Liver, Pancreas and Biliary Tract HCV infection in haemodialysed patients: A role for serum IL-10 and TGF-1 in liver damage?

Background. Hepatitis C virus (HCV) infection is often clinically silent in haemodialysed (HD) patients and their immune response may modulate liver damage in HCV infection. IL-10 and TGF-1 could play a role in this setting as, IL-10 down-regulates hepatic fibrosis, while TGF-1 is a pro-fibrotic cytokine. Aim. To evaluate the role of IL-10 and TGF-1 in HD/HCV+ patients. Patients. 71 HD/HCV+ patients (58 with normal [HD/HCV-N] and 13 with high serum transaminases [HD/HCV-H]), 40 non-uremic patients with chronic hepatitis C (HCV+), 56 HD anti-HCV− patients and 20 healthy volunteers (H). Methods. IL-10 and TGF-1 serum levels were assessed using ELISA tests. Liver histology was assessed by Ishak’s score. Results. IL-10 serum levels were significantly higher in HD patients, both HCV+ (3.7 ± 0.4 pg/ml; p < 0.01) and HCV− (3.8 ± 0.8 pg/ml; p < 0.05) than in non-uremic HCV patients (2.3 ± 0.4 pg/ml). Among the HD/HCV+ patients, IL-10 serum levels were similar in HD/HCV-N and in HD/HCV-H patients. Among the HD/HCV+ patients, IL-10 serum levels were similar in those with moderate histological damage compared to those with mild damage. TGF-1 serum levels were significantly lower in HD patients, both HCV+ (4.6 ± 0.9 ng/ml) and HCV− (6.0 ± 0.9 ng/ml) than in non-uremic HCV+ patients (8.1 ± 1.1 ng/ml; p < 0.001 and p < 0.01, respectively), but similar to the values found in H (5.3 ± 0.9 ng/ml; p = n.s.). No correlation was seen between IL-10 and TGF-1 serum levels in any of the groups considered. Conclusions. Patients on haemodialysis treatment to have high levels of IL-10, which remain high even when patients are anti-HCV+, whereas the opposite is true of TGF-1. The cytokine pattern observed in HD patients is compatible with the hypothesis explaining the relatively benign evolution of HCV-related liver disease in HD patients, and has a pathophysiological role. © 2008 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.