Potential conflict of interest: Nothing to report.
Elevated coffee consumption and reduced risk of insulin resistance in HIV-HCV coinfected patients (HEPAVIH ANRS CO-13)†
Article first published online: 31 OCT 2012
Copyright © 2012 American Association for the Study of Liver Diseases
Volume 56, Issue 5, page 2010, November 2012
How to Cite
Carrieri, M. P., Sogni, P., Cohen, J., Loko, M.-A., Winnock, M., Spire, B. and and the HEPAVIH Study Group (2012), Elevated coffee consumption and reduced risk of insulin resistance in HIV-HCV coinfected patients (HEPAVIH ANRS CO-13). Hepatology, 56: 2010. doi: 10.1002/hep.25813
- Issue published online: 31 OCT 2012
- Article first published online: 31 OCT 2012
- Accepted manuscript online: 26 APR 2012 05:42AM EST
- Manuscript Accepted: 22 APR 2012
To the Editor:
Molloy and colleagues1 report original results about the association between caffeine consumption and the low risk of insulin resistance (IR) and fibrosis progression in patients with nonalcoholic fatty liver disease (NAFLD). These results are consistent with previous reports on the association between elevated coffee consumption (ECC) and a lower risk of fibrosis progression2, 3 in other populations, including chronically infected hepatitis C virus (HCV) patients. In these HCV patients, an indirect protective effect of ECC on histological progression by the intermediary of a decrease in IR has never been investigated.
The possible relationship between ECC and IR could also be assessed in populations like human immunodeficiency virus (HIV)-HCV coinfected patients, where IR is common, multifactorial, and likely to predict negative liver disease outcomes.4 To test this hypothesis, we used enrollment data from the HEPAVIH ANRS CO-13 cohort of HIV-HCV infected patients. The study group consisted of 601 patients, 74% of whom were HIV-HCV coinfected through injected drug use. Median (interquartile range) age was 43 years (range, 40-46 years), 31% were female, 13% reported elevated alcohol consumption, and 26% of patients reported ECC (drinking ≥3 cups of coffee). Thirty-two percent of the patients presented advanced liver fibrosis (F3/F4), and those with homeostasis model assessment (HOMA)-IR ≤2.5 and ≥3 accounted for 59% and 69%, respectively.
In multiple logistic regression, ECC was significantly associated with HOMA-IR ≤3 (adjusted odds ratio [AOR] [95% confidence interval (CI)] = 1.62 [1.03-2.57], P = 0.04), after adjustment for body mass index, EAC, and liver fibrosis (F3/F4 vs. F0/F1/F2). When using a different cutoff for HOMA-IR (≤2.5), after multiple adjustment the association between ECC and HOMA-IR was confirmed, although it was less significant (P = 0.07).). ECC was also significantly associated with lower levels of fibrosis (F3/F4 vs. F0/F1/F2, AOR [95% CI] = 1.56 [1.04-2.34], P = 0.03), independently of EAC and HOMA-IR ≤3.
Despite some limitations, such as difficulty standardizing self-reported coffee intake and lack of data about other caffeine-containing products, our results are consistent with the hypothesis of a positive impact of ECC on IR and on liver fibrosis progression in HIV-HCV coinfected patients. Further research will help to better elucidate the causal mechanisms of this relationship and reveal whether polyphenols contained in coffee are also implicated. The use of coffee extracts to slow NAFLD and fibrosis progression is certain to soon become a clinical research concern.
- 1Association of coffee and caffeine consumption with fatty liver disease, nonalcoholic steatohepatitis, and degree of hepatic fibrosis. HEPATOLOGY 2012; 55: 429-436., , , , , .
- 2Coffee intake is associated with lower rates of liver disease progression in chronic hepatitis C. HEPATOLOGY 2009; 50: 1360-1369., , , , , , et al.
- 3Increased caffeine consumption is associated with reduced hepatic fibrosis. HEPATOLOGY 2010; 51: 201-209., , , , , , et al.
- 4Insulin resistance is associated with a higher risk of hepatocellular carcinoma in cirrhotic HIV/HCV-co-infected patients: results from ANRS CO13 HEPAVIH. J Hepatol 2012; 56: 862-868., , , , , , et al.
M. Patrizia Carrieri Ph.D.* , Philippe Sogni M.D.§ ¶, Julien Cohen M.D.* , Marc-Arthur Loko M.D.** , Maria Winnock Ph.D.** , Bruno Spire M.D., Ph.D.* , * INSERM, U912 (SESSTIM), Marseille, France, Université Aix Marseille, IRD, UMR-S912, Marseille, France, ORS PACA, Observatoire Régional de la Santé Provence Alpes Côte d'Azur, Marseille, France, § Institut Cochin, Université Paris-Descartes, INSERM U567-CNRS (UMR 8104), Paris, France, ¶ APHP, Hôpital Cochin, Service d'Hépatologie, Paris, ** University of Bordeaux, ISPED, Centre INSERM U897-Epidemiologie-Biostatistique, F-33000 Bordeaux, France, INSERM, ISPED, Centre INSERM U897-Epidemiologie-Biostatistique, F-33000 Bordeaux, France.