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HIV/Hepatitis & Insulin/Diabetes
Reported by Jules Levin
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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.
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