ABSTRACT
Aim: Hepatitis C virus [HCV] has been recognized as the cause of thrombocytopenia occurring in patients with chronic hepatitis C, possibly through autoimmune mechanisms. Prolactin [PRL] is a potent immunomodulator that may play a role in the pathogenesis of autoimmune diseases, including systemic lupus erythematosus [SLE]. The objective of this study was to estimate serum PRL level in patients with HCV-associated thrombocytopenia and those with chronic idiopathic thrombocytopenic purpura [ITP], in an attempt to find any possible role of this hormone in these autoimmune disorders. Subjects and The study was carried out on 70 patients divided into 3 groups: group I, included 30 patients with chronic HCV infection and thrombocytopenia [mean age: 47.25 +/- 8.6 years]; group II included 20 patients with chronic HCV and normal platelet counts [mean age: 42.2 +/- 8.5 years]; and group III, comprised 20 patients with chronic ITP [off-steroid therapy] who were HCV-negative. Their mean age was 42 +/- 12.5 years. Basal level of PRL was determined by chemiluminescence, and autoantibody profile [antinuclear antibodies [ANA], anti-double stranded DNA [anti-ds DNA], anti-smooth muscle antibodies [ASMA], anti-mitochondrial antibodies [AMA], and cryoglobulins] was performed in all patients. In group I, the mean platelet count was significantly lower compared to group II [P=0.00], but was significantly higher than group III [P=0.0002]. The mean serum PRL was higher in group I compared to group II and group III, however, the difference showed marginal statistical significance [P=0.058, P=0.057, respectively]. The autoantibody profile did not differ significantly between the three studied groups. The mean serum PRL was significantly higher in females than males in all studied groups [P<0.05]. Correlation studies in group I showed that the platelet count correlated negatively with the female sex. However, we found no significant correlation between serum PRL level and platelet count and no association between PRL level and the different autoantibodies studied. Conclusions: Our preliminary results suggest that the role of hyperprolactinemia in the triggering or promoting the autoimmune process responsible for HCV-associated thrombocytopenia is quite questionable. Prolactin seems to be poorly involved in the etiopathogenesis of both HDV-associated thrombocytopenia and chronic ITP. However, additional studies are warranted to elucidate the possible role of bromocriptine in the management of hyperprolactinemic thrombocytopenia in patients with chronic HCV infection