View source for Fatty liver disease

{{Short description|Medical condition where fat accumulates in the liver}}
{{Use dmy dates|date=December 2024}}
{{cs1 config |name-list-style=vanc |display-authors=6}}
{{Infobox medical condition (new)
| name           = Fatty liver
| synonyms       = Hepatic steatosis
| image          = Non-alcoholic_fatty_liver_disease1.jpg
| caption        = [[Micrograph]] showing a fatty liver ([[macrovesicular steatosis]]), as seen in [[metabolic dysfunction–associated steatotic liver disease]]. [[Trichrome staining|Trichrome stain]].
| field          = [[Gastroenterology]]
| symptoms        = None, tiredness, pain in the upper right side of the [[abdomen]]<ref name=NIH2016/><ref name=Sin2017/>
| complications   = [[Cirrhosis]], [[liver cancer]], [[esophageal varices]]<ref name=NIH2016/><ref name=Ant2019/>
| onset           =
| duration        =
| types           = [[Metabolic dysfunction–associated steatotic liver disease]] (MASLD), [[alcoholic liver disease]] (ALD)<ref name=NIH2016/>
| causes          = [[Ethanol|Alcohol]], [[diabetes]], [[obesity]]<ref name=Ant2019/><ref name=NIH2016/>
| risks           =
| diagnosis       = Based on the [[medical history]] supported by blood tests, [[medical imaging]], [[liver biopsy]]<ref name=NIH2016/>
| differential    = [[Viral hepatitis]], [[Wilson's disease]], [[primary sclerosing cholangitis]]<ref name=Ant2019/>
| prevention      =
| treatment       = Avoiding alcohol, weight loss<ref name=Ant2019/><ref name=NIH2016/>
| medication      =
| prognosis       = Good if treated early<ref name=Ant2019/>
| frequency       = NAFLD: 30% (Western countries)<ref name=Sin2017/><br />ALD: >90% of heavy drinkers<ref name=Bas2011/>
| deaths          =
}}
'''Fatty liver disease''' ('''FLD'''), also known as '''hepatic steatosis''' and '''steatotic liver disease''' ('''SLD'''), is a condition where excess [[fat]] builds up in the [[liver]].<ref name="NIH2016">{{Cite web |date=November 2016 |title=Nonalcoholic Fatty Liver Disease & NASH |url=https://www.niddk.nih.gov/health-information/liver-disease/nafld-nash/all-content |access-date=7 November 2018 |website=National Institute of Diabetes and Digestive and Kidney Diseases}}</ref> Often there are no or few symptoms.<ref name=NIH2016/><ref name=Sin2017/> Occasionally there may be tiredness or pain in the upper right side of the [[abdomen]].<ref name=NIH2016/> Complications may include [[cirrhosis]], [[liver cancer]], and [[esophageal varices]].<ref name=NIH2016/><ref name="Ant2019">{{Cite journal |last1=Antunes |first1=Catiele |last2=Azadfard |first2=Mohammadreza |last3=Hoilat |first3=Gilles J. |last4=Gupta |first4=Mohit |date=2022 |title=Fatty Liver |journal=StatPearls |publisher=StatPearls Publishing |pmid=28723021}}</ref>

The main subtypes of fatty liver disease are [[metabolic dysfunction–associated steatotic liver disease]] (MASLD) and [[alcoholic liver disease]] (ALD), with the category "metabolic and alcohol associated liver disease" (metALD) describing an overlap of the two.<ref name=":0">{{Cite journal |last1=Rinella |first1=Mary E. |last2=Lazarus |first2=Jeffrey V. |last3=Ratziu |first3=Vlad |last4=Francque |first4=Sven M. |last5=Sanyal |first5=Arun J. |last6=Kanwal |first6=Fasiha |last7=Romero |first7=Diana |last8=Abdelmalek |first8=Manal F. |last9=Anstee |first9=Quentin M. |last10=Arab |first10=Juan Pablo |last11=Arrese |first11=Marco |last12=Bataller |first12=Ramon |last13=Beuers |first13=Ulrich |last14=Boursier |first14=Jerome |last15=Bugianesi |first15=Elisabetta |date=2023 |title=A multi-society Delphi consensus statement on new fatty liver disease nomenclature |journal=Hepatology |language=en-US |volume=78 |issue=6 |pages=1966–1986 |doi=10.1097/HEP.0000000000000520 |issn=0270-9139 |pmc=10653297 |pmid=37363821 |s2cid=259260747 |doi-access=free |hdl-access=free |hdl=10807/245116}}</ref> 

