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  4th Intl Lipodystrophy Workshop
San Diego at Coronado Beach, Sept 22-25, 2002
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HIV/Hepatitis & Insulin/Diabetes
Reported by Jules Levin
  HBV and HCV Associated with Increased Insulin resistance and Diabetes in Patients with Body Changes: careful screening & management of insulin & diabetes recommended for HIV+ with viral hepatitis
This small study found that HCV and HBV+ patients were more likely to have glucose abnormalities than HIV+ patients without hepatitis. At last year's Retrovirus Conference a study reported finding that HCV/HIV coinfected patients were more likely to have body changes, elevated lipids, and glucose abnormalities than HIV+ patients without hepatitis.
Hadigan (abstract 34) and Boston researchers including Steve Grinspoon and Ray Chung, evaluated 91 HIV+ men and women with fat redistribution and elevated cholesterol & triglycerides, without a previous diagnosis of diabetes or symptoms for active hepatitis. Each patient completed a 2-hour oral glucose challenge test. Liver function tests, Hepatitis B Surface Antigen (HbsAg), antibody-HCV and HCV RNA by PCR were also dtermined. HOMA-IR was calcolated from fasting glucose and insulin levels as a measure of insulin resistance. 5 patients had HBV and 9 were HCV PCR+.
BASELINE CHARACTERISTICS: The ALT levels were not significantly different between the 3 groups: HIV+, HIV/HBV+. HIV/HCV+. Average age was 43. On average patients had HIV for 7 years, had been on ART for almost 5 years; 70% were on protease inhibior therapy; ALT was only 32-39. Fasting glucose was 92 mg/dL. Fasting insulin was 19 uIU/L. HOMA-IR was 4.6. Cholesterol was 226. Triglycerides were 331.
The HBV and HCV positive patients were significantly more likely to meet criteria for type 2 diabetes. Having hepatitis was a strong predictor of HOMA-IR (insulin resistance). The HBV+ patients had more glucose abnormalities than the HCV+ patients. The 9 HCV+ patients had higher insulin levels and HOMA-IR than the HIV+/hepatitis- patients. But the HBV+ patients had higher insulin levels than the HCV+ patients. But the HCV+ patients had the same fasting glucose and 2 hour fasting glucose levels as the HIV+ patients without hepatitis. The 5 HBV+ patients had more increased fasting glucose, a greater 2-hour challnge glucose, and HOMA-IR than the HCV+ patients and the HIV+ and hepatitis negative patients.
ALT was a significant predictor for fasting glucose, 2-hour glucose, fasting insulin, and insulin area under the curve. Fasting glucose was 90 mg/dL for HIV+ patients, 114 for the HBV+ patients, and 92 for the HCV+ patients. Asting 2-hour glucose was 132 mg/dL for the HIV+ patients, 195 for HBV+, and 133 for HCV+. Insulin was 17.5 uIU/L for HIV+, 39 for HBV+, and 23 for HCV+ patients. HOMA-IR (insulin resistance) was 4.0 for HIV+, 12.8 for HBV+, and 5.4 for HCV+.
The authors conclude that insulin resistance in patients with fat redistribution is associated with ALT elevation, after adjusting for having hepatitis. In addition, asymptomatic patients with HBV and HCV had significant insulin resistance and increased rates of diabetes. The authors suggest these findings suggest that fatty liver disease may correlate with the extent of insulin resistance, and are exacerbated by chronic viral hepatitis. The authors recommend careful screening and management of insulin resistance and diabetes among HIV-infected patients with fat redistribution and HBV or HCV.