Non-alcoholic fatty liver disease overview: Difference between revisions
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{{Non alcoholic fatty liver disease}} | {{Non alcoholic fatty liver disease}} | ||
'''Editor in Chief''': Elliot Tapper, M.D., Beth Israel Deaconess Medical Center, [[User:C Michael Gibson |C. Michael Gibson, M.S., M.D.]] [mailto:charlesmichaelgibson@gmail.com] | '''Editor in Chief''': Elliot Tapper, M.D., Beth Israel Deaconess Medical Center, [[User:C Michael Gibson |C. Michael Gibson, M.S., M.D.]] [mailto:charlesmichaelgibson@gmail.com] | ||
==Overview== | ==Overview== | ||
'''Non-alcoholic fatty liver disease''' ('''[[NAFLD]]''') is a spectrum of [[liver]] disease in the absence of excessive [[alcoholism|alcohol]] use that begins as fatty accumulation in the liver (hepatic [[steatosis]]). A fatty liver does not necessarily disturb the function of the liver, but by varying mechanisms and insults, it may progress to [[inflammation]] of the liver. When inflammation occurs in this setting, the condition is then called NASH - '''[[Non-alcoholic steatohepatitis]]'''. NASH, in turn, may progress to fibrosis and, later, cirrhosis. Studies of serial liver biopsies estimate a 26-37% rate of hepatic fibrosis and 2-15% rate of cirrhosis in less than 6 years. <ref>Adams LA, Sanderson S, Lindor KD, et al. The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies. J Hepatol 2005;42(1):132–8.</ref><ref>Harrison SA, Torgerson S, Hayashi PH. The natural history of nonalcoholic fatty liver disease:a clinical histopathological study. Am J Gastroenterol 2003;98(9):2042–7.</ref><ref>Ekstedt M, Franzén LE, Mathiesen UL, et al. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology 2006;44:865-73.</ref> In 2001, NASH represented 2.9% of the indications of liver transplantation.<ref name=Charlton> Charlton M et al. Frequency of Nonalcoholic Steatohepatitis as a Cause of Advanced Liver Disease. Liver Transpl 2001;7:608-614</ref> The impact of NAFLD is manifest at each step along the spectrum of the diease. Studies in the United States and Sweden have revealed that both simple steatosis as well as steatohepatitis significantly reduce life expectancy, even when the diagnosis is made in children.<ref>Adams et al. The Natural History of Nonalcoholic Fatty Liver Disease: A Population-Based Cohort Study. GASTROENTEROLOGY 2005;129:113–121</ref><ref>Feldstein AE et al. The natural history of non-alcoholic fatty liver disease in children: a follow-up study for up to 20 years. Gut 2009;58:1538–1544</ref> | '''Non-alcoholic fatty liver disease''' ('''[[NAFLD]]''') is a spectrum of [[liver]] disease in the absence of excessive [[alcoholism|alcohol]] use that begins as fatty accumulation in the liver (hepatic [[steatosis]]). A fatty liver does not necessarily disturb the function of the liver, but by varying mechanisms and insults, it may progress to [[inflammation]] of the liver. When inflammation occurs in this setting, the condition is then called NASH - '''[[Non-alcoholic steatohepatitis]]'''. NASH, in turn, may progress to fibrosis and, later, cirrhosis. Studies of serial liver biopsies estimate a 26-37% rate of hepatic fibrosis and 2-15% rate of cirrhosis in less than 6 years. <ref>Adams LA, Sanderson S, Lindor KD, et al. The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies. J Hepatol 2005;42(1):132–8.</ref><ref>Harrison SA, Torgerson S, Hayashi PH. The natural history of nonalcoholic fatty liver disease:a clinical histopathological study. Am J Gastroenterol 2003;98(9):2042–7.</ref><ref>Ekstedt M, Franzén LE, Mathiesen UL, et al. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology 2006;44:865-73.</ref> In 2001, NASH represented 2.9% of the indications of liver transplantation.<ref name=Charlton> Charlton M et al. Frequency of Nonalcoholic Steatohepatitis as a Cause of Advanced Liver Disease. Liver Transpl 2001;7:608-614</ref> The impact of NAFLD is manifest at each step along the spectrum of the diease. Studies in the United States and Sweden have revealed that both simple steatosis as well as steatohepatitis significantly reduce life expectancy, even when the diagnosis is made in children.<ref>Adams et al. The Natural History of Nonalcoholic Fatty Liver Disease: A Population-Based Cohort Study. GASTROENTEROLOGY 2005;129:113–121</ref><ref>Feldstein AE et al. The natural history of non-alcoholic fatty liver disease in children: a follow-up study for up to 20 years. Gut 2009;58:1538–1544</ref> | ||
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Editor in Chief: Elliot Tapper, M.D., Beth Israel Deaconess Medical Center, C. Michael Gibson, M.S., M.D. [1]
Overview
Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver disease in the absence of excessive alcohol use that begins as fatty accumulation in the liver (hepatic steatosis). A fatty liver does not necessarily disturb the function of the liver, but by varying mechanisms and insults, it may progress to inflammation of the liver. When inflammation occurs in this setting, the condition is then called NASH - Non-alcoholic steatohepatitis. NASH, in turn, may progress to fibrosis and, later, cirrhosis. Studies of serial liver biopsies estimate a 26-37% rate of hepatic fibrosis and 2-15% rate of cirrhosis in less than 6 years. [1][2][3] In 2001, NASH represented 2.9% of the indications of liver transplantation.[4] The impact of NAFLD is manifest at each step along the spectrum of the diease. Studies in the United States and Sweden have revealed that both simple steatosis as well as steatohepatitis significantly reduce life expectancy, even when the diagnosis is made in children.[5][6]
NAFLD/NASH was first described in a 1980 series of obese, non-alcoholic patients of the Mayo Clinic.[7] Since that seminal description, our understanding of NAFLD has progressed minimally. [8] The disease is most closely associated with the increasing obesity, insulin resistance, type two diabetes mellitus and hyperlipedmia endemic to the developed world. Roughly half of all patients with NAFLD, however, do not meet criteria for metabolic syndrome. [9]
References
- ↑ Adams LA, Sanderson S, Lindor KD, et al. The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies. J Hepatol 2005;42(1):132–8.
- ↑ Harrison SA, Torgerson S, Hayashi PH. The natural history of nonalcoholic fatty liver disease:a clinical histopathological study. Am J Gastroenterol 2003;98(9):2042–7.
- ↑ Ekstedt M, Franzén LE, Mathiesen UL, et al. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology 2006;44:865-73.
- ↑ Charlton M et al. Frequency of Nonalcoholic Steatohepatitis as a Cause of Advanced Liver Disease. Liver Transpl 2001;7:608-614
- ↑ Adams et al. The Natural History of Nonalcoholic Fatty Liver Disease: A Population-Based Cohort Study. GASTROENTEROLOGY 2005;129:113–121
- ↑ Feldstein AE et al. The natural history of non-alcoholic fatty liver disease in children: a follow-up study for up to 20 years. Gut 2009;58:1538–1544
- ↑ Ludwig J, Viggiano TR, McGill DB, Oh BJ. Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo Clin Proc. 1980;55:434-438. PMID 7382552.
- ↑ Day, CP. Non-alcoholic steatohepatitis (NASH): where are we now and where are we going? Gut. 2002 May; 50(5): 585–588.
- ↑ Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology. 2006;43:S99–S112.