Aspects of Viral Involvement in Chronic Immune Thrombocytopenic Purpura

The immune chronic thrombocytopenic purpura is an illness characterized by peripheral thrombocytopenia occurred through a mechanism of early hyper destruction of blood platelets or by deficient platelet synthesis in the medulla. The chronic immune purpura can be primary, autoimmune in nature, thrombocytopenic idiopathic or secondary in the context of other associated pathologies. The idiopathic thrombocytopenic purpura (P.T.I.) is an immune-mediated acquired disorder. It is characterized by isolated thrombocytopenia, defined as platelet count assessment from peripheral blood smear of less than 100.000/mm3, in the absence of a different cause of thrombocytopenia. The secondary immune isolated thrombocytopenia occurs in the context of some associated pathologies. The aim of the study is to highlight the involvement of some infectious agents in the etiopathogenesis of the secondary immune thrombocytopenic purpura. The immune thrombocytopenia can be subordinated to some chronic infections such as infection with virus B or C, infection with virus HIV, infection with Cytomegalovirus (CMV) or the Helicobacter Phylori infection. The study was conducted on a group of 40 patients, distributed into two groups: the first group of patients is the asymptomatic patients who do their common tests while the other group of patients is with bleeding symptoms: Petequiae, bruising, epistaxis, gum bleedings. The studied group puts into evidence a thrombocytopenia with a mean platelet count of 60.20 ± 19.75 × 103/μL. 80% of patients had positive anti-platelet antibodies. Out of these, 20% carry infections with virus B and C while 30% carry Cytometalovirus infection (CMV). The study found one case of HIV infection. Thus we highlight the involvement of infectious agents in the etipathogenesis of secondary immune thrombocytopenic purpura as well as the way they affect the platelet function.