Human platelet antigen-3 genotype predicts platelet count in patients with HCV infection.

Background/aim: A low platelet count is one of the most sensitive tests for cirrhosis detection in patients with hepatitis C virus (HCV) infection. We evaluated whether the human platelet antigen (HPA) genotype could predict platelet count in HCV-positive patients.

Materials And Methods: We genotyped the HPA 1, 2, 3, 5 and 15 polymorphisms in consecutive patients with HCV infection.

Complement fraction 3 binding on erythrocytes as additional mechanism of disease in paroxysmal nocturnal hemoglobinuria patients treated by eculizumab.

In paroxysmal nocturnal hemoglobinuria (PNH) hemolytic anemia is due mainly to deficiency of the complement regulator CD59 on the surface of red blood cells (RBCs). Eculizumab, an antibody that targets complement fraction 5 (C5), has proven highly effective in abolishing complement-mediated intravascular hemolysis in PNH; however, the hematologic benefit varies considerably among patients. In the aim to understand the basis for this variable response, we have investigated by flow cytometry the binding of complement fraction 3 (C3) on RBCs from PNH patients before and during eculizumab treatment.

Fetoneonatal alloimmune thrombocytopenia (FNAIT): our experience.

Objective: Fetoneonatal alloimmune thrombocytopenia (FNAIT) is a relatively rare clinical syndrome characterized by marked thrombocytopenia shortly after birth. It occurs when fetal platelets are destroyed, after sensitization, by a transplacental passage of maternal antibodies directed against a fetal platelet alloantigen inherited from the father. This article reviews some pathophysiologic and clinical aspects of FNAIT.

Thrombin-activated platelets induce proliferation of human skin fibroblasts by stimulating autocrine production of insulin-like growth factor-1.

Platelet components have found successful clinical utilization to initiate or to accelerate tissue-repair mechanisms. However, the molecular pathways by which platelet factors contribute to tissue regeneration have not been fully elucidated. We have studied the effect of thrombin-activated platelets (TAPs) on cell growth in vivo and in cultured cell systems.