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.

Effect of paraformaldehyde on platelet size and on measurement of surface IgG.

In many platelet assays, as in measurement of platelet-adherent IgG (PAIgG), platelets are fixed in paraformaldehyde (PFA). To better clarify the effect of PFA on platelet size and on PAIgG measurement we compared PAIgG levels in a series of 40 samples, with or without PFA fixing. We used an ELISA which was set up on unfixed platelets and gave excellent results in terms of linearity (r = 0.

The lack of correlation between the positivity of anti-platelet antibodies and the presence of thrombocytopenia in course of HIV infection.

The presence of anti-platelet autoantibodies has been reported in many cases of HIV infection, but there is no accordance about their pathogenic role in the onset of thrombocytopenia in the patients studied. In the present study surface anti-platelet antibodies (PAIgG) and serum anti-platelet antibodies (sPAIgG) were assayed in a group of 135 HIV-infected patients (109 men, 26 women), in different clinical stages by using an immunofluorescence test (PSIFT). In order to investigate the possible correlation of the positivity of these autoantibodies and the onset of thrombocytopenia, some of these patients were controlled in a follow-up study, with two successful controls: 10 months (II control: 89 patients) and 20 months (III control: 59 patients) after the first time.

Evidence of a cold immunoglobulin M autoantibody against 78-kD platelet glycoprotein in a case of EDTA-dependent pseudothrombocytopenia.

Pseudothrombocytopenia is a phenomenon in which the electronic count shows spuriously low platelet counts in subjects with normal platelet levels. The mechanism of anticoagulant-dependent pseudothrombocytopenia appears to involve cold reactive agglutinins against platelet antigens. The authors report a case of EDTA-dependent pseudothrombocytopenia with evidence of a cold immunoglobulin M antibody against 78-kD platelet membrane glycoprotein (GP).

[AIDS and the community. Preliminary data of an epidemiological study].

An epidemiological study into the prevalence and incidence of anti-H.I.V.