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Definitions & epidemiology

Definitions & epidemiology. NAFLD, NAFL, NASH?. Notes. References. NAFLD or alcoholic liver disease?. Exclusion of secondary causes of hepatic fat accumulation Absence of significant alcohol consumption

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Definitions & epidemiology

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  1. Definitions & epidemiology

  2. NAFLD, NAFL, NASH? Notes References

  3. NAFLD or alcoholic liver disease? • Exclusion of secondary causes of hepatic fat accumulation • Absence of significant alcohol consumption daily consumption ≥30 g for men and ≥20 g for women, or >21 standard drinks on average per week in men and >14 in women • Moderate amounts of alcohol + metabolic risk factors may predispose to NAFLD References

  4. Prevalence of NAFLD:25% of the global adult population • Increasing worldwide • 25% of the global adult population • Driven mainly by unhealthy lifestyles, obesity and diet Liver failure Hepatocellular carcinoma Cirrhosis NAFLD, 25% 25% 25% ?% NASH Stage 4 hepatic fibrosis with or without fat and inflammation Type 2 diabetes, Western diet and other factors Fat, hepatocyte ballooning, inflammation with or without fibrosis Fat, ballooning, inflammation, scarring and mutation (non-cirrhotic HCC in rare cases) No NAFLD, 75% ?% Progression: NAFLD: 1 stage fibrosis over 14 years; NASH: 1 stage fibrosis over 7 years References

  5. The globalisation of NAFLD Geographic variation in the daily energy availability per capita and in the prevalence of NAFLD References

  6. Prevalence of NASH increases with BMI in children and adolescents NAFLD prevalence by BMI population studies Across studies, prevalence of NAFLD increased considerably on average with increasing BMI category Prevalence of NAFLD among children and adolescents affects approximately 3% to 10% of all children and over one-third of obese children in developed countries Notes References

  7. NAFLD is largely driven by unhealthy lifestyles, ageing and genetics Visceral obesity and lipodystrophy-like phenotype Diabetes De-novo lipogenesis triglyceride synthesis Inflammation, fibrosis Fatty acids ceramides, cytokines, and dysregulated adipokines Insulin Gut dysbiosis Insulin resistance Genetics: PNPLA3, TM6SF2, MBOAT7 GCKR, and HSD17B13 DAMPs PAMPs SCFA, and ceramides Glucose DAMPs, damage-associated molecular patterns; GCKR, glucokinase regulator; HSD17B13, hydroxysteroid 17-beta dehydrogenase 13; MBOAT7, membrane-bound O-acyltransferase domain-containing 7; PAMPs, pathogen-associated molecular patterns; PNPLA3, patatin-like phospholipase domain-containing protein 3; SCFA, short-chain fatty acid; TM6SF2, transmembrane-6 superfamily member 2 Adapted from Stefan N et al. Lancet Diabetes Endocrinol2018; Aug 30 [Epub ahead of print]

  8. NASH: 261% increased risk of HCC*when compared to all other aetiologies of liver disease1 0.02 1 10 50 Heterogeneity τ² = 0.83; χ² = 130.68; df = 6 (P<0.00001), I² = 95% Test for overall effect: Z = 2.61 (P = 0.009) 0.1 Favours non-NASH Favours NASH NASH: the most common predisposing factor to HCC in the upcoming decades2 Notes References

  9. NASH: the most rapidly growing indication for liver transplantation Trends in liver transplantation for NASH and ALD between 2008 and 20142 Trends in liver transplantation by aetiology of liver disease1 HCV 1000 7000 2500 NASH ALD 950 HCV+ALD NASH: +50% 6000 2000 ALD: +42% 900 5000 HCV: +33% 850 1500 4000 Total annual liver transplant per etiology Total annual liver transplant surgeries ( ) 800 3000 NASH: +162% 1000 750 2000 ALD: +54% 500 700 1000 HCV+ALD: +17% 0 0 2011 2009 2012 2014 2008 2010 2013 2012 2014 2006 2011 2008 2013 2004 2010 2003 2005 2007 2009 Year Year By 2020, NASH is expected to be the leading cause of liver transplantation in the US3 References

  10. NAFLD is associated with a higher risk for CVD • Prevalence and incidence of CVD is higher in NAFLD than in matched controls and driven by the association between NAFLD and metabolic syndrome components • CVD is a more common cause of death than liver disease in NAFLD • Biochemical markers of atherosclerosis (low HDL cholesterol, high triacylglycerol) or inflammation (high-sensitive C reactive protein [CRP]) and increased levels of procoagulant/ prothrombotic factors are more common in NAFLD than in persons without steatosis • Pre-atherogenic lesions such as increased carotid intima-media thickness; coronary artery, abdominal aortic and aortic valve calcifications; endothelial dysfunction and functional unresponsiveness of the artery wall are more prevalent in NAFLD References

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