The common I148 M variant of PNPLA3 does not predict fibrosis progression after liver transplantation for hepatitis C

✍ Scribed by Nicole T. do O; Dennis Eurich; Christian Trautwein; Peter Neuhaus; Ulf P. Neumann; Hermann E. Wasmuth

• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: English
• Weight: 221 KB
• Volume: 54
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.24535

✦ Synopsis

We read with great interest the article by Martinot-Peignoux et al. 1 In this report from France, undetectable serum hepatitis C virus (HCV) RNA at 12 weeks (Wþ12) (409 patients) post-treatment follow-up was as relevant as undetectable serum HCV RNA at 24 weeks (Wþ24) (sustained virological response [SVR]; 408 patients) after the end of treatment.

Current standard therapy is based on a combination of pegylated interferon (PEG-IFN) and ribavirin, but it leads to only $50% SVR in patients with HCV genotype 1 and high viral loads. 2 IFN reduced the risk for HCC, especially among patients with SVR. 3,4 Then, we need to accurately judge whether the patient is SVR or non-SVR, applying the present standard for the judgment of SVR with the undetectability of serum HCV RNA at post-treatment Wþ24.

We investigated 102 patients with chronic hepatitis C genotype 1 treated with PEG-IFN-alfa 2a plus ribavirin for 48 weeks. Some of these patients had already been included in previous reports. 5,6 Serum HCV RNA was measured using the COBAS TaqMan HCV test with a detection limit of 1.2 logIU/mL. At the Wþ24 posttreatment follow-up, 40 (39.2%) patients had SVR, and 31 (48.4%) and 9 (23.6%) were treatment naı ¨ve and previously treated patients, respectively. At Wþ12, serum HCV RNA was undetectable in 42 patients, and 40 patients were SVR (PPV, 95.2%). We found two relapsers at Wþ24 (undetectable at Wþ12).

In the case of using direct-acting antivirals, earlier knowledge of treatment outcome would be useful for retreatment for the same patient. Taken together, our findings show that Wþ12 undetectable serum HCV RNA is not suitable for predicting persistent virological response. Further understanding of the mechanism of relapse could be useful in reducing the posttreatment follow-up period from the current standard of 24 weeks.