BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a common liver disease. The aim of the present study was to explore the relation of visfatin with underlying histopathological changes of NAFLD patients. SUBJECTS: A population of 55 NAFLD patients was analyzed in a cross-sectional study. A liver biopsy was realized. Weight, basal glucose, insulin, insulin resistance (HOMA), total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, and visfatin levels were measured. A bioimpedance was performed. RESULTS AND CONCLUSIONS: The mean age was 42.8 +/- 11.2 years, the mean BMI was 33.1 +/- 10.2 with 37 males (67.3%) and 18 females (32.7%). Probabilities to have; portal inflammation increased 1.11 (CI95%:1.03-1.50) with each increment of 1 ng/ml of visfatin concentration, high grade of steatosis increased 1.25 (CI 95%:1.06-1.61) with each unit of insulin concentrations, fibrosis increased 1.12 (CI 95%:1.02-1.43) with each unit of fat mass and lobulillar inflammation increased 13.4 (CI 95%:1.3-147) with each unit of HOMA-IR. Portal inflammation frequencies were different between groups (low visfatin group 13.07 < ng/ml: 37.5% versus high visfatin group 13.07 > ng/ml: 62.5%; P < 0.05). In conclusion, several histopathological changes in liver biopsies could be explained by insulin concentrations, HOMA-IR, and fat mass amount. Moreover, visfatin plasma concentrations could predict the presence of portal inflammation in NAFLD patients.
BACKGROUND:Non-alcoholic fatty liver disease (NAFLD) is a common liver disease. The aim of the present study was to explore the relation of visfatin with underlying histopathological changes of NAFLD patients. SUBJECTS: A population of 55 NAFLD patients was analyzed in a cross-sectional study. A liver biopsy was realized. Weight, basal glucose, insulin, insulin resistance (HOMA), total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, and visfatin levels were measured. A bioimpedance was performed. RESULTS AND CONCLUSIONS: The mean age was 42.8 +/- 11.2 years, the mean BMI was 33.1 +/- 10.2 with 37 males (67.3%) and 18 females (32.7%). Probabilities to have; portal inflammation increased 1.11 (CI95%:1.03-1.50) with each increment of 1 ng/ml of visfatin concentration, high grade of steatosis increased 1.25 (CI 95%:1.06-1.61) with each unit of insulin concentrations, fibrosis increased 1.12 (CI 95%:1.02-1.43) with each unit of fat mass and lobulillar inflammation increased 13.4 (CI 95%:1.3-147) with each unit of HOMA-IR. Portal inflammation frequencies were different between groups (low visfatin group 13.07 < ng/ml: 37.5% versus high visfatin group 13.07 > ng/ml: 62.5%; P < 0.05). In conclusion, several histopathological changes in liver biopsies could be explained by insulin concentrations, HOMA-IR, and fat mass amount. Moreover, visfatin plasma concentrations could predict the presence of portal inflammation in NAFLD patients.
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