Until June 2023, MASLD and its more advanced form, metabolic dysfunction associated steatohepatits (MASH), were referred to as non-alcoholic fatty liver disease (NALFD) and non-alcoholoc steatohepatitis (NASH), respectively.<ref>{{cite web |last1=DHANJAL |first1=Adonia |title=Multinational liver societies announce new "Fatty" liver disease nomenclature that is affirmative and non-stigmatising |url=https://easl.eu/news/new_fatty_liver_disease_nomenclature-2/ |website=EASL-The Home of Hepatology. |access-date=14 December 2025 |date=24 June 2023}}</ref>. The change in terminology was decided in a modified [[Delphi method|Delphi process]] led by three large pan-national liver associations (the [[American Association for the Study of Liver Diseases]], the [[European Association for the Study of the Liver]] and the Latin American Association for the Study of the Liver).<ref name=":0"></ref> 

The primary risks include [[ethanol|alcohol]], [[type 2 diabetes]], and [[obesity]].<ref name="NIH2016" /><ref name="Ant2019" /> Other risk factors include certain medications such as [[glucocorticoid]]s, and [[hepatitis C]].<ref name="NIH2016" /> It is unclear why some people with MASLD develop simple fatty liver and others develop metabolic dysfunction associated steatohepatitis (MASH), which is associated with poorer outcomes.<ref name="NIH2016" /> Diagnosis is based on the [[medical history]] supported by blood tests, [[medical imaging]], and occasionally [[liver biopsy]].<ref name="NIH2016" />

Treatment of MASLD is generally by dietary changes and exercise to bring about [[weight loss]].<ref name=NIH2016/> In those who are severely affected, [[liver transplantation]] may be an option.<ref name=NIH2016/> More than 90% of heavy drinkers develop fatty liver while about 25% develop the more severe [[alcoholic hepatitis]].<ref name="Bas2011">{{Cite journal |last=Basra |first=Sarpreet |date=2011 |title=Definition, epidemiology and magnitude of alcoholic hepatitis |journal=World Journal of Hepatology |volume=3 |issue=5 |pages=108–113 |doi=10.4254/wjh.v3.i5.108 |pmc=3124876 |pmid=21731902 |doi-access=free}}</ref> MASLD affects about 30% of people in Western countries and 10% of people in Asia.<ref name="Sin2017">{{Cite journal |last1=Singh |first1=S |last2=Osna |first2=NA |last3=Kharbanda |first3=KK |date=28 September 2017 |title=Treatment options for alcoholic and non-alcoholic fatty liver disease: A review. |journal=World Journal of Gastroenterology |volume=23 |issue=36 |pages=6549–6570 |doi=10.3748/wjg.v23.i36.6549 |pmc=5643281 |pmid=29085205 |doi-access=free}}</ref> MASLD affects about 10% of children in the United States.<ref name=NIH2016/> It occurs more often in older people and males.<ref name=Ant2019/><ref name="AFP2013">{{Cite journal |last1=Iser |first1=D |last2=Ryan |first2=M |date=July 2013 |title=Fatty liver disease—a practical guide for GPs. |journal=Australian Family Physician |volume=42 |issue=7 |pages=444–7 |pmid=23826593}}</ref>

== Classification ==
Until 2023, fatty liver disease was classified into:
* [[non-alcoholic fatty liver disease|Non-alcoholic fatty liver disease (NAFLD)]] made up of:<ref name="AFP2013" /><ref name="NIH2016" />
** [[Alcoholic liver disease|Non-alcoholic fatty liver (NAFL)]] or [[simple fatty liver]]
** [[non-alcoholic steatohepatitis|Non-alcoholic steatohepatitis (NASH)]]
* [[alcoholic liver disease|Alcoholic liver disease (ALD)]].<ref name="NIH2016" />
In 2023, a new nomenclature was chosen,<ref name=":0" /><ref>{{Cite web |title=A Liver Disease Gets a New Name, Diagnostic Criteria |url=http://www.medscape.com/viewarticle/994318 |access-date=2023-09-04 |website=[[Medscape]] |language=en}}</ref> with the classifications including:
* [[Metabolic dysfunction–associated steatotic liver disease]] (MASLD), including:
** [[Metabolic dysfunction-associated steatohepatitis]] (MASH)
* Metabolic and alcohol associated liver disease (metALD). Describes those with MASLD who consume greater amounts of alcohol per week but not enough to be categorized as ALD)
* [[Alcohol-associated liver disease]] (ALD)
* Specific aetiology SLD (including drug-induced, monogenic diseases and others)

==Signs and symptoms==
Often there are no or few symptoms.<ref name=NIH2016/> Occasionally there may be tiredness or pain in the upper right side of the abdomen.<ref name=NIH2016/>

===Complications===
Fatty liver can develop into hepatic fibrosis, cirrhosis or 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. |date=January 2018 |title=The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases |journal=Hepatology |volume=67 |issue=1 |pages=328–357 |doi=10.1002/hep.29367 |pmid=28714183 |doi-access=free |hdl-access=free |hdl=1805/14037}}</ref> For people affected by MASLD, the 10-year survival rate was about 80%. The rate of progression of fibrosis is estimated to be one per 7 years in MASH and one per 14 years in MASLD, 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 |date=April 2015 |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 |volume=13 |issue=4 |pages=643–654.e9 |doi=10.1016/j.cgh.2014.04.014 |pmc=4208976 |pmid=24768810}}</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 |date=20 September 2017 |title=Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention |journal=Nature Reviews Gastroenterology & Hepatology |volume=15 |issue=1 |pages=11–20 |doi=10.1038/nrgastro.2017.109 |pmid=28930295 |s2cid=31345431 |hdl-access=free |hdl=2318/1659230}}</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 [[hepatocellular carcinoma]],<ref name="Qian_2005">{{Cite journal |vauthors=Qian Y, Fan JG |date=May 2005 |title=Obesity, fatty liver and liver cancer |journal=Hepatobiliary & Pancreatic Diseases International |volume=4 |issue=2 |pages=173–7 |pmid=15908310}}</ref> the most common type of primary liver cancer in adults, but up to 45% people with MASH without cirrhosis can develop hepatocellular carcinoma.<ref>{{Cite journal |last=Bellentani |first=Stefano |date=January 2017 |title=The epidemiology of non-alcoholic fatty liver disease |journal=Liver International |volume=37 |pages=81–84 |doi=10.1111/liv.13299 |pmid=28052624 |doi-access=free}}</ref>

The condition is also associated with other diseases that influence fat [[metabolism]].<ref name="Reddy_2006">{{Cite journal |vauthors=Reddy JK, Rao MS |date=May 2006 |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 |doi=10.1152/ajpgi.00521.2005 |pmid=16603729}}</ref>

==Causes==
[[Image:Stage of liver damage.JPG|thumb|upright=1.4|Different stages of liver damage]]
Fatty liver (FL) is commonly associated with [[metabolic syndrome]] ([[diabetes]], [[hypertension]], [[obesity]], and [[dyslipidemia]]), but can also be due to any one of many causes:<ref name="Angulo_2002" /><ref name="Bayard_2006" />
;Alcohol: [[Alcohol use disorder]] 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 alcohol use disorder.
;Metabolic: [[abetalipoproteinemia]], [[glycogen storage disease]]s, [[Weber–Christian disease]],  [[acute fatty liver of pregnancy]], [[lipodystrophy]]
;Nutritional: [[obesity]], [[malnutrition]], [[total parenteral nutrition]], severe [[weight loss]], [[refeeding syndrome]], [[jejunoileal bypass]], [[gastric bypass]], jejunal [[diverticulosis]] with [[bacterial overgrowth]]
;Drugs and toxins: [[amiodarone]], [[methotrexate]], [[diltiazem]], expired [[tetracycline]], [[highly active antiretroviral therapy]], [[glucocorticoids]], [[tamoxifen]],<ref name="Osman_2007">{{Cite journal |vauthors=Osman KA, Osman MM, Ahmed MH |date=January 2007 |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 |doi=10.1517/14740338.6.1.1 |pmid=17181445 |s2cid=33505288}}</ref> environmental [[hepatotoxin]]s (e.g., [[phosphorus]], [[mushroom poisoning]])
;Other: [[celiac disease]],<ref name="Marciano_2016">{{Cite journal |vauthors=Marciano F, Savoia M, Vajro P |date=February 2016 |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 |doi=10.1016/j.dld.2015.11.013 |pmid=26711682}}</ref> [[inflammatory bowel disease]], [[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 |date=October 2006 |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 |doi=10.1002/hep.21329 |pmid=17006922 |s2cid=26068505 |doi-access=free|hdl=11380/304217 |hdl-access=free }}</ref>

==Pathology==
[[Image:Periportal hepatosteatosis intermed mag.jpg|thumb|right|[[Micrograph]] of [[liver lobule|periportal]] [[liver|hepatic]] steatosis, as may be seen due to [[steroid]] use, [[trichrome stain]]]]
The fatty change represents the [[cytoplasm|intracytoplasmatic]] accumulation of triglycerides (neutral fats). At the beginning, the hepatocytes present small fat vacuoles ([[liposomes]]) around the [[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 a 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 [[cyst]]s, which are irreversible lesions. Macrovesicular [[steatosis]] is the most common form and is typically associated with [[alcohol (drug)|alcohol]], diabetes, [[obesity]], and [[corticosteroids]]. 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 |title=Cecil Textbook of Medicine – 2-Volume Set, Text with Continually Updated Online Reference |publisher=W.B. Saunders Company |year=2003 |isbn=978-0-7216-4563-6 |location=Philadelphia}}{{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 |date=July 2005 |title=The natural history of nonalcoholic fatty liver disease: a population-based cohort study |journal=Gastroenterology |volume=129 |issue=1 |pages=113–21 |doi=10.1053/j.gastro.2005.04.014 |pmid=16012941 |doi-access=free}}</ref><ref name="Crabb_2004">{{Cite journal |vauthors=Crabb DW, Galli A, Fischer M, You M |date=August 2004 |title=Molecular mechanisms of alcoholic fatty liver: role of peroxisome proliferator-activated receptor alpha |journal=Alcohol |volume=34 |issue=1 |pages=35–8 |doi=10.1016/j.alcohol.2004.07.005 |pmid=15670663}}</ref>

