Visceral adiposity index is associated with histological findings and high viral load in patients with chronic hepatitis C due to genotype 1

Abstract

Metabolic factors have been associated with liver damage in patients with genotype 1 chronic hepatitis C (G1 CHC). We tested visceral adiposity index (VAI), a new marker of adipose dysfunction in G1 CHC, patients to assess its association with host and viral factors and its link to both histological findings and sustained virological response (SVR). Two hundred thirtysix consecutive G1 CHC patients were evaluated by way of liver biopsy and anthropometric and metabolic measurements, including insulin resistance (IR), homeostasis model assessment (HOMA), and VAI using waist circumference, body mass index, triglycerides, and highdensity lipoprotein cholesterol. All biopsies were scored by one pathologist for staging and grading and graded for steatosis, which was considered moderate to severe if !30%. Multiple linear regression analysis revealed that VAI score was independently associated with higher HOMA score (P 5 0.009), log10 hepatitis C virus RNA levels (P 5 0.01), necroinflammatory activity (P 5 0.04), and steatosis (P 5 0.04). Multiple logistic regression analysis revealed that IR (OR 3.879, 95% CI 1.727-8.713, P 5 0.001), higher VAI score (OR 1.472, 95% CI 1.051-2.062, P 5 0.02), and fibrosis (OR 2.255, 95% CI 1.349-3.768, P 5 0.002) were linked to steatosis !30%. Logistic regression analysis revealed that older age (OR 1.030, 95% CI 1.002-1.059, P 5 0.03), higher VAI score (OR 1.618, 95% CI 1.001-2.617, P 5 0.04), and fibrosis (OR 2.608, 95% CI 1.565-4.345, P < 0.001) were independently associated with moderate to severe necroinflammatory activity. No independent associations were found between VAI score and both fibrosis and SVR. Conclusion: In G1 CHC patients, higher VAI score is independently associated with both steatosis and necroinflammatory activity and has a direct correlation with viral load. (HEPATOLOGY 2010;52:1543-1552

Volume-dependent effect of supervised exercise training on fatty liver and visceral adiposity index in subjects with type 2 diabetes The Italian Diabetes Exercise Study (IDES)

“…Moreover, VAI, a marker of visceral fat distribution and dysfunction which correlates with cardiovascular risk [27], was recently found to be independently associated with fibrosis in subjects with NAFLD [11] and with steatosis and necroinflammatory activity in those with chronic C hepatitis [12], though another report showed that VAI was not more powerful than waist circumference in discriminating NAFLD from NASH [29].…”

“…Among these, fatty liver index (FLI) has been shown to predict NAFLD [9,10], whereas visceral adiposity index (VAI), a marker of visceral fat distribution and function, has been correlated with histology in subjects with NAFLD [11] and chronic hepatitis C [12].…”

Does visceral adiposity index signify early metabolic risk in children and adolescents?: Association with insulin resistance, adipokines, and subclinical inflammation

“…In this context, visceral adiposity index (VAI)-a novel index derived from anthropometric (BMI and WC) and lipid parameters-has been shown to be associated with visceral adipose tissue and, moreover, with adipokine levels, mainly adiponectin, insulin resistance, and glucose disturbances in adults (12)(13)(14)(15). In addition, this index seems to have predictive value in terms of an increased risk for cardiovascular events (13) and has served as a marker of insulin resistance in several different nosologic entities (16)(17)(18)(19)(20)(21). Furthermore, our group recently reported, for the first time, the strong relationship of VAI with adipose tissue secretion and with functional glycemic disorders (22).…”

Role of insulin resistance and hepatic steatosis in the progression of fibrosis and response to treatment in hepatitis C

“…Interestingly, in genotype 1 chronic hepatitis C patients, a higher visceral adiposity index was independently associated with both steatosis and necroinflammatory activity and has a direct correlation with viral load (17).…”