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Article Type

Original Study

Abstract

Objective The aim of this work was to explore the role prolactin (PRL) in hepatitis C (HCV)-related thrombocytopenia. Background PRL is involved in the activation of a number of immunological responses. It enhances the progression of the immune process in autoimmune diseases. Autoimmunity is a common finding in chronic hepatitis C, and a significant association between hyperprolactinemia (HPRL) and infection with HCV genotype 4 has been reported. Materials and methods This study was carried at the Internal Medicine Department, Menoufia University Hospital, in the period between May 2014 and December 2014. Three groups were involved: group I, which included 41 chronic hepatitis C patients with thrombocytopenia; group II, which included 35 chronic hepatitis C patients without thrombocytopenia; and group III, which included 25 healthy individuals with matched age and sex. Results Patients with HCV-related thrombocytopenia had HPRL and their serum PRL levels were significantly higher compared with HCV patients with normal platelet count and compared with normal controls (P = 0.02 and 0.001, respectively). We demonstrated negative correlation between HPRL and platelet count (r = 0.32 and P = 0.04). In addition, there was a significant difference in platelet count among different stages of liver fibrosis as the platelet count dropped steadily in line with the stage of fibrosis (P = 0.004). Conclusion This study shows that HPRL is present in a subset of patients with HCV-related thrombocytopenia and can be a contributing factor in the pathogenesis of thrombocytopenia in those patients. Thus, anti-PRL may be a treatment option in this category of patients.

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