Patients with chronic hepatitis C are at risk of developing type 2 diabetes mellitus (DM) and impaired fasting glucose (IFG), and this risk may increase among hepatitis C virus (HCV) patients not responding to an antiviral therapy.
To compare the incidence of glucose abnormalities (IFG or DM) after an antiviral therapy between HCV+ patients with a long-term virological response (LTR) and nonresponders (NR; persistently positive HCV-RNA).
All 202 HCV+ patients without the baseline glucose abnormalities enrolled by our center in investigational trials or routinely treated with interferon (IFN)/peginterferon (Peg-IFN) (+/– ribavirin) from 1988 to 2001, with the available baseline sera stored at −80°C, were considered. The baseline data included age, sex, body mass index (BMI), viral load, genotype, liver histologic staging and steatosis, glucose, and cholesterol. The homeostatic assessment of insulin resistance (HOMA-IR) was calculated in the baseline serum. The incidence of IFG or DM at the end of follow-up was compared between patients with LTR and NR.
After a median follow-up of 8.0 yr (range 5–16), the cumulative risk of DM (N = 7) or IFG (N = 33) among the 202 HCV+ included patients was 16.9% (95% confidence interval [CI] 11.3–22.5). The 8-yr risk was not significantly lower between LTRs (14.5%) compared to NRs (18.8%) (hazard ratio [HR] 0.60, CI 0.30–1.20, P= 0.16). The HR adjusted for the baseline risk factors for DM and the predictors of a poor response (age, sex, HOMA-IR, BMI, family history of diabetes, HCV genotype 1, high viral load, cirrhosis, and steatosis) was 0.88 (CI 0.38–2.02, P= 0.76). Among other factors, those more associated to IFG-DM were an increasing age (P= 0.017), a higher BMI (P= 0.054), and a family history of DM (P= 0.065).
After adjustment for several baseline risk factors, the incidence of glucose abnormalities was not significantly different between LTRs and NRs. Our data suggest that HCV clearance does not significantly reduce the risk of glucose intolerance.
Departments of 1Gastroenterology; 2Internal Medicine, Molinette Hospital, Turin, Italy; 3Unità di Epidemiologia dei Tumori, CPO Piemonte, Turin, Italy
Reprint requests and correspondence: Giorgio Saracco, M.D., Department of Gastroenterology, Molinette Hospital, Corso Bramante 88, 10126 Turin, Italy.
CONFLICT OF INTEREST
Guarantor of the article: Giorgio Saracco, M.D.
Specific author contributions: Chiara Giordanino was responsible for patients' recall and completion of the patients' database; Elisabetta Bugianesi contributed to the design of the study; Antonina Smedile, Alessia Ciancio, Rinaldo Pellicano, and Simona Bo contributed to patients' recruitment; Maria Lorena Abate and Antonella Olivero were involved in the long-term storage of patients' sera and performed the virological assays; Maurizio Cassader and Roberto Gambino performed the insulin and cholesterol dosage; Giovanni Ciccone performed the statistical analysis; Mario Rizzetto revised the manuscript; and Giorgio Saracco created the study design, analyzed the results, and wrote the article.
Financial support: The study received a grant of 4,000 Euros by the School of Medicine, University of Turin, Italy.
Potential competing interests: None.
Received January 5, 2008; accepted April 14, 2008.