Treatment of Chronic Hepatitis C in HIV-infected Patients With Compensated Liver Cirrhosis

L. Martín-Carbonero; P. Tuma, E. Vispo; J. Medrano, P. Labarga; J. González-Lahoz; P. Barreiro; V. Soriano


J Viral Hepat. 2011;18(8):542-548. 

In This Article

Patients and Methods

Study Population

A retrospective review of all HIV–HCV-coinfected patients who had received peginterferon plus weight-based ribavirin (1000 mg/day if ≤75 kg and 1200 mg/day if >75 kg) at our institution was carried out. Only individuals naïve for interferon in whom liver fibrosis had been assessed using elastometry within the year before being treated were chosen. Response rates and toxicities were compared in cirrhotics (>14.5 KPa) and noncirrhotics. Patients with cirrhosis were excluded if they had had any previous liver decompensation as ascites, variceal bleeding, hepatic encephalopathy and hepatorenal syndrome.

For each patient, a case report form specially designed for this study was filled. It recorded the main demographic characteristics, clinical, biochemical and virological data at different time-points, including baseline (before treatment was started) and at months 1, 3, 6, 12 and 18 of treatment.

The planned duration of HCV treatment was 24, 48, 60 or 72 weeks, depending on HCV genotype, viral response at week 4 and participation in different trials conducted at our centre during the last years.[18–20] Following international guidelines,[2] early stopping rules had been applied according to virological response at weeks 12 and 24. Therefore, patients experiencing a decline in serum HCV-RNA <2 log10 IU/mL at week 12 or displaying still detectable HCV-RNA (>10 IU/mL) at week 24 discontinued treatment and were considered as virological failures. Sustained virological response (SVR) was considered when serum HCV-RNA was undetectable 6 months after treatment discontinuation.

Serum HCV-RNA was measured using a commercial real-time PCR assay (Cobas Taqman, Roche, Pleasanton, CA, USA), which has a lower limit of detection of 10 IU/mL. HCV genotypes were determined using a commercial reverse hybridization assay (InnoLiPA HCV II; Innogenetics, Ghent, Belgium).

Liver Fibrosis Assessment

Estimation of hepatic fibrosis was examined measuring liver stiffness using transient elastography by Fibroscan (EchoSens, Paris, France). Details of this examination procedure have been described elsewhere.[21] Briefly, an ultrasound wave is produced and spread through the liver. There is a good correlation between the speed of the wave propagation and the degree of liver fibrosis, making possible to estimate liver fibrosis staging. At least ten successful measurements were performed on the right lobe of each patient's liver. The median value of all tests was deemed as representative and expressed in kilopascal (kPa) units. As reported elsewhere,[22] Metavir estimates were as follows: F0–F1 if <7.2 KPa; F2 if 7.2–9.4 KPa; F3 if 9.5–14.5 KPa; and cirrhosis (F4) if >14.5 KPa.

Statistical Analyses

Baseline characteristics, response rates and toxicities were compared in cirrhotics and noncirrhotic patients. Descriptive statistics were expressed as median and interquartile ranges and percentages for continuous and categorical variables, respectively. Baseline characteristics between the two groups were compared using the chi-square test or nonparametric tests, as needed. Univariate and multivariate logistic regression analysis was performed to calculate the odds ratio (OR) and 95% confidence intervals (95% CI) of different parameters associated with the achievement of SVR. All analyses were performed using the SPSS software package (version 15.0; Chicago, IL, USA).


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