While sickle cell disease and other chronic hereditary and acquired hemolytic anemias are considered hypercoagulable states, a unifying mechanism explaining the hemostatic activation has been elusive.[1][1] Patients with sickle cell disease exhibit increased thrombin and fibrin generation,[2][2], [3
No takes yet. Share an insight, caveat, or question.
Gladwin et al. (2007) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: