View source for Medicine:Fatty liver

{{Infobox medical condition (new)
| name           = Fatty liver
| synonyms       = Fatty liver disease (FLD), hepatic steatosis, simple steatosis
| image          = Non-alcoholic_fatty_liver_disease1.jpg
| caption        = [[Micrograph]] showing a fatty liver (macrovesicular steatosis), as seen in [[Medicine:Non-alcoholic fatty liver disease|non-alcoholic fatty liver disease]]. Trichrome stain.
| field          = [[Medicine:Gastroenterology|Gastroenterology]]
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'''Fatty [[Biology:Liver|liver]]''', or hepatic steatosis or simple steatosis, is a reversible condition wherein large [[Biology:Vacuole|vacuole]]s of [[Chemistry:Triglyceride|triglyceride]] fat accumulate in [[Biology:Hepatocyte|liver cells]] via the process of [[Medicine:Steatosis|steatosis]] (i.e., abnormal retention of [[Chemistry:Lipid|lipid]]s within a cell). Despite having multiple causes, fatty [[Biology:Liver|liver]] can be considered a single [[Disease|disease]] that occurs worldwide in those with excessive [[Chemistry:Alcohol|alcohol]] intake and the obese (with or without effects of insulin resistance). The condition is also associated with other diseases that influence fat [[Biology:Metabolism|metabolism]].<ref name="Reddy_2006">{{cite journal | vauthors = Reddy JK, Rao MS | title = Lipid metabolism and liver inflammation. II. Fatty liver disease and fatty acid oxidation | journal = American Journal of Physiology. Gastrointestinal and Liver Physiology | volume = 290 | issue = 5 | pages = G852-8 | date = May 2006 | pmid = 16603729 | doi = 10.1152/ajpgi.00521.2005 }}</ref> When this process of fat metabolism is disrupted, the fat can accumulate in the liver in excessive amounts, thus resulting in a fatty liver.<ref>{{cite web|last1=Cutler|first1=Nicole | name-list-format = vanc |url=http://www.liversupport.com/fattyliver.htm |title=Symptoms of Fatty Liver|access-date=18 November 2014}}</ref> It is difficult to distinguish alcoholic FLD, which is part of [[Medicine:Alcoholic liver disease|alcoholic liver disease]], from nonalcoholic FLD (NAFLD), and both show microvesicular and macrovesicular fatty changes at different stages.

The accumulation of fat in alcoholic or non-alcoholic steatosis may also be accompanied by a progressive inflammation of the liver ([[Medicine:Hepatitis|hepatitis]]), called [[Medicine:Steatohepatitis|steatohepatitis]]. This more severe condition may be termed either alcoholic steatohepatitis or non-alcoholic steatohepatitis (NASH).

==Signs and symptoms==
===Complications===
Fatty liver can develop into a fibrosis or a liver cancer.<ref name="AASLD2018">{{cite journal |last1=Chalasani |first1=Naga |last2=Younossi |first2=Zobair |last3=Lavine |first3=Joel E. |last4=Charlton |first4=Michael |last5=Cusi |first5=Kenneth |last6=Rinella |first6=Mary |last7=Harrison |first7=Stephen A. |last8=Brunt |first8=Elizabeth M. |last9=Sanyal |first9=Arun J. |title=The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases |journal=Hepatology |date=January 2018 |volume=67 |issue=1 |pages=328–357 |doi=10.1002/hep.29367}}</ref> For people affected by NAFLD, the 10-year survival rate was about 80%. The rate of progression of fibrosis in NASH is estimated to one per 7 years and 14 years for NAFLD, with an increasing speed.<ref>{{cite journal |last1=Singh |first1=Siddharth |last2=Allen |first2=Alina M. |last3=Wang |first3=Zhen |last4=Prokop |first4=Larry J. |last5=Murad |first5=Mohammad H. |last6=Loomba |first6=Rohit |title=Fibrosis Progression in Nonalcoholic Fatty Liver vs Nonalcoholic Steatohepatitis: A Systematic Review and Meta-analysis of Paired-Biopsy Studies |journal=Clinical Gastroenterology and Hepatology |date=April 2015 |volume=13 |issue=4 |pages=643–654.e9 |doi=10.1016/j.cgh.2014.04.014|pmc=4208976 }}</ref><ref name=Younossi2017>{{cite journal |last1=Younossi |first1=Zobair |last2=Anstee |first2=Quentin M. |last3=Marietti |first3=Milena |last4=Hardy |first4=Timothy |last5=Henry |first5=Linda |last6=Eslam |first6=Mohammed |last7=George |first7=Jacob |last8=Bugianesi |first8=Elisabetta |title=Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention |journal=Nature Reviews Gastroenterology & Hepatology |date=20 September 2017 |volume=15 |issue=1 |pages=11–20 |doi=10.1038/nrgastro.2017.109}}</ref> There is a strong relationship between these pathologies and metabolic illnesses (diabetes type II, metabolic syndrome). These pathologies can also affect non-obese people, who are then at a higher risk.<ref name="AASLD2018" />

Less than 10% of people with cirrhotic alcoholic FLD will develop [[Medicine:Hepatocellular carcinoma|hepatocellular carcinoma]],<ref name = "Qian_2005">{{cite journal | vauthors = Qian Y, Fan JG | title = Obesity, fatty liver and liver cancer | journal = Hepatobiliary & Pancreatic Diseases International | volume = 4 | issue = 2 | pages = 173–7 | date = May 2005 | pmid = 15908310 }}</ref> the liver cancer, but up to 45% people with NASH without cirrhosis can develop hepatocellular carcinoma.<ref>{{cite journal |last1=Bellentani |first1=Stefano |title=The epidemiology of non-alcoholic fatty liver disease |journal=Liver International |date=January 2017 |volume=37 |pages=81–84 |doi=10.1111/liv.13299}}</ref>

==Causes==
[[Image:Stage of liver damage.JPG|thumb|Different stages of liver damage]]
Fatty liver (FL) is commonly associated with [[Medicine:Metabolic syndrome|metabolic syndrome]] ([[Medicine:Diabetes|diabetes]], [[Medicine:Hypertension|hypertension]], obesity, and dyslipidemia), but can also be due to any one of many causes:<ref name="Angulo_2002"/><ref name="Bayard_2006"/>
;Metabolic: [[Medicine:Abetalipoproteinemia|abetalipoproteinemia]], [[Medicine:Glycogen storage disease|glycogen storage disease]]s, Weber–Christian disease,  [[Medicine:Acute fatty liver of pregnancy|acute fatty liver of pregnancy]], lipodystrophy
;Nutritional: obesity, [[Medicine:Malnutrition|malnutrition]], total parenteral nutrition, severe weight loss, [[Medicine:Refeeding syndrome|refeeding syndrome]], jejunoileal bypass, gastric bypass, jejunal [[Medicine:Diverticulosis|diverticulosis]] with bacterial overgrowth
;Drugs and toxins: [[Chemistry:Amiodarone|amiodarone]], [[Chemistry:Methotrexate|methotrexate]], [[Chemistry:Diltiazem|diltiazem]], expired [[Chemistry:Tetracycline|tetracycline]], highly active antiretroviral therapy, glucocorticoids, [[Chemistry:Tamoxifen|tamoxifen]],<ref name = "Osman_2007" >{{cite journal | vauthors = Osman KA, Osman MM, Ahmed MH | title = Tamoxifen-induced non-alcoholic steatohepatitis: where are we now and where are we going? | journal = Expert Opinion on Drug Safety | volume = 6 | issue = 1 | pages = 1–4 | date = January 2007 | pmid = 17181445 | doi = 10.1517/14740338.6.1.1 }}</ref> environmental [[Chemistry:Hepatotoxin|hepatotoxin]]s (e.g., [[Chemistry:Phosphorus|phosphorus]], [[Medicine:Mushroom poisoning|mushroom poisoning]])
;Alcohol: Alcoholism is one of the causes of fatty liver due to production of toxic metabolites like aldehydes during metabolism of alcohol in the liver. This phenomenon most commonly occurs with chronic alcoholism.
;Other: celiac disease,<ref name="Marciano_2016">{{cite journal | vauthors = Marciano F, Savoia M, Vajro P | title = Celiac disease-related hepatic injury: Insights into associated conditions and underlying pathomechanisms | journal = Digestive and Liver Disease | volume = 48 | issue = 2 | pages = 112–9 | date = February 2016 | pmid = 26711682 | doi = 10.1016/j.dld.2015.11.013 }}</ref> [[Medicine:Inflammatory bowel disease|inflammatory bowel disease]], [[Biology:HIV|HIV]], hepatitis C (especially genotype 3), and alpha 1-antitrypsin deficiency<ref name = "Valenti_2006">{{cite journal | vauthors = Valenti L, Dongiovanni P, Piperno A, Fracanzani AL, Maggioni M, Rametta R, Loria P, Casiraghi MA, Suigo E, Ceriani R, Remondini E, Trombini P, Fargion S | title = Alpha 1-antitrypsin mutations in NAFLD: high prevalence and association with altered iron metabolism but not with liver damage | journal = Hepatology | volume = 44 | issue = 4 | pages = 857–64 | date = October 2006 | pmid = 17006922 | doi = 10.1002/hep.21329 }}</ref>

==Pathology==
[[Image:Periportal hepatosteatosis intermed mag.jpg|thumb|right|[[Micrograph|Micrograph]] of periportal hepatic steatosis, as may be seen due to steroid use, trichrome stain]]
Fatty change represents the [[Biology:Cytoplasm|intracytoplasmatic]] accumulation of triglycerides (neutral fats). At the beginning, the hepatocytes present small fat vacuoles (liposomes) around the [[Biology:Cell nucleus|nucleus]] (microvesicular fatty change). In this stage, liver cells are filled with multiple fat droplets that do not displace the centrally located nucleus. In the late stages, the size of the vacuoles increases, pushing the nucleus to the periphery of the cell, giving characteristic signet ring appearance (macrovesicular fatty change). These vesicles are well-delineated and optically "empty" because fats dissolve during tissue processing. Large vacuoles may coalesce and produce fatty cysts, which are irreversible lesions. Macrovesicular [[Medicine:Steatosis|steatosis]] is the most common form and is typically associated with [[Chemistry:Alcohol|alcohol]], [[Medicine:Diabetes|diabetes]], obesity, and corticosteroids. [[Medicine:Acute fatty liver of pregnancy|Acute fatty liver of pregnancy]] and Reye's syndrome are examples of severe liver disease caused by microvesicular fatty change.<ref>{{cite book | last = Goldman | first = Lee | name-list-format = vanc | title = Cecil Textbook of Medicine – 2-Volume Set, Text with Continually Updated Online Reference | publisher = W.B. Saunders Company | location = Philadelphia | year = 2003 | isbn = 978-0-7216-4563-6 }}{{page needed|date=May 2018}}</ref> The diagnosis of steatosis is made when fat in the liver exceeds 5–10% by weight.<ref name="Reddy_2006"/><ref name="Adams_2005">{{cite journal | vauthors = Adams LA, Lymp JF, St Sauver J, Sanderson SO, Lindor KD, Feldstein A, Angulo P | title = The natural history of nonalcoholic fatty liver disease: a population-based cohort study | journal = Gastroenterology | volume = 129 | issue = 1 | pages = 113–21 | date = July 2005 | pmid = 16012941 | doi = 10.1053/j.gastro.2005.04.014 }}</ref><ref name="Crabb_2004">{{cite journal | vauthors = Crabb DW, Galli A, Fischer M, You M | title = Molecular mechanisms of alcoholic fatty liver: role of peroxisome proliferator-activated receptor alpha | journal = Alcohol | volume = 34 | issue = 1 | pages = 35–8 | date = August 2004 | pmid = 15670663 | doi = 10.1016/j.alcohol.2004.07.005 }}</ref>

[[Image:Steatosis.jpg|thumb|left|Mechanism leading to hepatic steatosis]]
Defects in [[Biology:Fatty acid metabolism|fatty acid metabolism]] are responsible for [[Medicine:Pathogenesis|pathogenesis]] of FLD, which may be due to imbalance in energy consumption and  its combustion,  resulting in lipid storage, or can be a consequence of peripheral resistance to insulin, whereby the transport of fatty acids from adipose tissue to the liver is increased.<ref name="Reddy_2006"/><ref name = "Medina_2004">{{cite journal | vauthors = Medina J, Fernández-Salazar LI, García-Buey L, Moreno-Otero R | title = Approach to the pathogenesis and treatment of nonalcoholic steatohepatitis | journal = Diabetes Care | volume = 27 | issue = 8 | pages = 2057–66 | date = August 2004 | pmid = 15277442 | doi = 10.2337/diacare.27.8.2057 }}</ref>
Impairment or inhibition of receptor molecules ([[Biology:Peroxisome proliferator-activated receptor|PPAR-α]], [[Biology:Peroxisome proliferator-activated receptor|PPAR-γ]] and SREBP1) that control the enzymes responsible for the oxidation and synthesis of fatty acids appears to contribute to fat accumulation. In addition, alcoholism is known to damage mitochondria and other cellular structures, further impairing cellular energy mechanism. On the other hand, non-alcoholic FLD may begin as excess of unmetabolised energy in liver cells. Hepatic steatosis is considered reversible and to some extent nonprogressive if the underlying cause is reduced or removed.

[[Image:Steatohepatitis high mag.jpg|thumb|right|Micrograph of inflamed fatty liver (steatohepatitis)]]
Severe fatty liver is sometimes accompanied by [[Medicine:Inflammation|inflammation]], a situation referred to as [[Medicine:Steatohepatitis|steatohepatitis]]. Progression to alcoholic steatohepatitis (ASH) or non-alcoholic steatohepatitis (NASH) depends on the persistence or severity of the inciting cause. Pathological lesions in both conditions are similar. However, the extent of inflammatory response varies widely and does not always correlate with degree of fat accumulation. Steatosis (retention of [[Chemistry:Lipid|lipid]]) and onset of steatohepatitis may represent successive stages in FLD progression.<ref name="Day_1998">{{cite journal | vauthors = Day CP, James OF | title = Steatohepatitis: a tale of two "hits"? | journal = Gastroenterology | volume = 114 | issue = 4 | pages = 842–5 | date = April 1998 | pmid = 9547102 | doi = 10.1016/S0016-5085(98)70599-2 }}</ref>

Liver disease with extensive inflammation and a high degree of steatosis often progresses to more severe forms of the disease.<ref name="Gramlich_2004">{{cite journal | vauthors = Gramlich T, Kleiner DE, McCullough AJ, Matteoni CA, Boparai N, Younossi ZM | title = Pathologic features associated with fibrosis in nonalcoholic fatty liver disease | journal = Human Pathology | volume = 35 | issue = 2 | pages = 196–9 | date = February 2004 | pmid = 14991537 | doi = 10.1016/j.humpath.2003.09.018 }}</ref> [[Biology:Hepatocyte|Hepatocyte]] ballooning and [[Biology:Necrosis|necrosis]] of varying degrees are often present at this stage. Liver cell death and inflammatory responses lead to the activation of [[Biology:Hepatic stellate cell|hepatic stellate cell]]s, which play a pivotal role in hepatic [[Medicine:Fibrosis|fibrosis]]. The extent of fibrosis varies widely. [[Biology:Sinusoid (blood vessel)|Perisinusoidal]] fibrosis is most common, especially in adults, and predominates in zone 3 around the terminal hepatic veins.<ref name= "Zafrani _2004">{{cite journal | vauthors = Zafrani ES | title = Non-alcoholic fatty liver disease: an emerging pathological spectrum | journal = Virchows Archiv | volume = 444 | issue = 1 | pages = 3–12 | date = January 2004 | pmid = 14685853 | doi = 10.1007/s00428-003-0943-7 }}</ref>

The progression to cirrhosis may be influenced by the amount of fat and degree of steatohepatitis and by a variety of other sensitizing factors. In alcoholic FLD, the transition to cirrhosis related to continued alcohol consumption is well-documented, but the process involved in non-alcoholic FLD is less clear.

==Diagnosis==
[[File:Liversteatosis.png|thumb|Liver steatosis (fatty liver disease) as seen on CT]]
[[File:Steatosis hepatis - Sonographie 001.jpg|thumb|Ultrasound showing diffuse increased echogenicity of the liver.]]
{|align="centre"
|-Elevated liver enzyme
!align="center"|Flow chart for diagnosis, modified from<ref name="Bayard_2006">{{cite journal | vauthors = Bayard M, Holt J, Boroughs E | title = Nonalcoholic fatty liver disease | journal = American Family Physician | volume = 73 | issue = 11 | pages = 1961–8 | date = June 2006 | pmid = 16770927 }}</ref>
|-
|{{familytree/start}}
{{familytree |border=1|boxstyle=background:#dfd; | | | | A01| | | |A01=Elevated liver enzyme}}
{{familytree |border=1|boxstyle=background:#dfd; | | | | |!| | | | |}}
{{familytree |border=1|boxstyle=background:#dfd; | | | | B01| | | |B01=Serology to exclude viral hepatitis}}
{{familytree |border=1|boxstyle=background:#dfd; | | | | |!| | | | |}}
{{familytree |border=1|boxstyle=background:#dfd; | | | | C01| | | |C01=Imaging study showing<br />fatty infiltrate}}
{{familytree |border=1|boxstyle=background:#dfd; | | | | |!| | | | |}}
{{familytree |border=1|boxstyle=background:#dfd; | | | | D01| | | |D01=Alcohol intake}}
{{familytree |border=1|boxstyle=background:#dfd; | | |,|-|^|-|.| | |}}
{{familytree |border=1|boxstyle=background:#dfd; | |E01| |E02| | |E01=Less than two drinks per day‡|E02=More than two drinks per day‡}}
{{familytree |border=1|boxstyle=background:#dfd; | | |!| | | |!| | |}}
{{familytree |border=1|boxstyle=background:#dfd; | |F01| |F02| | |F01=Nonalcoholic fatty liver disease likely|F02=Alcoholic liver disease likely}}
{{familytree/end}}
|-
|align="center"|‡ <small>Criteria for nonalcoholic fatty liver disease:<br /> consumption of ethanol less than 20&nbsp;g/day for women and 30&nbsp;g/day for men<ref name="Adams _2005">{{cite journal | vauthors = Adams LA, Angulo P, Lindor KD | title = Nonalcoholic fatty liver disease | journal = CMAJ | volume = 172 | issue = 7 | pages = 899–905 | date = March 2005 | pmid = 15795412 | pmc = 554876 | doi = 10.1503/cmaj.045232 }}</ref></small>
|}

Most individuals are asymptomatic and are usually discovered incidentally because of abnormal liver function tests or hepatomegaly noted in unrelated medical conditions. Elevated liver biochemistry is found in 50% of patients with simple steatosis.<ref>{{cite book | last = Sleisenger | first = Marvin | name-list-format = vanc | title = Sleisenger and Fordtran's Gastrointestinal and Liver Disease | publisher = W.B. Saunders Company | location = Philadelphia | year = 2006 | isbn = 978-1-4160-0245-1 }}{{page needed|date=May 2018}}</ref> The serum [[Biology:Alanine transaminase|alanine transaminase]] level usually is greater than the [[Biology:Aspartate transaminase|aspartate transaminase]] level in the nonalcoholic variant and the opposite in alcoholic FLD (AST:ALT more than 2:1).

