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Pulmonary hypertension (PHT) is increasingly recognized as cause for significant morbidity and mortality in thalassemia patients. However, the prevalence in non-selected thalassemia patients, the clinical risk factors and mechanism of its development are not fully understood, resulting in sub-optimal screening and inadequate treatment. Hypercoagulability has been known to occur in thalassemia and thought to play a major role in the pathogenesis of PHT.

The specific aims of Dr. Singerís current research are:

  1. To determine the factors responsible for the development of PHT and identify associated coagulation and inflammatory markers.
  2. To determine if commonly applied treatment with an anti-coagulant (coumadin) or a platelet-inhibitor (aspirin), beneficially affect these physiological markers.

As no controlled studies have been done for treatment of this complication, this information is fundamental prior to initiation of randomized controlled clinical trials for PHT in thalassemia. Dr Singer has demonstrated that platelet activation and thrombin generation are associated with PHT and that they can result in endothelial and inflammatory changes; hence specific anti-platelet or anti-thrombin agents may be a new and specific intervention which could prevent or improve PHT in thalassemia patients, in future studies.

Successful completion of this research is expected to substantially increase our knowledge of the pathogenesis of PHT and on the potential utility of specific therapeutic agents, which could improve life expectancy and quality of life for these patients.


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