Insulin resistance is not a relevant predictor of sustained virological response to pegylated interferon plus ribavirin in HIV/HCV co-infected patients☆

Received 23 September 2008; received in revised form 31 October 2008; accepted 31 October 2008. published online 29 December 2008.

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 600.000IU/mL [AOR 2.97; 95% CI 1.03–8.57; p=0.04] and baseline LDL cholesterol above 100mg/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.

Associate Editor: M.U. Mondelli

Keywords: HIV/HCV co-infection, HOMA, Insulin resistance, Pegylated interferon, SVR

1 Unidad de Enfermedades Infecciosas, Servicio de Medicina Interna, Hospital Universitario de Valme, Sevilla, Spain

2 Servicio de Medicina Interna-Enfermedades Infecciosas, Hospital Universitario de La Princesa, Madrid, Spain

3 Servicio de Medicina Interna, Hospital Juan Ramón Jiménez, Huelva, Spain

4 Unidad de Enfermedades Infecciosas, Hospital Universitario Virgen de la Victoria, Málaga, Spain

5 Servicio de Análisis Clínicos, Hospital Universitario de Valme, Sevilla, Spain

6 Unidad de Enfermedades Infecciosas, Hospital Universitario de Valme, Ctra. de Cadiz s/n, 41014 Sevilla, Spain

Corresponding author. Tel.: +34 955015787/+34 955015747; fax: +34 955015747.

☆ 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.

† Grupo Andaluz para el Estudio de las Hepatitis Víricas (HEPAVIR) de la Sociedad Andaluza de Enfermedades Infecciosas (SAEI).

PII: S0168-8278(08)00806-4

doi:10.1016/j.jhep.2008.10.032

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