Background/Aims
To evaluate the possible influence of baseline insulin resistance in sustained virological
response.
Methods
One hundred and fifty-five consecutive individuals from a multicentric cohort of HIV/HCV
co-infected patients who underwent therapy with pegylated interferon plus ribavirin
were included. The main outcome variable was sustained virological response, defined
as undetectable plasma HCV RNA at week 24 after the end of the therapy. Insulin resistance
was determined using the HOMA method.
Results
Sustained virological response was achieved in 55 (36%) patients. Forty-two (38%)
patients with a HOMA lower than 4 developed sustained virological response vs 13 (29%)
of those with a HOMA above 4 (p = 0.27). Analyses restricted to patients harbouring genotype 1 or 4 showed similar rates
of sustained virological response among patients with a HOMA below and above 4 [19
(27%) vs 7 (24%); p = 0.8]. In the multivariate analysis, genotype 3 [AOR 9.26; 95% CI 3.03–28.30; p < 0.0001], a baseline HCV viral load below 600.000 IU/mL [AOR 2.97; 95% CI 1.03–8.57; p = 0.04] and baseline LDL cholesterol above 100 mg/dL [AOR 6.62; 95% CI 1.97–22.19; p = 0.002] were independently associated with sustained virological response.
Conclusions
Insulin resistance is not a relevant predictor of sustained virological response to
pegylated interferon plus ribavirin in HIV/HCV co-infected patients.
Abbreviations:
HAART (highly active antiretroviral therapy), HCV (hepatitis C virus), SVR (sustained virological response), IR (insulin resistance), CHC (chronic hepatitis C), ETR (end of treatment response), HOMA (homeostasis model assessment), BMI (body mass index), ALT (alanine-aminotransferase), LDL (low-density lipoprotein), HDL (high-density lipoprotein), AOR (adjusted odds ratio), CI (confidence interval), EVR (early virological response), RVR (rapid virological response)Keywords
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Article info
Publication history
Published online: December 29, 2008
Accepted:
October 31,
2008
Received in revised form:
October 31,
2008
Received:
September 23,
2008
Associate Editor: M.U. MondelliFootnotes
☆The authors who have taken part in the research of this paper declared that they do not have a relationship with the manufacturers of the drugs involved either in the past or present and they did not receive funding from the manufacturers to carry out their research.
Identification
Copyright
© 2008 European Association for the Study of the Liver. Published by Elsevier Inc. All rights reserved.
