https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.27406

The global burden of liver disease: The major impact of China

New trends on obesity and NAFLD in Asia

Non-alcoholic fatty liver disease is marked by hepatic fat accumulation not due to alcohol abuse. Several studies have demonstrated that NAFLD is associated with insulin resistance leading to a resistance in the antilipolytic effect of insulin in the adipose tissue with an increase of free fatty acids (FFAs). The increase of FFAs induces mitochondrial dysfunction and development of lipotoxicity. Moreover, in subjects with NAFLD, ectopic fat also accumulates as cardiac and pancreatic fat. In this review we analyzed the mechanisms that relate NAFLD with metabolic syndrome and dyslipidemia and its association with the development and progression of cardiovascular disease.

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Non-Alcoholic Fatty Liver Disease (NAFLD) and Its Connection with Insulin Resistance, Dyslipidemia, Atherosclerosis and Coronary Heart Disease

https://www.soard.org/article/S1550-7289(08)00630-8/pdf

American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery Medical Guidelines for Clinical Practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient.

http://forensic.sc.su.ac.th/seminar/seminarii52/51312338.pdf

Epidemiology of non-alcoholic fatty liver disease in China

Background: Obesity is a chronic inflammatory condition, with related steatohepatitis and liver fibrosis. The authors analyzed the hepatic histopathology in morbidly obese patients and predictors of concurrence of clinical and/ or histopathologic findings of steatohepatitis with other forms of chronic liver disease. Methods: The histopathologic findings in the liver of 160 patients who were undergoing laparoscopic gastric bypass or gastric banding for morbid obesity, were examined. Clinical data (gender, age, BMI and associated diseases) and laboratory evaluation were obtained from the patient records. The degree of steatosis, ballooning degeneration, lobular inflammation and fibrosis were determined and scored. Results: Among the patients, 62.5% (n=100) were females and 37.5% (n=60) were males, age 27 ± 12 years, with mean BMI 43 ± 5.8 kg/m2. 63, 54, 26, 15 and 2 patients were diagnosed as non-nonalcoholic steatohepatitis (non-NASH), NASH, chronic hepatitis B (CHB), alcoholic steatohepatitis and chronic hepatitis C (CHC), respectively. The prevalence of NASH was 33.8%, of which 5 patients (9.2%) had bridging fibrosis, but no cirrhosis was found in the NASH group. The prevalence of CHB was 16.3%, of which 3 patients (11.6%) had bridging fibrosis and/or cirrhosis. Multivariate analysis showed an association between steatosis and AST, ALT, GGT, C-peptide, insulin, HOMA-IR and adiponectin. The predictors of ballooning degeneration were serum sugar and AST, whereas the predictors of lobular inflammation were AST and ALT. There was a trend toward a correlation between abnormal liver function, insulin resistance, steatosis, liver cell injury and Mallory body in the NASH population. BMI, C-peptide, steatosis, ballooning degeneration and portal inflammation were significantly different between NASH and CHB groups, but only steatosis and ballooning degeneration were independent factors of NASH compared with CHB group after multivariate analysis. Overall, AST, AST/ALT ratio, uric acid and portal inflammation were independently associated with advanced fibrosis, while only Mallory body (P=0.033) and portal inflammation (P=0.015) were significantly different between mild-moderate fibrosis and advanced fibrosis in the NASH patients. Conclusion: Hepatic steatosis, features of metabolic syndrome and liver cell injuries were common in morbidly obese patients. Abnormal liver function and portal inflammation were related to hepatic fibrosis. The coexistance of clinical and histologic features of steatohepatitis with another chronic liver disease may reflect the biological significance of the chronic inflammatory condition in the obese population, which requires further investigation.

Hepatic histopathology of morbid obesity: concurrence of other forms of chronic liver disease.

Metabolic syndrome (MetS) and nonalcoholic fatty liver disease (NAFLD), ranging from simple steatosis to steatohepatitis (NASH), have become important health issues in obese subjects. In this study, we investigated the relationship between MetS and NASH in severely obese subjects. A total of 111 non-alcoholic obese patients who underwent laparoscopic bariatric surgery (BMI 45.4 ± 5.7 kg/m2) were enrolled from February to September 2004 in a referral center in North Taiwan. MetS and its individual components were defined using the American Heart Association/National Heart, Lung, and Blood Institute criteria. Based on liver biopsy during surgery, subjects were classified into either having NASH or not. The relationship among NASH, adiponectin, insulin resistance, MetS and its individual components was examined using a multivariate logistic regression analysis. The prevalence of NASH and MetS in these subjects was 79.3% and 68.5%, respectively. Using a multivariate logistic regression analysis with NASH as the outcome variable, odds ratio (OR) of NASH for subjects with MetS versus without MetS was 2.96 (95% CI = 1.14–7.68) adjusted for age, gender, and BMI. Also, high blood pressure (OR = 2.97, 1.31–6.73) and high fasting glucose (OR = 2.94, 1.13–7.67) were independently associated with NASH after adjustment for age, gender, and BMI. Insulin resistance measured as HOMA-IR and serum adiponectin level were not significantly different between the NASH and non-NASH group. MetS and NASH were common in severely obese Taiwanese adults. Presence of MetS, high blood pressure, and high fasting glucose was independently related to increased risk of NASH.The underlying mechanism deserves to be explored in the future.

Metabolic syndrome is related to nonalcoholic steatohepatitis in severely obese subjects.

Background: Helicobacter pylori (HP) infection is linked to weight control through gastric inflammation-induced deregulation of satiety-related hormone, and eradication of HP before a weight reduction operation has been advocated. We aimed to examine the impact of HP infection and corpus gastritis on preoperative patient characteristics, postoperative complications and weight loss following laparoscopic vertical banded gastroplasty (LVBG). Methods: A prospective cohort of 152 patients undergoing LVBG was enrolled. Gastric specimens at the corpus were obtained during LVBG operation and scored histologically according to the Sydney classification of gastritis. Excess weight loss, and early and late complications following LVBG, were recorded and correlated. Results: 63 and 89 patients were identified as HP positive and negative groups respectively. The prevalence of individual components of the metabolic syndrome was comparable in both groups except hypertension. The occurrence of early and late complications, either minor or major, in both groups was similar. The severity of gastritis was correlated positively with age and negatively with preoperative BMI and excess weight. Patients with higher neutrophil activity, chronic inflammation, and HP density experienced less excess weight loss at 24 to 48 months follow-up. The impact of gastritis on weight loss became less recognizable after 48 months follow-up. Conclusions: HP infection and gastric inflammation play a significant role in the amount of weight loss after LVBG. Further prospective studies should examine possible mechanisms and long-term effects on weight loss to determine the utility of preventive eradication of HP in different types of bariatric surgery.

Hsih Hsi Wang

Papers

Hepatic histopathology of morbid obesity: concurrence of other forms of chronic liver disease.

Metabolic syndrome is related to nonalcoholic steatohepatitis in severely obese subjects.

The Influence of Helicobacter pylori Infection and Corpus Gastritis on the Postoperative Outcomes of Laparoscopic Vertical Banded Gastroplasty