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Insulin Resistance Imperils Response to Interferon in People With HCV/HIV
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11th European AIDS Conference
October 24-27, 2007
Madrid
Mark Mascolini
People coinfected with HIV and hepatitis C virus (HCV) stood a much better chance of responding to interferon plus ribavirin if they did not have insulin resistance when they began therapy, according to results of a 29-person single-center study reported at the 11th European AIDS Conference [1]. Insulin resistance thwarted responses to interferon/ribavirin in people with HCV genotype 3, who usually respond well to anti-HCV therapy.
Insulin resistance independently dims the chance of sustained virologic response to interferon in people without HIV [2]. Two earlier studies linked HCV to a higher insulin resistance risk in people coinfected with or at risk for HIV, but these studies did not weigh the repercussions of insulin resistance on response to interferon/ribavirin [3,4].
To gauge the impact of insulin resistance on early virologic response (EVR) and rapid virologic response (RVR) in HCV/HIV-coinfected adults, University of Milan clinicians studied 29 coinfected patients starting pegylated interferon alfa-2a (180 mcg/week) plus ribavirin (1000 to 1200 mg daily depending on weight). They defined insulin resistance as a HOMA value above 3.8, RVR as an HCV RNA below 15 IU/mL after 1 month of therapy, and EVR as an HCV RNA below 15 IU/mL after 3 months.
Before interferon/ribavirin began, 10 people had insulin resistance and 19 did not. Rates of insulin resistance did not vary significantly by gender, age, body mass index, CD4 count, HIV load, use of antiretrovirals, or HIV load below 60 copies/mL. Seventeen people without insulin resistance (89.5%) and 9 with insulin resistance (90%) were taking antiretrovirals, and everyone on antiretroviral therapy had an undetectable HIV load. Median CD4 count for the study group stood at 430 (interquartile range 356 to 552).
The groups with and without insulin resistance compared closely in median triglycerides (139 mg/dL for the whole group), total cholesterol (176 mg/dL), aspartate aminotransferase (AST) (108 IU/L), alanine aminotransferase (ALT) (102 IU/L), and platelets (197 cells/mmc). Equivalent proportions with and without insulin resistance had HCV genotype 1 (50% and 42%), genotype 3 (30% and 42%), and genotype 4 (20% and 16%).
After 3 months of therapy, AST and ALT fell significantly more in people with insulin resistance (Table). But no one with insulin resistance had an RVR or an EVR, while half of the non-insulin-resistant group had an RVR and most had an EVR (Table).
None of 3 people with relatively easy-to-treat genotype 3 and insulin resistance had a rapid or early virologic response. Of the 3 people without insulin resistance who did not achieve an early virologic response, 1 had genotype 1a, 1 had genotype 3a, and 1 had genotype 4c/4d.
Caution is appropriate in interpreting these results because they involve a relatively small number of people from a single center, where HIV and HCV treatment practices are probably consistent but may vary from practices at other centers. The findings do indicate a need for further study of insulin resistance in HCV/HIV-coinfected people starting interferon/ribavirin.
References
1. Bongiovanni M, Ranieri R, Casana M, et al. Insulin resistance affects early virologic response in HIV-infected subjects treated for hepatitis C infection. 11th European AIDS Conference. October 24-27, 2007. Madrid. Abstract P13.2/09.
2. Conjeevaram HS, Kleiner DE, Everhart JE, et al. Race, insulin resistance and hepatic steatosis in chronic hepatitis C. Hepatology. 2007;45:80-87.
3. Howard AA, Lo Y, Floris-Moore M, et al. Hepatitis C virus infection is associated with insulin resistance among older adults with or at risk of HIV infection. AIDS. 2007;21:633-641.
4. Duong M, Petit JM, Piroth L, et al. Association between insulin resistance and hepatitis C virus chronic infection in HIV-hepatitis C virus-coinfected patients undergoing antiretroviral therapy. J Acquir Immune Defic Syndr. 2001;27:245-250.
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