blood picture, serum ferritin, screening tests for
coagulation, prothrombin and partial thromboplastin times(PT,PTT) and
prothrombin activity (P activity %) have been estimated. The mean TFPI was higher
in patients than controls but did not reach statistical significance, TBARS and serum
ferritin were significantly higher in patients than controls(p=0.000)reflecting the
presence of oxidative stress. No relation was found between TFPI and chelating agent
(desferrioxamine) intake, splenectomy or TBARS. In conclusion, tissue factor pathway
(TFP) as reflected by increased TFPI could be, at least in part incriminated in the
thalassemia-induced hypercoagulable state.

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