Background: Our study aimed to elucidate the possible relationship between apoptosis, inflammation, and fibrosis in hepatitis C virus (HCV) patients. Methods: Patients aged 18 to 60 years with HCV were included and underwent clinical and pathological examinations. Patients with chronic renal failure, malignancies, alcohol abuse, or pregnancy and/or those who were taking immunosuppressant agents were excluded. Body mass index, glucose, insulin, HOMA-IR, lipid profile, and the extent of fibrosis (METAVIR) were determined, as were the serum levels of CK-18 (M30-Apoptosense, ELISA -Lausen, Switzerland), Fas, Fas-L, I-CAM, V-CAM, MIF, and PAI (HSEP-63k, Milliplex, Millipore, Copenhagen, Denmark). Results: Of the 55 patients, 23 were treatment-naïve, 15 demonstrated a sustained virologic response (SVR) and 17 were non-responders (NR). The levels of CK-18 did not differ between the groups. Inflammation, as assessed by sVCAM, was directly associated with advanced fibrosis (p = 0.009). sFas-L and sVCAM were increased in the SVR group compared with the treatment-naïve group (p = 0.006 and 0.019, respectively). sVCAM was associated with both sFas-L (r s = 0.778, p < 0.001) and MIF (r s = 0.621, p < 0.001). MIF and sFas-L were also correlated (r s = 0.526, p = 0.001). Conclusions: Advanced fibrosis was positively correlated with inflammation according to the levels of sVCAM. Furthermore, apoptosis, as assessed by the levels of sFas-L, and inflammation, as determined by sVCAM, were increased in the patients who achieved viral clearance compared with the treatment-naïve patients. The patients with advanced fibrosis were also more likely to present with higher levels of MIF.
