Visceral Adipose Tissue Area as an Independent Risk Factor for Elevated Liver Enzyme in Nonalcoholic Fatty Liver Disease

Self Cite

Section: Methodsmentioning

confidence: 99%

Section: Hepatic Ultrasonographic Examinationsmentioning

confidence: 99%

The preventive effect of sustained physical activity on incident nonalcoholic fatty liver disease

Kwak

Kim

Chung

et al. 2016

Self Cite

“…In fact, a correlation between the visceral abdominal fat detected by CT scan and the degree of hepatic steatosis has previously been demonstrated. 19,23 Therefore patients with steatosis might feature an increase in mesenteric visceral fat that displaces the bowel, particularly the colon, thereby hampering the visualization of the liver and the pancreas and mimicking the presence of excessive intestinal gas. However, these…”

Section: Discussionmentioning

confidence: 99%

Intestinal gas and liver steatosis: a casual association? A prospective multicentre assessment

Maconi

Furfaro

Fries

et al. 2016

“…Visceral adipose tissue (VAT) area is more directly related to NAFLD than is the body mass index (BMI) as a surrogate marker of general obesity . We previously reported that increased VAT area is independently associated with NASH or significant fibrosis .…”

Section: Introductionmentioning

confidence: 99%

“…Visceral adipose tissue (VAT) area is more directly related to NAFLD than is the body mass index (BMI) as a surrogate marker of general obesity. 7,8 We previously reported that increased VAT area is independently associated with NASH or significant fibrosis. 9 Several studies have reported that an increased visceral fat is associated with metabolic syndrome in metabolically obese, normal-weight (MONW) subjects.…”

Section: Introductionmentioning

confidence: 99%

Predictors of nonalcoholic steatohepatitis and significant fibrosis in non‐obese nonalcoholic fatty liver disease

Kim

Joo

et al. 2018

Self Cite

Aims We compared (a) demographic and clinical characteristics and (b) determinants of nonalcoholic steatohepatitis and significant fibrosis in non‐obese and obese nonalcoholic fatty liver disease. Methods A cross‐sectional study of 664 Asian subjects (mean age 53.1 years; men 50.3%) with biopsy‐proven nonalcoholic fatty liver disease and controls was conducted. Subjects were divided by their body mass index into obese (body mass index ≥25 kg/m2) and non‐obese (body mass index <25 kg/m2). Results Observations in subjects with non‐obese nonalcoholic fatty liver disease were in between non‐obese controls and subjects with obese nonalcoholic fatty liver disease for body mass index, sagittal abdominal diameter, aminotransferase levels, insulin resistance and abdominal visceral adipose tissue area. There was no significant difference in histology between non‐obese and obese subjects with nonalcoholic fatty liver disease except for lower grade of hepatic steatosis in nonobese nonalcoholic fatty liver disease and higher severity of hepatic fibrosis in nonobese nonalcoholic steatohepatitis. Predictors of nonalcoholic steatohepatitis in nonobese subjects included females (odds ratio 2.49), higher alanine aminotransferase (odds ratio 1.03), lower high‐density lipoprotein cholesterol (odds ratio 0.96), higher prevalence of diabetes (odds ratio 3.65) and higher visceral adipose tissue area (odds ratio 1.63 per standard deviation increase of visceral adipose tissue area) while age (odds ratio 1.04), higher aspartate aminotransferase (odds ratio 1.02), diabetes (odds ratio 2.76) and higher visceral adipose tissue area (odds ratio 1.57 per standard deviation increase) were associated with significant fibrosis in the non‐obese. Sagittal abdominal diameter was independently associated with nonalcoholic steatohepatitis or significant fibrosis among subjects with non‐obese nonalcoholic fatty liver disease. Conclusion While there were a few phenotypic differences from obese subjects, non‐obese subjects with nonalcoholic fatty liver disease displayed a similar severity of histological liver damage. Potential factor(s) beyond obesity may play a role as non‐obese nonalcoholic fatty liver disease advances to more severe disease.