Original paper
The role of NK cells in pathogenesis of thrombocytopenia in hepatitis C infection

Aim: The aim of this study was to discuss the pathomechanism of thrombocytopenia in HCV infection. Material and methods: Twenty-four HCV positive patients with thrombocytopenia (HCV-TP) and twelve HCV positive patients with normal count of platelets (HCV-NP) as a control group were enrolled in this study. Subpopulations of lymphocytes and serum platelet-associated immunoglobulin (PAIg) levels were determined and correlation analyses were performed. Results: The percentages of T lymphocytes (mainly CD8+) were higher in the HCV-NP group than in the HCV-TP group (p<0.04). There were no differences in lymphocyte B (CD19+) levels between patients with HCV-TP and HCV-NP. Elevated titres of PAIg were detected in 14/24 (58.3%) of HCV-TP cases, whereas PAIg were negative in the HCV-NP patients. There was not a relationship between severity of thrombocytopenia and serum PAIg. A significant decrease in NK cells (79.1%) was observed in the HCV-TP group compared with the HCV-NP group (58.3%). Moreover, NK cells were not detected in 11 patients from the HCV-MP group (45.8%) and in 1 patient from the HCV-NP group (8.3%) (p<0.004, p<0.04). Correlation analyses demonstrated a significant negative correlation between NK cells count and PAIgG levels (p<0.005). We conclude that thrombocytopenia in our HCV-positive patients appears to be autoimmune mediated. Conclusions: The above findings show a direct correlation between deficient NK cells and PAIg level and suggest an important role of NK population as a mechanism contributing to thrombocytopenia in HCV-infected patients.