[[Image:Steatosis.jpg|thumb|left|Mechanism leading to hepatic steatosis]]
Defects in [[fatty acid metabolism]] are responsible for [[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 |date=August 2004 |title=Approach to the pathogenesis and treatment of nonalcoholic steatohepatitis |journal=Diabetes Care |volume=27 |issue=8 |pages=2057–66 |doi=10.2337/diacare.27.8.2057 |pmid=15277442 |doi-access=free}}</ref>
Impairment or inhibition of receptor molecules ([[Peroxisome proliferator-activated receptor|PPAR-α]], [[Peroxisome proliferator-activated receptor|PPAR-γ]] and [[sterol regulatory element binding protein|SREBP1]]) that control the enzymes responsible for the oxidation and synthesis of fatty acids appears to contribute to fat accumulation. In addition, alcohol use disorder 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.{{cn|date=May 2025}}

[[Image:Steatohepatitis high mag.jpg|thumb|right|Micrograph of inflamed fatty liver ([[steatohepatitis]])]]
Severe fatty liver is sometimes accompanied by [[inflammation]], a situation referred to as [[steatohepatitis]]. Progression to alcoholic steatohepatitis (ASH) or metabolic dysfunction associated steatohepatitis (MASH) 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 [[lipid]]) and onset of steatohepatitis may represent successive stages in FLD progression.<ref name="Day_1998">{{Cite journal |vauthors=Day CP, James OF |date=April 1998 |title=Steatohepatitis: a tale of two "hits"? |journal=Gastroenterology |volume=114 |issue=4 |pages=842–5 |doi=10.1016/S0016-5085(98)70599-2 |pmid=9547102 |doi-access=free}}</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 |date=February 2004 |title=Pathologic features associated with fibrosis in nonalcoholic fatty liver disease |journal=Human Pathology |volume=35 |issue=2 |pages=196–9 |doi=10.1016/j.humpath.2003.09.018 |pmid=14991537}}</ref> [[Hepatocyte]] ballooning and [[necrosis]] of varying degrees are often present at this stage. Liver cell death and inflammatory responses lead to the activation of [[hepatic stellate cell]]s, which play a pivotal role in hepatic [[fibrosis]]. The extent of fibrosis varies widely. [[Sinusoid (blood vessel)|Perisinusoidal]] fibrosis is most common, especially in adults, and predominates in [[Hepatic lobule|zone 3]] around the terminal [[hepatic veins]].<ref name="Zafrani _2004">{{Cite journal |vauthors=Zafrani ES |date=January 2004 |title=Non-alcoholic fatty liver disease: an emerging pathological spectrum |journal=Virchows Archiv |volume=444 |issue=1 |pages=3–12 |doi=10.1007/s00428-003-0943-7 |pmid=14685853 |s2cid=7708476}}</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.{{cn|date=May 2025}}

==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<ref name="Bayard_2006">{{Cite journal |vauthors=Bayard M, Holt J, Boroughs E |date=June 2006 |title=Nonalcoholic fatty liver disease |journal=American Family Physician |volume=73 |issue=11 |pages=1961–8 |pmid=16770927}}</ref>
|-
|{{tree chart/start}}
{{tree chart|border=1|boxstyle=background:#dfd; | | | | A01| | | |A01=Elevated liver enzyme}}
{{tree chart|border=1|boxstyle=background:#dfd; | | | | |!| | | | |}}
{{tree chart|border=1|boxstyle=background:#dfd; | | | | B01| | | |B01=Serology to exclude viral hepatitis}}
{{tree chart|border=1|boxstyle=background:#dfd; | | | | |!| | | | |}}
{{tree chart|border=1|boxstyle=background:#dfd; | | | | C01| | | |C01=Imaging study showing<br />fatty infiltrate}}
{{tree chart|border=1|boxstyle=background:#dfd; | | | | |!| | | | |}}
{{tree chart|border=1|boxstyle=background:#dfd; | | | | D01| | | |D01=Alcohol intake}}
{{tree chart|border=1|boxstyle=background:#dfd; | | |,|-|^|-|.| | |}}
{{tree chart|border=1|boxstyle=background:#dfd; | |E01| |E02| | |E01=Less than two drinks per day‡|E02=More than two drinks per day‡}}
{{tree chart|border=1|boxstyle=background:#dfd; | | |!| | | |!| | |}}
{{tree chart|border=1|boxstyle=background:#dfd; | |F01| |F02| | |F01=Nonalcoholic fatty liver disease likely|F02=Alcoholic liver disease likely}}
{{tree chart/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 |last1=Adams |first1=L. A. |last2=Angulo |first2=P |last3=Lindor |first3=KD |date=29 March 2005 |title=Nonalcoholic fatty liver disease |journal=Canadian Medical Association Journal |volume=172 |issue=7 |pages=899–905 |doi=10.1503/cmaj.045232 |pmc=554876 |pmid=15795412}}</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 enzymes are found in as many as 50% of patients with simple steatosis.<ref>{{Cite book |last=Reid |first=Andrea E. |url=https://archive.org/details/sleisengerfordtr0000unse_j1o5 |title=Sleisenger and Fordtran's Gastrointestinal and Liver Disease |publisher=W.B. Saunders Company |year=2006 |isbn=978-1-4160-0245-1 |editor-last=Feldman |editor-first=Mark |edition=8th |location=Philadelphia |chapter=Chapter 82: Nonalcoholic Fatty Liver Disease |access-date=4 July 2023 |editor-last2=Friedman |editor-first2=Lawrence S. |editor-last3=Brandt |editor-first3=Lawrence J. |url-access=registration |via=Internet Archive}}</ref>{{rp|1794}} The serum [[alanine transaminase]] (ALT) level usually is greater than the [[aspartate transaminase]] (AST) level in the nonalcoholic variant and the opposite in alcoholic FLD (AST:ALT more than 2:1). Simple blood tests may help to determine the magnitude of the disease by assessing the degree of liver fibrosis.<ref>{{Cite journal |last1=Peleg |first1=Noam |last2=Issachar |first2=Assaf |last3=Sneh-Arbib |first3=Orly |last4=Shlomai |first4=Amir |date=October 2017 |title=AST to Platelet Ratio Index and fibrosis 4 calculator scores for non-invasive assessment of hepatic fibrosis in patients with non-alcoholic fatty liver disease |journal=Digestive and Liver Disease |volume=49 |issue=10 |pages=1133–1138 |doi=10.1016/j.dld.2017.05.002 |pmid=28572039}}</ref> For example, AST-to-platelets ratio index (APRI score) and several other scores, calculated from the results of blood tests, can detect the degree of liver fibrosis and predict the future formation of liver cancer.<ref>{{Cite journal |last1=Peleg |first1=Noam |last2=Sneh Arbib |first2=Orly |last3=Issachar |first3=Assaf |last4=Cohen-Naftaly |first4=Michal |last5=Braun |first5=Marius |last6=Shlomai |first6=Amir |date=14 August 2018 |title=Noninvasive scoring systems predict hepatic and extra-hepatic cancers in patients with nonalcoholic fatty liver disease |journal=PLOS ONE |volume=13 |issue=8 |article-number=e0202393 |bibcode=2018PLoSO..1302393P |doi=10.1371/journal.pone.0202393 |pmc=6091950 |pmid=30106985 |doi-access=free}}</ref>

Imaging studies are often obtained during the evaluation process. [[Ultrasonography]] reveals a "bright" liver with increased [[echogenicity]]. Pocket-sized [[ultrasound]] devices might be used as point-of-care screening tools to diagnose liver steatosis.<ref>{{cite journal|vauthors=Miles DA, Levi CS, Uhanova J, Cuvelier S, Hawkins K, Minuk GY|title=Pocket-Sized Versus Conventional Ultrasound for Detecting Fatty Infiltration of the Liver|journal=Dig Dis Sci|year=2020|volume=65|series=1|issue=1 |pages=82–85|doi=10.1007/s10620-019-05752-x|pmid=31376083}}</ref> [[Medical imaging]] can aid in diagnosis of fatty liver; fatty livers have lower [[density]] than [[spleen]]s on [[computed tomography]] (CT), and fat appears bright in [[Relaxation (NMR)|T1-weighted]] [[Magnetic resonance imaging|magnetic resonance images]] (MRIs). 

[[Histology|Histological]] diagnosis by [[liver biopsy]] is the most accurate measure of fibrosis and liver fat progression as of 2018.<ref name="AASLD2018" /> Conventional imaging methods, such as ultrasound, CT and MRI, are not specific enough to detect fatty liver disease unless fat occupies at least 30% of the liver volume.<ref name="pmid28652891">{{Cite journal |vauthors=Benedict M, Zhang X |date=June 2017 |title=Non-alcoholic fatty liver disease: An expanded review |journal=World Journal of Hepatology |volume=9 |issue=16 |pages=715–732 |doi=10.4254/wjh.v9.i16.715 |pmc=5468341 |pmid=28652891 |doi-access=free}}</ref>

