INTRODUCTION: Leptin has been implicated in the pathogenesis of nonalcoholic steatohepatitis. It has also been suggested that adiponectin plays an important role in the transition from fatty liver disease to nonalcoholic steatohepatitis. OBJECTIVE: To evaluate whether leptin and adiponectin levels are related to the degree of necroinflammatory activity and fibrosis in patients with nonalcoholic steatohepatitis. METHODS: Leptin and adiponectin levels were determined in 52 patients with nonalcoholic steatohepatitis and in 49 controls by enzyme-linked immunosorbent analysis. RESULTS: Median (interquartile range) leptin levels were higher in patients with nonalcoholic steatohepatitis than in the controls (5.75 (12.3) ng mL-1 and 2.80 (2.40) ng mL-1, respectively; P = 0.0035). Adiponectin levels were lower in patients with nonalcoholic steatohepatitis than in the controls (6.55 (5.05) mg mL-1 and 9.30 (6.70) mg mL-1, respectively; P = 0.0218). Leptin levels were lower in overweight patients than in obese patients (2.25 (6.73) and 8.0 (16.0) ng mL-1, respectively; P = 0.0025). The amount of necroinflammatory activity observed in liver biopsies correlated positively with the amount of fibrosis (P < 0.0001). Increased lactate dehydrogenase correlated with increased fibrosis in patients with nonalcoholic steatohepatitis (P = 0.0012). Necroinflammatory activity correlated with adiponectin, g-glutamyltranspeptidase, the quantitative insulin-sensitivity check index, and ferritin (P < 0.05). Risk factors for nonalcoholic steatohepatitis in the logistic regression analysis were leptin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and g-glutamyltranspeptidase (P < 0.0001). Only lactate dehydrogenase (P = 0.0012) was significantly associated with advanced fibrosis on logistic regression analysis. CONCLUSIONS: Lactate dehydrogenase was associated with fibrosis and advanced fibrosis. Leptin was associated with nonalcoholic steatohepatitis but not with fibrosis or necroinflammatory activity. Adiponectin was related to necroinflammatory activity. Risk factors for nonalcoholic steatohepatitis were leptin and liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gama-glutamyltranspeptidase).
INTRODUCTION: Leptin has been implicated in the pathogenesis of nonalcoholic steatohepatitis. It has also been suggested that adiponectin plays an important role in the transition from fatty liver disease to nonalcoholic steatohepatitis. OBJECTIVE: To evaluate whether leptin and adiponectin levels are related to the degree of necroinflammatory activity and fibrosis in patients with nonalcoholic steatohepatitis. METHODS: Leptin and adiponectin levels were determined in 52 patients with nonalcoholic steatohepatitis and in 49 controls by enzyme-linked immunosorbent analysis. RESULTS: Median (interquartile range) leptin levels were higher in patients with nonalcoholic steatohepatitis than in the controls (5.75 (12.3) ng mL-1 and 2.80 (2.40) ng mL-1, respectively; P = 0.0035). Adiponectin levels were lower in patients with nonalcoholic steatohepatitis than in the controls (6.55 (5.05) mg mL-1 and 9.30 (6.70) mg mL-1, respectively; P = 0.0218). Leptin levels were lower in overweight patients than in obesepatients (2.25 (6.73) and 8.0 (16.0) ng mL-1, respectively; P = 0.0025). The amount of necroinflammatory activity observed in liver biopsies correlated positively with the amount of fibrosis (P < 0.0001). Increased lactate dehydrogenase correlated with increased fibrosis in patients with nonalcoholic steatohepatitis (P = 0.0012). Necroinflammatory activity correlated with adiponectin, g-glutamyltranspeptidase, the quantitative insulin-sensitivity check index, and ferritin (P < 0.05). Risk factors for nonalcoholic steatohepatitis in the logistic regression analysis were leptin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and g-glutamyltranspeptidase (P < 0.0001). Only lactate dehydrogenase (P = 0.0012) was significantly associated with advanced fibrosis on logistic regression analysis. CONCLUSIONS: Lactate dehydrogenase was associated with fibrosis and advanced fibrosis. Leptin was associated with nonalcoholic steatohepatitis but not with fibrosis or necroinflammatory activity. Adiponectin was related to necroinflammatory activity. Risk factors for nonalcoholic steatohepatitis were leptin and liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gama-glutamyltranspeptidase).
Authors: James H Tabibian; Mariana Lazo; Francisco A Durazo; Hsin-Chieh Yeh; Myron J Tong; Jeanne M Clark Journal: J Gastroenterol Hepatol Date: 2011-03 Impact factor: 4.029
Authors: Stergios A Polyzos; Konstantinos N Aronis; Jannis Kountouras; Dimitrios D Raptis; Maria F Vasiloglou; Christos S Mantzoros Journal: Diabetologia Date: 2015-09-26 Impact factor: 10.122