Plasma Thrombopoietin Level in Thrombocytopenic Patients with or without Liver Cirrhosis Chronically Infected by the Hepatitis C Virus
Aiman Al-Qtaitat *
Department of Anatomy and Histology, Faculty of Medicine, Mutah University, Karak, Jordan
Said Al-Dalaen
Department of Pharmacology, Faculty of Medicine, Mutah University, Karak, Jordan
Samir Mahgoub
Department of Biochemistry and Molecular Biology, Faculty of Medicine, Mutah University, Karak, Jordan
Nedal Alnawaiseh
Department of Public Health, Faculty of Medicine, Mutah University, Karak, Jordan
Jehad Al-Shuneiqat
Department of Biochemistry and Molecular Biology, Faculty of Medicine, Mutah University, Karak, Jordan
Sameeh Al-Sarayreh
Department of Biochemistry and Molecular Biology, Faculty of Medicine, Mutah University, Karak, Jordan.
Yousef Al –Saraireh
Department of Pharmacology, Faculty of Medicine, Mutah University, Karak, Jordan
*Author to whom correspondence should be addressed.
Abstract
Background and Aim: Thrombocytopenia is a frequent problem in patients with post- hepatitis C (HCV) liver cirrhosis and also occurs in chronic HCV-infected patients without liver cirrhosis. The aim of this study was to evaluate the role of plasma thrombopoietin (TPO) in the occurrence of thrombocytopenia in both conditions.
Method: Platelet count and plasma thrombopoietin level and liver function tests were measured in four groups of patients: twenty chronic patients with post-hepatitis C liver cirrhosis and thrombocytopenia (group I), ten chronic HCV-positive patients with liver cirrhosis without thrombocytopenia (group II), ten chronic HCV-positive patients without liver cirrhosis with thrombocytopenia (group III) and chronic ten HCV-positive patients without liver cirrhosis and without thrombocytopenia (group IV). Ten normal healthy individuals were included as a control group.
Results: Plasma levels of albumin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), TPO and platelet counts in the four groups of patients were significantly different from their corresponding levels in the control group (P <0.001). There was a significant positive correlation between plasma TPO levels and platelet counts in group III patients (ρ (Spearman's [rho]) = 0.661, P= 0 .038). There was no significant correlation between TPO levels and platelet counts in the other three groups of patients. The logistic regression analysis in the three designated models, using dependent variables (chronic HCV infection, liver cirrhosis and thrombocytopenia) and an independent variable (TPO plasma level) revealed that liver cirrhotic patient and the thrombocytopenic patient have equally the best prediction model for the low plasma TPO.
Conclusion: Decreased thrombopoietin production has a role in the pathogenesis of thrombocytopenia in liver cirrhosis.
Keywords: Thrombopoietin, thrombocytopenia, liver cirrhosis, hepatitis C infection