الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Non-alcoholic fatty liver disease (NAFLD) covers a spectrum of disease states ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) to end-stage liver disease (ESLD). NAFLD is the most common form of chronic liver disease in the Western world and is increasing in importance in other parts of the world. The prevalence is expected to increase as the epidemics of obesity and diabetes evolve. New data suggest that the incidence of NAFLD is significant. The development of NAFLD is preceded by weight gain. There are differences in the prevalence of NAFLD according to age, gender, and race or ethnicity in the general population. The natural history of NAFLD depends on the histologic subtype. Those who have fatty liver or fatty liver-non specific inflammation (FL or FL-NI) generally have a benign long-term prognosis, whereas those who have NASH can progress to cirrhosis. NASH-related cirrhosis may have a similar prognosis as cirrhosis from other causes. HCC is part of the spectrum of NAFLD, and screening for HCC seems reasonable in patients who have NASH-related cirrhosis. There are many risk factors associated with NAFLD. Medications, surgical procedures, and total parenteral nutrition can lead to fatty liver disease and are classified by some experts as secondary causes of NAFLD. Primary NAFLD comprises those persons who have NAFLD associated with the metabolic syndrome or insulin resistance. NAFLD is considered to be the hepatic manifestation of the metabolic syndrome. Many patients who have NAFLD fulfill criteria for the metabolic syndrome. The traditional ‘2-hit’ hypothesis of NAFLD pathogenesis has been modified several times; in most patients however NAFLD does appear to begin with lipid accumulation, or steatosis, which is in turn driven by obesity and IR. Progression to steatohepatitis and fibrosis depends on additional factors such as FFAs, inflammatory cytokines and adipokines, oxidative stress and mitochondrial dysfunction in a complex interplay with genetic predisposition. Aim of study: This review discussed NAFLD and NASH covering the epidemiology, pathogenesis, clinical implications and focuses on a number of novel molecular targets for the treatment of NASH, as well as the evidence for currently available therapy. Conclusion: NAFLD is now acknowledged to be the commonest liver condition in the western world, largely because of the considerable increase in metabolic diseases such as obesity and diabetes. NAFLD leads to liver related morbidity and mortality in a subset of people, particularly those who are obese, diabetic, and who have NASH. Treatment of NAFLD should begin with screening and managing metabolic risk factors that may modify the risk of liver disease. First line treatment should consist of lifestyle change with weight loss and exercise to improve insulin sensitivity. However, because of long term compliance difficulties, pharmaceutical agents aimed at reducing insulin resistance or protecting the liver from additional insults are needed.