الفهرس 
Hepatitis C Virus Associated ThrombocytopeniaOnly 14 pages are availabe for public view
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Abstract
Thrombocytopenia in chronic HCV infection is a major problem, particularly in patients with advanced liver disease. The risk of serious bleeding with severe thrombocytopenia can prevent invasive procedures including biopsies for staging. Thrombocytopenia can also complicate bleeding manifestations such as variceal bleeding. It may impede the initiation and continuation of antiviral therapy, potentially decreasing the probability of successful HCV treatment. Recent studies have evaluated the underlying mechanism of thrombocytopenia in chronic HCV infection and assessed the usefulness of several therapeutic options.
A variety of pathogenic mechanisms are reported to be implicated in thrombocytopenia related to chronic HCV infection: (1) Auto-immunity (2) sequestration of platelets in the enlarged spleen secondary to portal hypertension (hyper-splenism) , (3) inadequate production of thrombopoietin in advanced stage liver disease , (4) Anti-viral for HCV.
Several authors have suggested that persistent infections with HCV are associated with ITP, and several studies have demonstrated improvement of platelet counts with suppression or eradication of infection, suggesting a role of persistent antigen exposure to the pathogenesis of ITP.
CD59 encodes a 77-amino acid glycosylphosphatid-ylinositol (GPI)-anchored cell surface glycol protein, synthesized as a 128-amino acid protein that includes a signal sequence and the sequence for a GPI anchor replacement. The CD59 protein, formerly known as a membrane inhibitor of reactive lysis (MIRL), inhibits the final and most important step of membrane attack complex (MAC) formation. Erythrocytes that are deficient in GPI-anchored membrane proteins, including CD59, undergo complement-mediated hemolysis.
There are many studies had been done specially on autoimmune diseases and found that abnormalities in the expression of CD55 and CD59 surface molecules on peripheral blood cells and they are not specific to paroxysmal nocturnal hemoglobinuria.
The aim of this study is to assess the expression of CD59 on the platelet surface in patients with HCV associated thrombocytopenia specially if the cause of thrombocytopenia is autoimmune.
This cross section study included two groups, a group of 30 adult patients with Hepatitis C Virus (HCV) associated thrombocytopenia, compared with another control group of 20 healthy individuals don’t have niether (HCV) nor thrombocytopenia.
The inclusion criteria of the patient group :
1.Adut patients.
2.Seropositive for anti-HCV antibody and had detectable HCV-RNA by Polymerase Chain Reaction (PCR) for HCV.
3.Compensated liver disease (child A) .
4. With no splenomegaly .
5.Naïve for anti- viral treatment.
6. Not known to have any other concomitant disease that may induce thrombocytopenia such as collagen disease.
All patients subjected to:
1.Detailed medical history and physical examination .
2.CBC , Liver function test( ALT, AST, Bil , PT, PTT, ALB) and ESR.
3.Pelvi-abdominal ultra sound.
4.Flowcytometric determination of the expression of human CD59 using CD61 for platelet gating on peripheral blood samples.
Our study showed that there is significant difference between the patient group (30 patient) which have thrombocytopenia associated with HCV and the healthy control group (20 healthy individual) according to CD59 on the platelet surface.
As regard the correlation between CD59 and the platelet count, there is a significant positive correlation between CD59 and platelet count.