Epidemiologic data suggest that patients with chronic hepatitis C virus (HCV) infection have an increased risk for insulin resistance—and for overt diabetes.1,2 Specifically, Serfaty and Capteau have reported evidence for “a triangular interaction” between steatosis, inflammatory processes, and insulin resistance.1
Averting these metabolic risks is essential for several reasons: Most importantly, their development is associated with increased liver inflammation and progression to fibrosis and cirrhosis, as well as impaired response to antiviral medications.3,4 Additionally, type 2 diabetes in patients with chronic HCV has been associated with a 1.7-fold increased risk for hepatocellular carcinoma (HCC) and other malignancies.5,6
Though never directly linked with the metabolic syndrome, HCV has been associated with impaired insulin signaling and insulin resistance, in addition to hypocholesterolemia and steatosis. Lonardo et al went so far as to mark this constellation of effects as “a distinct HCV-associated dysmetabolic syndrome.” 4
The dysmetabolic syndrome places affected patients at increased risk for cardiovascular disease, according to Rzouq et al. Statins, they report, are safe and effective in patients with chronic HCV and appear to confer anti-HCV proliferative benefits, making them a potentially “life-saving therapy.”7
Because insulin resistance in the hepatic and peripheral tissues is at the very least “an obvious and significantly detrimental pathophysiologic feature of HCV infection,” Kawaguchi and Mazuta suggest that patients with chronic HCV be encouraged to follow the same dietary and lifestyle recommendations made to those with diabetes, obesity, and metabolic syndrome.2 Maintaining a healthy body weight and following a reasonable regimen of diet and exercise help protect the liver in HCV-infected patients, whereas overweight and obesity, high cholesterol levels, and fatty liver are associated with accelerated liver damage.3
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