Imaging studies are often obtained during the evaluation process. Ultrasonography reveals a "bright" liver with increased [[Physics:Echogenicity|echogenicity]]. [[Medicine:Medical imaging|Medical imaging]] can aid in diagnosis of fatty liver; fatty livers have lower [[Physics:Density|density]] than [[Biology:Spleen|spleen]]s on computed tomography (CT), and fat appears bright in [[Physics:Relaxation (NMR)|T1-weighted]] [[Physics:Magnetic resonance imaging|magnetic resonance images]] (MRIs). [[Physics:Magnetic resonance elastography|Magnetic resonance elastography]], a variant of magnetic resonance imaging, is investigated as a non-invasive method to diagnose fibrosis progression.<ref>{{cite journal |last1=Singh |first1=Siddharth |last2=Venkatesh |first2=Sudhakar K. |last3=Loomba |first3=Rohit |last4=Wang |first4=Zhen |last5=Sirlin |first5=Claude |last6=Chen |first6=Jun |last7=Yin |first7=Meng |last8=Miller |first8=Frank H. |last9=Low |first9=Russell N. |last10=Hassanein |first10=Tarek |last11=Godfrey |first11=Edmund M. |last12=Asbach |first12=Patrick |last13=Murad |first13=Mohammad Hassan |last14=Lomas |first14=David J. |last15=Talwalkar |first15=Jayant A. |last16=Ehman |first16=Richard L. |title=Magnetic resonance elastography for staging liver fibrosis in non-alcoholic fatty liver disease: a diagnostic accuracy systematic review and individual participant data pooled analysis |journal=European Radiology |date=28 August 2015 |volume=26 |issue=5 |pages=1431–1440 |doi=10.1007/s00330-015-3949-z}}</ref> [[Biology:Histology|Histological]] diagnosis by [[Medicine:Liver biopsy|liver biopsy]] is the most accurate measure of fibrosis and liver fat progression as of 2018.<ref name="AASLD2018" />

==Treatment==
The treatment of fatty liver depends on its cause, and, in general, treating the underlying cause will reverse the process of steatosis if implemented at an early stage. Fatty liver can be caused by different factors that are not all identified. However, two known causes of fatty liver disease are an excess consumption of alcohol and a prolonged diet with a high proportion of calories coming from carbohydrates. For people with NAFLD or NASH, weight loss via a combination of diet and exercise was shown to improve or resolve the disease.<ref name="AASLD2018" /> In more serious cases, medications that decrease insulin resistance, hyperlipidemia, and those that induce weight loss such as bariatric surgery as well as Vitamin E have been shown to improve or resolve liver function.<ref name="AASLD2018" /><ref name="Bayard_2006"/>

Bariatric surgery, while not recommended in 2017 as a treatment for fatty liver disease (FLD) alone, has been shown to revert FLD, NAFLD, NASH and advanced [[Medicine:Steatohepatitis|steatohepatitis]] in over 90% of people who have undergone this surgery for the treatment of obesity.<ref name="AASLD2018" /><ref>{{Cite journal|date=2017-01-25|title=Fatty Liver: Overview, Pathophysiology, Etiology|url=http://emedicine.medscape.com/article/175472-overview#a12}}</ref>

In the case of long-term total parenteral nutrition induced fatty liver disease, [[Chemistry:Choline|choline]] has been shown to alleviate symptoms.<ref name="Buchman_1995">{{cite journal | vauthors = Buchman AL, Dubin MD, Moukarzel AA, Jenden DJ, Roch M, Rice KM, Gornbein J, Ament ME | title = Choline deficiency: a cause of hepatic steatosis during parenteral nutrition that can be reversed with intravenous choline supplementation | journal = Hepatology | volume = 22 | issue = 5 | pages = 1399–403 | date = November 1995 | pmid = 7590654 | doi = 10.1002/hep.1840220510 }}</ref><ref name="Buchman_1992">{{cite journal | vauthors = Buchman AL, Dubin M, Jenden D, Moukarzel A, Roch MH, Rice K, Gornbein J, Ament ME, Eckhert CD | title = Lecithin increases plasma free choline and decreases hepatic steatosis in long-term total parenteral nutrition patients | journal = Gastroenterology | volume = 102 | issue = 4 Pt 1 | pages = 1363–70 | date = April 1992 | pmid = 1551541 | doi = 10.1016/0016-5085(92)70034-9 }}</ref><ref name="Buchman_2016">{{cite journal | vauthors = Buchman AL, Ament ME, Sohel M, Dubin M, Jenden DJ, Roch M, Pownall H, Farley W, Awal M, Ahn C | title = Choline deficiency causes reversible hepatic abnormalities in patients receiving parenteral nutrition: proof of a human choline requirement: a placebo-controlled trial | journal = JPEN. Journal of Parenteral and Enteral Nutrition | volume = 25 | issue = 5 | pages = 260–8 | year = 2016 | pmid = 11531217 | doi = 10.1177/0148607101025005260 }}</ref> This may be due to a deficiency in the [[Biology:Methionine synthase|methionine cycle]].<ref>{{cite journal | vauthors = Hollenbeck CB | title = The importance of being choline | journal = Journal of the American Dietetic Association | volume = 110 | issue = 8 | pages = 1162–5 | date = August 2010 | pmid = 20656090 | doi = 10.1016/j.jada.2010.05.012 }}</ref>

