Reuters Health Information (2003-12-17): Hepatitis C virus-induced insulin resistance contributes to hepatic fibrogenesis
Hepatitis C virus-induced insulin resistance contributes to hepatic fibrogenesis
Last Updated: 2003-12-17 11:45:20 -0400 (Reuters Health)
NEW YORK (Reuters Health) - Hepatitis C virus (HCV) induces insulin resistance that may contribute to the progression of fibrotic liver disease in chronic hepatitis C infection, Australian researchers report in the December issue of Gastroenterology.
As senior investigator Dr. Jacob George told Reuters Health, "hepatitis C is the first significant cause of type 2 diabetes apart from obesity and genetics that we know of. Insulin resistance in hepatitis C," he added, " may be a consequence of the effects of the virus on the liver or ... through mechanisms that are as yet unknown."
To investigate further, Dr. George from University of Sydney at Westmead Hospital, and colleagues examined the association of insulin resistance (as determined by the homeostasis model assessment (HOMA)-IR method) with HCV infection and with hepatic fibrotic progression in 260 patients with chronic HCV infection.
Compared to controls, the HCV patients had significantly higher levels of all markers of insulin resistance.
Factors independently associated with increased HOMA-IR included portal or periportal inflammatory grade, higher body-mass index, and previous treatment. HCV genotype 3 was associated with a lower risk of insulin resistance.
HOMA-IR independently predicted the degree of hepatic fibrosis, the researchers note, as did portal or periportal inflammatory grade, past alcohol intake, age, and ALT level. HOMA-IR was also independently associated with an increased rate of fibrosis progression in a multiple linear regression model.
"It is important to implement strategies to reduce insulin resistance in patients infected with chronic hepatitis C," Dr. George continued," as this may reduce the rate of progression of hepatic fibrosis. " In particular, "I usually recommend an intervention program comprising diet and exercise."
This, he suggested, should be done " in concert with or prior to commencing antiviral therapy."
In an accompanying editorial, Dr. Arun J. Sanyal from Virginia Commonwealth University, Richmond, notes that "these new insights may lead to innovative new therapies to modulate chronic inflammation and fibrosis in a variety of diseases, including chronic liver disease."