To identify and examine the different causes of liver disease in Sri Lanka

© 2017 The Authors. Published by International Journal of Science and Research. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://www.ijsr.net/get_abstract.php?paper_id=ART20178732Liver disease is one of the main causes for deaths in Sri Lanka, this is the second most common disease causing deaths in hospitals in Sri Lanka after the heart disease. Sri Lanka ranks eighty-nine (89) in the world rankings for liver disease causing 3349 deaths according to the data published by the World Health Organization (WHO) for the 2014 calendar year and an average of 15.28 deaths per hundred thousand. The two most common forms of this disease is non-alcoholic fatty liver disease and alcoholic fatty liver disease. The data collected by the WHO is analyzed and the different causes for the liver disease is identified between the period of 1980-2010, using the different factors responsible for the cause of the disease data is distinguished. Of the data collected and analyzed most causes of liver disease in Sri Lanka is due to the non-alcoholic fatty liver disease (NAFLD) or alcoholic fatty liver disease which leads to severe complications such as renal failure, liver cirrhosis and eventually deat

Endocannabinoid receptor blockade increases hepatocyte growth factor and reduces insulin levels in obese women with polycystic ovary syndrome

There is evidence from animal and in-vitro studies that activation of the endocannabinoid system (EC) through cannabinoid receptor 1 (CB-1) is associated with liver injury, inflammation and hepatocellular carcinoma.1 Data suggests endogenous cannabinoids (EC) are related to fatty liver metabolism with a role in non-alcoholic fatty liver disease (NAFLD) through modulating lipid metabolism that may be ameliorated by CB1 receptor antagonism with rimonabant.2 This is of particular importance as NAFLD is the most common cause of chronic liver disease with liver dysfunction leading liver cirrhosis. The diagnosis of NAFLD can only be confirmed by a liver biopsy, as liver enzymes such as alanine aminotransferase (ALT) used, as a serum marker may not be elevated

The role of lipid and lipoprotein metabolism in non-alcoholic fatty liver disease

Due to the epidemic of obesity across the world, nonalcoholic fatty liver disease (NAFLD) has become one of the most prevalent chronic liver disorders in children and adolescents. NAFLD comprises a spectrum of fat-associated liver conditions that can result in end-stage liver disease and the need for liver transplantation. Simple steatosis, or fatty liver, occurs early in NAFLD and may progress to nonalcoholic steatohepatitis, fibrosis and cirrhosis with increased risk of hepatocellular carcinoma. The mechanism of the liver injury in NAFLD is currently thought to be a multiple-hit process where the first hit is an increase in liver fat, followed by multiple additional factors that trigger the inflammatory activity. At the onset of disease, NAFLD is characterized by hepatic triglyceride accumulation and insulin resistance. Liver fat accumulation is associated with increased lipotoxicity from high levels of free fatty acids, free cholesterol and other lipid metabolites. As a consequence, mitochondrial dysfunction with oxidative stress and production of reactive oxygen species and endoplasmic reticulum stress-associated mechanisms, are activated. The present review focuses on the relationship between intra-cellular lipid accumulation and insulin resistance, as well as on lipid and lipoprotein metabolism in NAFLD

Non-alcoholic fatty liver disease and associated factors among type 2 diabetic patients in southwest Ethiopia

