Session Title: Category 5g. VIRAL HEPATITIS: g. HEPATITIS C - CLINICAL (THERAPY)
Presentation Date: Apr 15, 2010
SHIFTS IN CHILD-PUGH SCORE IN PATIENTS COINFECTED WITH HIV-HCV UNDERGOING TREATMENT WITH PEGINTERFERON ALFA-2A (40KD) AND RIBAVIRIN ARE NOT PREDICTIVE OF HEPATIC DECOMPENSATION
M. Sulkowski1*, R.T. Chung2, J. Slim3, L. Bhatti4, R. Sterling5, T. Hassanein6, R. Serrão7, R. Solà8, A. Bertasso9, S. Stancic9, M. Rodriguez-Torres10, on behalf of the PARADIGM Study Investigators
1Johns Hopkins University School of Medicine, Baltimore, MD, 2Massachusetts General Hospital, Harvard Medical School, Boston, MA, 3St. Michael's Medical Center, Newark, NJ, 4Aids Healthcare Foundation, LA, CA, 5Virginia Commonwealth University, Richmond, VA, 6University of California San Diego, San Diego, CA, USA, 7Hospital São João, Porto, Portugal, 8Hospital del Mar, Barcelona, Spain, 9Roche, Nutley, NJ, 10Fundacion de Investigacion De Diego Santurce,Puerto Rico and Ponce School of Medicine, Santurce, PR, USA. *firstname.lastname@example.org
Background: The Child-Pugh (CP) score is a clinical tool that may be used to predict the risk of hepatic decompensation in patients with compensated cirrhosis. The score comprises two clinical parameters, ascites and encephalopathy, and three laboratory parameters, albumin, total bilirubin and INR. Increases in CP score may indicate worsening of liver disease. We examined data from HIV-HCV co‑infected patients enrolled in the randomised double-blind PARADIGM study to determine whether shifts in the CP score predict hepatic decompensation.
Methods: Eligible interferon treatment-naive adults with HIV-HCV (genotype 1) co‑infection, stable HIV disease (on stable anti-retroviral therapy [ART] or not requiring ART) and ≥100 CD4+ cells/mm3 were randomised (1:2) to receive ribavirin 800mg/day or 1000/1200mg/day for 48 weeks in combination with PegIFNα2a 180µg/week. Patients with cirrhosis were eligible (maximum 20%) provided they had compensated liver disease (CP< 6). CP scores were assessed at 1 to 6 week intervals during treatment and follow-up.
Results: At study entry 46 patients had cirrhosis, 45 of these had baseline CP scores. Shifts in CP score (Table) occurred in approximately half (22/45) of cirrhotic patients all secondary to decreases in serum albumin and/or increases in total bilirubin. There was one episode of hepatic decompensation on study day 299 (baseline CP=5; last CP score prior to decompensation was 5 on day 238) characterised by bleeding oesophageal varices (unrelated to study drug in the investigator's opinion), which developed 3 months after the patient discontinued treatment due to insufficient therapeutic response and resolved without sequelae.
Conclusions: During this study, shifts in CP score occurred in approximately 50% of co-infected patients with compensated cirrhosis but hepatic decompensation was a rare event. Shifts in CP score may be related to decreased albumin (≤35g/L) secondary to treatment-related anorexia, and weight loss and/or increased total bilirubin (≥34.2µmol/L) may reflect ribavirin-induced haemolysis and/or atazanavir-related (or other drug-related) indirect hyperbilirubinemia. These results suggest that a shift in CP score is not a reliable predictor of hepatic decompensation among co-infected cirrhotic patients treated with PegIFNα2a plus ribavirin.