==Epidemiology==
The prevalence of FLD in the general population ranges from 10% to 24% in various countries.<ref name="Angulo_2002"/> However, the NAFLD condition is observed in up to 80% of obese people, 35% of whom progress to NASH,<ref name="Hamaguchi_2005">{{cite journal | vauthors = Hamaguchi M, Kojima T, Takeda N, Nakagawa T, Taniguchi H, Fujii K, Omatsu T, Nakajima T, Sarui H, Shimazaki M, Kato T, Okuda J, Ida K | title = The metabolic syndrome as a predictor of nonalcoholic fatty liver disease | journal = Annals of Internal Medicine | volume = 143 | issue = 10 | pages = 722–8 | date = November 2005 | pmid = 16287793 | doi = 10.7326/0003-4819-143-10-200511150-00009 }}</ref> and in up to 20% of normal weight people,<ref name=Younossi2017 /> despite no evidence of excessive alcohol consumption. FLD is the most common cause of abnormal liver function tests in the {{wipe|United States}}.<ref name="Angulo_2002">{{cite journal | vauthors = Angulo P | title = Nonalcoholic fatty liver disease | journal = The New England Journal of Medicine | volume = 346 | issue = 16 | pages = 1221–31 | date = April 2002 | pmid = 11961152 | doi = 10.1056/NEJMra011775 }}</ref> Fatty liver is more prevalent in hispanic people than white, with black people having the lowest susceptibility.<ref name=Younossi2017 />

== See also ==
{{Columns-list|colwidth=30em|
*[[Medicine:Steatosis|Steatosis]]
*[[Medicine:Steatohepatitis|Steatohepatitis]]
*[[Medicine:Alcoholic liver disease|Alcoholic liver disease]]
*[[Medicine:Non-alcoholic fatty liver disease|Non-alcoholic fatty liver disease]]
*[[Medicine:Metabolic syndrome|Metabolic syndrome]]
*[[Medicine:Cirrhosis|Cirrhosis]]
*Focal fatty liver
*[[Medicine:Acute fatty liver of pregnancy|Acute fatty liver of pregnancy]]
*Feline hepatic lipidosis
*Foie gras
}}

== References ==
{{Reflist|32em}}

== External links ==
{{Medical resources
 | DiseasesDB     = 18844
 | ICD10          = {{ICD10|K|70||k|70}}, {{ICD10|K|76|0|k|70}}
 | ICD9           = {{ICD9|571.0}}, {{ICD9|571.8}}
 | ICDO           = 
 | OMIM           = 
 | MedlinePlus    = 
 | eMedicineSubj  = med
 | eMedicineTopic = 775
 | eMedicine_mult = {{eMedicine2|article|170409}}
 | MeshName       = Fatty+Liver
 | MeshNumber     = C06.552.241
}}
* [http://www.aasld.org American Association for the Study of Liver Diseases]
* [http://www.liverfoundation.org American Liver Foundation]
* [http://www.liver.ca/liver-disease/types/fatty-liver.aspx Fatty Liver Disease], Canadian Liver Foundation
* {{Chorus|00474}}
* Photo at [http://www.pathologyatlas.ro/fatty-change-liver-steatosis-pathology.php Atlas of Pathology]
* [http://www.healthdirect.gov.au/fatty-liver Healthdirect] 
{{Gastroenterology}}

{{DEFAULTSORT:Fatty Liver}}
[[Category:Histopathology]]

no:Steatose
pl:Alkoholowe stłuszczenie wątroby

{{Sourceattribution|Fatty liver|1}}