Peginterferon alfa-2b biosimilar(Nanogen Biopharmaceutical Co)

Summary.  Twenty to fifty per cent of patients with chronic hepatitis C (CHC) experience nonresponse to current antiviral therapy, which may relate in part to ribavirin or PEG‐interferon pharmacodynamics. We evaluated potential relevance of various factors for nonresponse. Two hundred forty‐two naive CHC patients who received in a previous trial at least 24 weeks of antiviral therapy, including PEG‐interferon alfa‐2b and ribavirin, were analysed. Of them, 53% were infected with hepatitis C virus (HCV) genotype 1–4, 71% exhibited high viral load and 32% had severe fibrosis/cirrhosis. After 24 weeks of treatment, 39 patients (16%) were nonresponders. In multivariate analysis, lower serum ribavirin concentrations, HCV genotype 1–4 and higher baseline γ‐GT predicted nonresponse. Week‐24 ribavirin concentrations (2.2 vs 2.8 mg/L, P < 0.001), average ribavirin doses (14.5 vs 15.2 mg/kg per day, P = 0.03) and week‐24 haemoglobin decreases (1.7 vs 2.0 mm, P = 0.02) were lower in nonresponders. Nonresponse rates increased progressively at decreasing ribavirin concentrations: 4%, 11%, 13% and 36% in case of serum ribavirin concentrations ≥4, 3–4, 2–3 and ≤2 mg/L, respectively (P = 0.001). Ribavirin concentrations correlated with both week‐24 haemoglobin decreases (r = 0.42, P < 0.001) and ribavirin doses (r = 0.17, P = 0.01). Subgroup analysis in HCV genotype 1–4 patients revealed essentially the same results. Nonresponse was exceptional in HCV genotype 2–3 patients and associated with ribavirin concentrations <2 mg/L. Presumed interferon‐related factors (average PEG‐interferon doses and decreases in leucocytes, granulocytes, platelets and body weight) did not differ between nonresponders and responders. In conclusion, ribavirin‐ rather than PEG‐interferon‐related factors are independent and potentially modifiable predictors of nonresponse in treatment‐naive CHC patients.

Chronic hepatitis C virus (HCV) infection exists in a large proportion of patients undergoing renal transplantation. Nowadays it is not considered to be an absolute contraindication to transplantation; however, it is associated with an increased risk for the patient and accounts for a shorter half-life of the renal allograft. We present three transplant recipients who displayed serious hepatic dysfunction after renal transplantation due to an HCV infection. In two of these cases, the liver biopsies established the diagnosis of FCH. In the third case, the liver biopsy was compatible with the early stages of FCH. All patients were started on peg-interferon alfa 2-b and ribavirin with subsequent normalization of hepatic function and early complete viral responses.