December 6, 2013

Prediction of Hepatic Fibrosis in Patients Coinfected With HIV and Hepatitis C Virus Based on Genetic Markers

J Acquir Immune Defic Syndr. 2013 Dec 15;64(5):434-42. doi: 10.1097/QAI.0b013e3182a06eb6.

Fernández-Rodríguez A, Berenguer J, Jiménez-Sousa MA, Guzmán-Fulgencio M, Micheloud D, Miralles P, López JC, Bellón JM, Aldamiz-Echevarria T,García-Broncano P, Carrero A, Alvarez E, Resino S.

*Viral Infection and Immunity Unit, National Centre of Microbiology, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain; †Infectious Diseases and HIV Unit, Hospital General Universitario Gregorio Marañón, Madrid, Spain; ‡Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Madrid, Spain; and Departments of §Internal Medicine; ‖Pathology, Hospital General Universitario, Gregorio Marañón, Madrid, Spain.

Abstract

OBJECTIVE: To assess the ability of the cirrhosis risk score (CRS) to predict liver fibrosis progression in HIV/hepatitis C virus (HCV)-coinfected patients.

DESIGN: Retrospective follow-up study.

METHODS: Based on a minimum follow-up time of 10 years with HCV infection, 190 HIV/HCV-coinfected patients were classified according to their METAVIR score: (1) 25 nonprogressor patients who did not develop fibrosis (F0) and (2) 165 progressor patients who developed fibrosis (F ≥ 1). Seven polymorphisms of CRS signature and IL28B genotype were performed using the GoldenGate assay. The CRS signature was calculated by naive Bayes formula as previously described.

RESULTS: Nonprogressors had CRS values significantly lower than progressors (0.61 versus 0.67; P = 0.043). Among the progressors, we observed similar CRS values through all the fibrosis stages (F1/F2/F3/F4). The percentage of patients with CRS > 0.70 (high risk of developing fibrosis) was higher in progressors than in nonprogressors; but the percentages with values between 0.50 and 0.70 (intermediate risk) and <0.50 (low risk) were quite similar for each of the fibrosis stages (P = 0.047). The area under the receiver-operating characteristic curve of CRS for discriminating nonprogressor versus progressor was 0.625 (P = 0.043). When clinical variables were considered (age at HCV infection, intravenous drug use, gender, IL28B, and HCV genotype), the area under the receiver-operating characteristic curve of CRS improved up to 0.739 (P < 0.001).

CONCLUSIONS: CRS itself seems not to be a good marker for identifying HIV/HCV-coinfected patients who are at high risk of developing liver fibrosis. However, CRS score coupled with clinical factors might help to distinguish between nonprogressors and progressors patients.

PMID: 23797694 [PubMed - in process]

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