Background: Non-alcoholic Fatty Liver Disease (NAFLD) among type 2 diabetic patients is completely ignored in developing regions like Africa paving the way for public health and economic burden in the region. Therefore, the main objective of this research was to evaluate non-alcoholic fatty liver disease and associatedfactors among type 2 diabetic patients in Southwestern Ethiopia attending Diabetic Clinic of Jimma University Specialized Hospital (JUSH).Methods: Facility based cross-sectional study design was used. Anthropometry, fatty liver (using utrasonography), liver enzymes, and lipid profiles were measured among type 2 diabetic patients who fulfilled the inclusion criteria. Socio-demographic and clinical characteristics were assessed using standard questionnaires.Results: Ninety-six (96) type 2 diabetic patients were enrolled and non-alcoholic fatty liver disease prevalence was 73%. Of nonalcoholic fatty Liver disease documented patients, 35.4%, 31.3% and 6.3% exhibited mild, moderate and severe fatty liver diseases, respectively. Alanine aminotransferase (p ≤0.001), Triacyglycerol (p ≤0.001), total bilirubin (p ≤0.05), direct bilirubin (p ≤0.05) and diabetic duration (p ≤0.01) were significantly associated with nonalcoholic fatty liver disease among type 2 diabetic patients. The Aspartate aminotransferase/ Alanine aminotransferase ratio among non alcoholic fatty liver disease patients was greater than one.Conclusions: The magnitude of non-alcoholic fatty liver disease is high among study groups and it needs urgent action by healthcare systems. Therefore, targeted treatment approach inclusive of non-alcoholic fatty liver disease should be designed.Keywords: Africa, Ethiopia, Nonalcoholic Fatty Liver Disease, Type 2 DM, Liver Enzymes, Lipid Profil

Identifying nonalcoholic fatty liver disease patients with active fibrosis by measuring extracellular matrix remodeling rates in tissue and blood.

Excess collagen synthesis (fibrogenesis) in the liver plays a causal role in the progression of nonalcoholic fatty liver disease (NAFLD). Methods are needed to identify patients with more rapidly progressing disease and to demonstrate early response to treatment. We describe here a novel method to quantify hepatic fibrogenesis flux rates both directly in liver tissue and noninvasively in blood. Twenty-one patients with suspected NAFLD ingested heavy water (2 H2 O, 50-mL aliquots) two to three times daily for 3-5 weeks prior to a clinically indicated liver biopsy. Liver collagen fractional synthesis rate (FSR) and plasma lumican FSR were measured based on 2 H labeling using tandem mass spectrometry. Patients were classified by histology for fibrosis stage (F0-F4) and as having nonalcoholic fatty liver or nonalcoholic steatohepatitis (NASH). Magnetic resonance elastography measurements of liver stiffness were also performed. Hepatic collagen FSR in NAFLD increased with advancing disease stage (e.g., higher in NASH than nonalcoholic fatty liver, positive correlation with fibrosis score and liver stiffness) and correlated with hemoglobin A1C. In addition, plasma lumican FSR demonstrated a significant correlation with hepatic collagen FSR.ConclusionUsing a well-characterized cohort of patients with biopsy-proven NAFLD, this study demonstrates that hepatic scar in NASH is actively remodeled even in advanced fibrosis, a disease that is generally regarded as static and slowly progressive. Moreover, hepatic collagen FSR correlates with established risks for fibrotic disease progression in NASH, and plasma lumican FSR correlates with hepatic collagen FSR, suggesting applications as direct or surrogate markers, respectively, of hepatic fibrogenesis in humans. (Hepatology 2017;65:78-88)

The association of vitamin D deficiency with non-alcoholic fatty liver disease

OBJECTIVE: Vitamin D deficiency has been related to diabetes, hypertension, hyperlipidemia and peripheral vascular disease. In this study, we aimed to investigate the role of vitamin D status in non-alcoholic fatty liver disease. METHODS: We included 211 consecutive subjects to examine the presence of non-alcoholic fatty liver disease. Of these subjects, 57 did not have non-alcoholic fatty liver disease and 154 had non-alcoholic fatty liver disease. RESULTS: The non-alcoholic fatty liver disease group had significantly higher fasting blood glucose (p = 0.005), uric acid (p = 0.001), aspartate aminotransferase (

Targeting a phospho-STAT3-miRNAs pathway improves vesicular hepatic steatosis in an in vitro and in vivo model

Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease. Although genetic predisposition and epigenetic factors contribute to the development of NAFLD, our understanding of the molecular mechanism involved in the pathogenesis of the disease is still emerging. Here we investigated a possible role of a microRNAs-STAT3 pathway in the induction of hepatic steatosis. Differentiated HepaRG cells treated with the fatty acid sodium oleate (fatty dHepaRG) recapitulated features of liver vesicular steatosis and activated a cell-autonomous inflammatory response, inducing STAT3-Tyrosine-phosphorylation. With a genome-wide approach (Chromatin Immunoprecipitation Sequencing), many phospho-STAT3 binding sites were identified in fatty dHepaRG cells and several STAT3 and/or NAFLD-regulated microRNAs showed increased expression levels, including miR-21. Innovative CARS (Coherent Anti-Stokes Raman Scattering) microscopy revealed that chemical inhibition of STAT3 activity decreased lipid accumulation and deregulated STAT3-responsive microRNAs, including miR-21, in lipid overloaded dHepaRG cells. We were able to show in vivo that reducing phospho-STAT3-miR-21 levels in C57/BL6 mice liver, by long-term treatment with metformin, protected mice from aging-dependent hepatic vesicular steatosis. Our results identified a microRNAs-phosphoSTAT3 pathway involved in the development of hepatic steatosis, which may represent a molecular marker for both diagnosis and therapeutic targeting

Fatty Liver Degeneration In Children: Association With Obstructive Sleep Apnea

Fatty liver degeneration, also termed hepatic steatosis, is a condition in which lipids accumulate in the hepatocytes causing cellular dysfunction and eventually cell death. Hepatic steatosis is diagnosed histologically when liver fat exceeds more than 5% of the liver weight. In adults, fatty liver degeneration is typically associated with excessive alcohol intake as in alcoholic fatty liver disease or with sedentary lifestyle and high-calorie diet as in non-alcoholic fatty liver disease (NAFLD). With the rise of obesity in recent decades, fatty liver disease has become the leading cause of chronic liver disease, not only in adults but in children as well. Besides liver disease, obesity is associated with several conditions among which is obstructive sleep apnea.The aim of this article is to review the pathogenesis of fatty liver degeneration focusing on NAFLD and its relationship with obstructive sleep apnea in children

Endothelial dysfunction in adolescents and young adults with nonalcoholic liver disease

Nonalcoholic liver disease is a global public health problem that increases cardiovascular morbidity and mortality in these patients. This paper discusses endothelial dysfunction among patients (adolescents and young adults) with nonalcoholic liver disease. On the one hand, evidence suggests that cardiovascular disease is the leading cause of mortality in patients with advanced nonalcoholic liver disease and that nonalcoholic fatty liver is associated with an increased risk of cardiovascular disease independent of the presence of cardiovascular risk factors and metabolic syndrome components. On the other hand, nonalcoholic liver disease, especially the non-inflammatory form of nonalcoholic steatohepatitis, may not only be a marker of cardiovascular damage but also a factor involved in its pathogenesis. Such patients are candidates not only for the treatment of liver disease but also for the early treatment of cardiovascular risk factors because many of them, especially those with severe nonalcoholic liver disease, will develop major cardiovascular events and may eventually die of cardiovascular disease before the advanced liver disease occurs

Intakes of magnesium, calcium and risk of fatty liver disease and prediabetes

Objective Obesity and insulin resistance play important roles in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Mg intake is linked to a reduced risk of metabolic syndrome and insulin resistance; people with NAFLD or alcoholic liver disease are at high risk of Mg deficiency. The present study aimed to investigate whether Mg and Ca intakes were associated with risk of fatty liver disease and prediabetes by alcohol drinking status. Design We analysed the association between Ca or Mg intake and fatty liver disease, prediabetes or both prediabetes and fatty liver disease in cross-sectional analyses. Setting Third National Health and Nutrition Examination Survey (NHANES III) follow-up cohort of US adults. Subjects Nationally representative sample of US adults in NHANES (n 13 489). Results After adjusting for potential confounders, Mg intake was associated with approximately 30 % reduced odds of fatty liver disease and prediabetes, comparing the highest intake quartile v. the lowest. Mg intake may only be related to reduced odds of fatty liver disease and prediabetes in those whose Ca intake is less than 1200 mg/d. Mg intake may also only be associated with reduced odds of fatty liver disease among alcohol drinkers. Conclusions The study suggests that high intake of Mg may be associated with reduced risks of fatty liver disease and prediabetes. Further large studies, particularly prospective cohort studies, are warranted to confirm the findings