More advanced imaging techniques are under investigation for both the diagnosis and monitoring of fatty liver disease patients, including [[elastography]] techniques (both [[elastography#Ultrasound_elastography|ultrasound-based techniques]] and using [[magnetic resonance elastography]]) to measure the stiffness of the liver, which increases due to the accumulation of liver fibrosis.<ref>{{cite journal |last1=Selvaraj |first1=EA |last2=Mózes |first2=FE |last3=Jayaswal |first3=ANA |last4=Zafarmand |first4=MH |last5=Vali |first5=Y |last6=Lee |first6=JA |last7=Levick |first7=CK |last8=Young |first8=LAJ |last9=Palaniyappan |first9=N |last10=Liu |first10=CH |last11=Aithal |first11=GP |last12=Romero-Gómez |first12=M |last13=Brosnan |first13=MJ |last14=Tuthill |first14=TA |last15=Anstee |first15=QM |last16=Neubauer |first16=S |last17=Harrison |first17=SA |last18=Bossuyt |first18=PM |last19=Pavlides |first19=M |last20=LITMUS |first20=Investigators |title=Diagnostic accuracy of elastography and magnetic resonance imaging in patients with NAFLD: A systematic review and meta-analysis. |journal=Journal of Hepatology |date=October 2021 |volume=75 |issue=4 |pages=770–785 |doi=10.1016/j.jhep.2021.04.044 |pmid=33991635|hdl=2434/1156671 |hdl-access=free }}</ref> Several studies have also explored the use of quantitative MRI techniques such as proton density fat-fraction mapping<ref>{{cite journal |last1=Caussy |first1=C |last2=Reeder |first2=SB |last3=Sirlin |first3=CB |last4=Loomba |first4=R |title=Noninvasive, Quantitative Assessment of Liver Fat by MRI-PDFF as an Endpoint in NASH Trials. |journal=Hepatology (Baltimore, Md.) |date=August 2018 |volume=68 |issue=2 |pages=763–772 |doi=10.1002/hep.29797 |pmid=29356032|pmc=6054824 }}</ref> and iron-corrected [[Spin–lattice relaxation|T1]] (cT1) mapping techiques.<ref>{{cite journal |last1=Andersson |first1=A |last2=Kelly |first2=M |last3=Imajo |first3=K |last4=Nakajima |first4=A |last5=Fallowfield |first5=JA |last6=Hirschfield |first6=G |last7=Pavlides |first7=M |last8=Sanyal |first8=AJ |last9=Noureddin |first9=M |last10=Banerjee |first10=R |last11=Dennis |first11=A |last12=Harrison |first12=S |title=Clinical Utility of Magnetic Resonance Imaging Biomarkers for Identifying Nonalcoholic Steatohepatitis Patients at High Risk of Progression: A Multicenter Pooled Data and Meta-Analysis. |journal=Clinical Gastroenterology and Hepatology |date=November 2022 |volume=20 |issue=11 |pages=2451–2461.e3 |doi=10.1016/j.cgh.2021.09.041 |pmid=34626833|doi-access=free }}</ref>

==Treatment==
Decreasing caloric intake by at least 30% or by approximately 750–1,000 kcal/day results in improvement in hepatic steatosis.<ref name="AASLD2018" /> For people with MASLD or MASH, 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 FLD alone, has been shown to revert FLD, MASLD, MASH and advanced [[steatohepatitis]] in over 90% of people who have undergone this surgery for the treatment of [[obesity]].<ref name="AASLD2018" /><ref>{{EMedicine|article|175472|Fatty Liver}}</ref>

In the case of long-term total-parenteral-nutrition-induced fatty liver disease, [[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 |date=November 1995 |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 |doi=10.1002/hep.1840220510 |pmid=7590654 |s2cid=20227016}}</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 |date=April 1992 |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 |doi=10.1016/0016-5085(92)70034-9 |pmid=1551541}}</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 |year=2016 |title=Choline deficiency causes reversible hepatic abnormalities in patients receiving parenteral nutrition: proof of a human choline requirement: a placebo-controlled trial |journal=Journal of Parenteral and Enteral Nutrition |volume=25 |issue=5 |pages=260–8 |doi=10.1177/0148607101025005260 |pmid=11531217}}</ref> This may be due to a deficiency in the [[Methionine synthase|methionine cycle]].<ref>{{Cite journal |vauthors=Hollenbeck CB |date=August 2010 |title=The importance of being choline |journal=Journal of the American Dietetic Association |volume=110 |issue=8 |pages=1162–5 |doi=10.1016/j.jada.2010.05.012 |pmid=20656090}}</ref>

