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Visceral adiposity index may not effectively predict NAFLD severity

Visceral adiposity scores were not more effective than waist circumference measurements in predicting hepatic inflammation or fibrosis among patients with nonalcoholic fatty liver disease in recent study results.

Researchers calculated the visceral adiposity index (VAI) of 190 patients with nonalcoholic fatty liver disease (NAFLD), along with a 129-patient control group. The NAFLD patients were further categorized into patients with steatosis (n=61) and nonalcoholic steatohepatitis (NASH) (n=129).

A multivariate linear regression analysis independently associated VAI with a diagnosis of steatosis vs. nonalcoholic steatohepatitis (P<.05) and with fasting glucose levels (P<.05). Type 2 diabetes was present in 19.7% of the steatosis group, 34.1% in the NASH group and none of the control group. Criteria for a metabolic syndrome diagnosis were met by 5.6% of the control group, 31% of patients with steatosis and 52% of patients with NASH.

The mean VAI was 1.5 for the control group, compared with 2.3 in the steatosis group and 3.2 in the VAI group (P<.001). Waist circumference (WC) also increased significantly across the three groups in this order (P<.001). VAI was associated with an increased number of metabolic syndrome components, as well as diagnosis of metabolic syndrome (P<.001). However, the same associations were observed with WC (P<.001), and there was no significant difference between the strength of VAI and WC’s associations.

VAI was not associated with liver inflammation or fibrosis, while WC was considered a marker for liver fibrosis (P=.01). Investigators also observed a correlation between VAI and visceral fat percentage when quantified by MRI (r=0.39, P<.05), but a stronger association was found between visceral fat percentage and both WC (r=0.52, P<.01) and BMI (r=0.43, P<.01).

“In NAFLD, VAI is not associated with steatosis, inflammation or fibrosis,” the researchers wrote. “VAI is no more powerful than WC in discriminating steatosis from steatohepatitis, reflecting limitations of the formula with what is known about the pathogenesis of NAFLD.”