Day 1 :
- Gastroenterology and Digestive Disorders Conference
Session Introduction
Nafiseh Bahadori birgani
Shahid Beheshti University of Medical Sciences, Tehran, Iran
Title: Nutritional recommendations for patients with non-alcoholic fatty liver diseases
Biography:
Nafiseh Bahadori birgani, Department of National Nutrition And Food Technology Research, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Fatty liver is the most common liver disease worldwide. Hyperglycemia and hyperinsulinemia induce lipogenesis, thereby increasing the hepatic pool of fatty acid. Nutritional consultations and lifestyle modification are important in the treatment of non-alcoholic fatty liver disease (NAFLD). The usual management of NAFLD includes lifestyle counseling to achieve a gradual weight reduction and an increase in physical activity. An intensive lifestyle intervention focused on diet, exercise and behavior modification with a goal of 7–10% weight reduction that leads to significant improvement in liver histology in patients with NASH. Indeed, weight loss improves steatosis, reduces hepatic inflammation and hepatocellular injury and improves cardiovascular risk profile. Several changes in dietary intake have occurred in the past few years, including increased energy intake (24%), and increases in added sugars, flour and cereal products, fruit, added fats and total fat intake. Fatty liver disease in humans is an insulin-resistant condition and the liver over-produces glucose and triglycerides due to impaired insulin action. Fatty liver is an independent predictor of diabetes and cardiovascular disease. There are three major sources for increased liver faat accumulation: excessive delivery of free fatty acids from lipolysis of superficial and visceral fat depots (60%), increased de novo hepatic lipogenesis (30%), and increased nutritional intake (10%)[
Biography:
Tarek A Elshazly, Department of Internal Medicine, Faculty of Medicine, Mansoura University, Egypt
Abstract:
Quantitative estimation of serum levels of hepatitis B surface antigen (HBsAg) and HB viral DNA load (HB VDL) in chronic hepatitis B (CHB) patients and their applicability for differentiating between disease phases and to predict the outcome of liver biopsy. Patients & Methods: The study included 113 patients; 67 males and 46 females; with mean age of 42.6±10.8 years and mean disease duration of 5.6±1.1 years. All patients underwent clinical examination, and blind liver biopsy was taken for necrosis and fibrosis histopathological scoring. Fasting venous blood samples were collected for estimation of serum AST and ALT, estimation of hepatitis B serological markers by ELISA and quantitative estimation of serum HBsAg by Roche Cobas e 411 analyzer and estimation of HB VDL by real time PCR. Results: Fifty-three patients were HB e antigen (HBeAg)-positive, while
60 patients were HBeAg-negative. Mean total serum HB VDL was 2907.2±1060 IU/ml; 32 patients had low and 81 patients had high HB VDL. Mean total serum HBsAg level was 24.7±5.9x103 IU/ml. The ratio of the median log10 of serum HB VDL/ serum HBsAg level was 0.42 in low VDL patients and 0.4 in high VDL patients. Regression analysis defined high log10 of serum HBsAg level as the persistently significant determinant of cases with immune tolerance (IT) and/or immune reactive (IR), liver necrosis score, high log10 of serum VDL, the ratio of log10 values of serum VDL to serum HBsAg and male gender. ROC curve analysis defined high log10 of serum HBsAg level as a significant specific and the ratio of log10 of serum HB VDL to serum HBsAg as a significant sensitive predictor for IT cases and high log10 of serum HB VDL and positive HBeAg as significant predictors for presence of fibrosis. Conclusion: Quantitative estimation of serum level of HBsAg and viral load could differentiate between phases of CHB disease and predict histopathological status of the liver, so could spare liver biopsy with its inherent complications.