==Epidemiology==
NAFLD affects about 30% of people in Western countries and 10% of people in Asia.<ref name=Sin2017/>
In the United States, rates are around 35% with about 7% having the severe form NASH.<ref name=NIH2016/> NAFLD affects about 10% of children in the United States.<ref name=NIH2016/>  Recently the term Metabolic dysfunction-associated fatty liver disease (MAFLD) has been proposed to replace NAFLD.  MAFLD is a more inclusionary diagnostic name as it is based on the detection of fatty liver by histology (biopsy), medical imaging or blood biomarkers but should be accompanied by either overweight/obesity, type 2 diabetes mellitus, or metabolic dysregulation.<ref name="Liu_2021">{{Cite journal |last1=Liu |first1=Jiaye |last2=Ayada |first2=Ibrahim |last3=Zhang |first3=Xiaofang |last4=Wang |first4=Ling |last5=Li |first5=Yang |last6=Wen |first6=Tianfu |last7=Ma |first7=Zhongren |last8=Bruno |first8=Marco J. |last9=de Knegt |first9=Robert J. |last10=Cao |first10=Wanlu |last11=Peppelenbosch |first11=Maikel P. |last12=Ghanbari |first12=Mohsen |last13=Li |first13=Zhihui |last14=Pan |first14=Qiuwei |date=February 2021 |title=Estimating Global Prevalence of Metabolic Dysfunction-Associated Fatty Liver Disease in Overweight or Obese Adults |journal=Clinical Gastroenterology and Hepatology |volume=20 |issue=3 |pages=e573–e582 |doi=10.1016/j.cgh.2021.02.030 |pmid=33618024 |s2cid=232018678 |doi-access=free}}</ref> The new definition no longer excludes alcohol consumption or coexistence of other liver diseases such as viral hepatitis. Using this more inclusive definition, the global prevalence of MAFLD is an astonishingly high 50.7%.<ref name="Liu_2021" /> Indeed, also using the old NAFLD definition, the disease is observed in up to 80% of obese people, 35% of whom progress to NASH,<ref name="Hamaguchi_2005">{{Cite journal |last1=Hamaguchi |first1=Masahide |last2=Kojima |first2=Takao |last3=Takeda |first3=Noriyuki |last4=Nakagawa |first4=Takayuki |last5=Taniguchi |first5=Hiroya |last6=Fujii |first6=Kota |last7=Omatsu |first7=Tatsushi |last8=Nakajima |first8=Tomoaki |last9=Sarui |first9=Hiroshi |last10=Shimazaki |first10=Makoto |last11=Kato |first11=Takahiro |last12=Okuda |first12=Junichi |last13=Ida |first13=Kazunori |date=15 November 2005 |title=The Metabolic Syndrome as a Predictor of Nonalcoholic Fatty Liver Disease |journal=Annals of Internal Medicine |volume=143 |issue=10 |pages=722–728 |doi=10.7326/0003-4819-143-10-200511150-00009 |pmid=16287793 |s2cid=22475943}}</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 test]]s in the [[United States]].<ref name="Angulo_2002">{{Cite journal |last=Angulo |first=Paul |date=18 April 2002 |title=Nonalcoholic Fatty Liver Disease |journal=New England Journal of Medicine |volume=346 |issue=16 |pages=1221–1231 |doi=10.1056/NEJMra011775 |pmid=11961152}}</ref> Fatty liver is more prevalent in Hispanic people than white, with black people having the lowest prevalence.<ref name="Younossi2017" />

In the study [[Children of the 90s]], 2.5% born in 1991 and 1992 were found by ultrasound at the age of 18 to have non-alcoholic fatty liver disease; five years later [[transient elastography]] found over 20% to have the fatty deposits on the liver, indicating non-alcoholic fatty liver disease; half of those were classified as severe. The scans also found that 2.4% had a degree of liver fibrosis, which can lead to cirrhosis.<ref>{{Cite web |last=Sarah Boseley |date=12 April 2019 |title=Experts warn of fatty liver disease 'epidemic' in young people |url=https://www.theguardian.com/society/2019/apr/12/experts-warn-of-fatty-liver-disease-epidemic-in-young-people |access-date=4 July 2023 |newspaper=The Guardian}}</ref><ref>{{Cite press release |title=Nonalcoholic fatty liver disease found in large numbers of teenagers and young adults |date=11 April 2019 |publisher=American Association for the Advancement of Science |url=https://www.eurekalert.org/news-releases/750779 |access-date=4 July 2023 |website=EurekAlert! |author=SPINK HEALTH}}</ref>

After the [[COVID-19 pandemic lockdowns|lockdown of the COVID-19 pandemic]], a study demonstrated that 48% of patients with liver steatosis gained weight, while 16% had a worsened steatosis grade. Weight gain was associated with poor adherence to the suggested diet, reduced levels of physical activity, and increased prevalence of homozygosity for the ''[[PNPLA3]]'' rs738409 single nucleotide polymorphism.<ref>{{Cite journal |last1=Cinque |first1=Felice |last2=Cespiati |first2=Annalisa |last3=Lombardi |first3=Rosa |last4=Costantino |first4=Andrea |last5=Maffi |first5=Gabriele |last6=Alletto |first6=Francesca |last7=Colavolpe |first7=Lucia |last8=Francione |first8=Paolo |last9=Oberti |first9=Giovanna |last10=Fatta |first10=Erika |last11=Bertelli |first11=Cristina |last12=Sigon |first12=Giordano |last13=Dongiovanni |first13=Paola |last14=Vecchi |first14=Maurizio |last15=Fargion |first15=Silvia |date=January 2022 |title=Interaction between Lifestyle Changes and PNPLA3 Genotype in NAFLD Patients during the COVID-19 Lockdown |journal=Nutrients |language=en |volume=14 |issue=3 |page=556 |doi=10.3390/nu14030556 |issn=2072-6643 |pmc=8838646 |pmid=35276911 |doi-access=free |last16=Fracanzani |first16=Anna Ludovica}}  [[File:CC-BY icon.svg|50px]]  Text was copied from this source, which is available under a [https://creativecommons.org/licenses/by/4.0/  Creative Commons Attribution 4.0 International License].</ref> ''PNPLA3'' rs738409 is already a known risk factor for NAFLD.<ref>Liu, Y.L.; Patman, G.L.; Leathart, J.B.; Piguet, A.C.; Burt, A.D.; Dufour, J.F.; Day, C.P.; Daly, A.K.; Reeves, H.L.; Anstee, Q.M. Carriage of the PNPLA3 rs738409 C >G polymorphism confers an increased risk of non-alcoholic fatty liver disease associated hepatocellular carcinoma. J. Hepatol. 2014, 61, 75–81.</ref><ref>Eslam, M.; Valenti, L.; Romeo, S. Genetics and epigenetics of NAFLD and NASH: Clinical impact. J. Hepatol. 2018, 68, 268–279.</ref>

== Research ==
A systematic review and meta-analysis, published in 2024, found that [[growth hormone]] therapy may help in the management of fatty liver disease.<ref>{{cite journal | vauthors = Dutta D, Nagendra L, Mohindra R, Bhattacharya S, Joshi A, Kamrul-Hasan A | title = Role of Growth Hormone Therapy in Metabolic-Dysfunction-Associated Steatotic Liver Disease: A Systematic Review and Meta-Analysis | journal = Indian Journal of Endocrinology and Metabolism | volume = 28 | issue = 4 | pages = 336–342 | date = 2024 | pmid = 39371653 | pmc = 11451958 | doi = 10.4103/ijem.ijem_488_23 | doi-access = free | title-link = doi }}</ref>

==In animals==
Fatty liver disease can occur in pets such as reptiles (particularly [[Testudines|turtle]]s<ref>{{Cite journal |last=Lock |first=Brad |date=8 August 2017 |title=Hepatic Lipidosis (Fatty Liver Disease) in Reptiles |url=https://veterinarypartner.vin.com/default.aspx?pid=19239&catId=102919&id=8017925 |access-date=29 December 2020 |website=Vin.com}}</ref>) and birds<ref>{{Cite web |title=Fatty Liver Disease in Birds |url=https://www.animalhouseofchicago.com/news/birds-fatty-liver |access-date=29 December 2020 |website=Animal House of Chicago}}</ref> as well as mammals like [[Feline hepatic lipidosis|cats]] and dogs.<ref>{{Cite web |title=Fatty Liver Disease in Cats |url=https://www.petmd.com/cat/conditions/digestive/c_ct_hepatic_lipidosis |access-date=29 December 2020 |website=PetMD}}</ref> The most common cause is [[overnutrition]]. A distinct sign in birds is a misshapen beak.  Fatty livers can be induced via [[gavage]] in geese or ducks to produce [[foie gras]]. Fatty liver can also be induced in ruminants such as sheep by a high-caloric diet.<ref>{{Cite journal |last1=Kalyesubula |first1=Mugagga |last2=Mopuri |first2=Ramgopal |last3=Rosov |first3=Alexander |last4=Alon |first4=Tamir |last5=Edery |first5=Nir |last6=Moallem |first6=Uzi |last7=Dvir |first7=Hay |date=December 2020 |title=Hyperglycemia-stimulating diet induces liver steatosis in sheep |journal=Scientific Reports |volume=10 |issue=1 |page=12189 |bibcode=2020NatSR..1012189K |doi=10.1038/s41598-020-68909-z |pmc=7376193 |pmid=32699301}}</ref><ref>{{Cite journal |last1=Kalyesubula |first1=Mugagga |last2=Mopuri |first2=Ramgopal |last3=Asiku |first3=Jimmy |last4=Rosov |first4=Alexander |last5=Yosefi |first5=Sara |last6=Edery |first6=Nir |last7=Bocobza |first7=Samuel |last8=Moallem |first8=Uzi |last9=Dvir |first9=Hay |date=1 March 2021 |title=High-dose vitamin B1 therapy prevents the development of experimental fatty liver driven by overnutrition |journal=Disease Models & Mechanisms |volume=14 |issue=3 |pages=dmm048355 |doi=10.1242/dmm.048355 |pmc=7988776 |pmid=33608323}}</ref>

== References ==
{{Reflist}}

== 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
}}
* {{Chorus|00474}}
* Photo at [http://www.pathologyatlas.ro/fatty-change-liver-steatosis-pathology.php Atlas of Pathology]

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{{DEFAULTSORT:Fatty Liver}}
[[Category:Diseases of liver]]
[[Category:Medical conditions related to obesity]]
[[Category:Histopathology]]
[[Category:Wikipedia medicine articles ready to translate]]

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