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| '''Editor in Chief''': Elliot Tapper, M.D., Beth Israel Deaconess Medical Center
| | {{Non alcoholic fatty liver disease}} |
| | {{CMG}}; {{AE}} {{VKG}} |
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| {{Editor Help}} | | {{See also|Fatty liver}} |
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| ==Overview==
| | '''For the patient information page on this topic, click [[non-alcoholic fatty liver disease (patient information)|here]].''' |
| {{DiseaseDisorder infobox |
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| Name = Non-alcoholic steatohepatitis |
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| Image = |
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| Caption = |
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| DiseasesDB = 29786|
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| ICD10 = {{ICD10|K|76|0|k|70}} |
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| ICD9 = {{ICD9|571.8}} |
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| OMIM = |
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| MedlinePlus = |
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| eMedicineSubj = med |
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| eMedicineTopic = 775 |
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| {{SI}}
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| '''Non-alcoholic fatty liver disease''' ('''[[NAFLD]]''') is a spectrum of [[liver]] disease in the absence of excessive [[alcoholism|alcohol]] use that begins with fatty infiltration and can proceed to inflammation - '''[[Non-alcoholic steatohepatitis]]''' ([[NASH]]) - and even cirrhosis. At present, estimates are that between 30- 90 million Americans have some degree of NAFLD and 5-6% have NASH. <ref name=McCullough> McCullough, AJ. Thiazolidinediones for NASH. NEJM 2006;355(22):2361-2363.</ref> | |
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| NAFLD/NASH was first described in 1980 in a series of patients of the [[Mayo Clinic]]<ref>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.</ref>. Since that seminal description, our understanding of NAFLD/NASH has progressed minimally. <ref>Day, CP. Non-alcoholic steatohepatitis (NASH): where are we now and where are we going? Gut. 2002 May; 50(5): 585–588.</ref> 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 NASH, however, do not meet criteria for metabolic syndrome <ref>Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology. 2006;43:S99–S112.</ref>.
| | {{SK}} NASH, NAFLD, non-alcoholic steatohepatitis, metabolic dysfunction-associated steatotic liver disease (MASLD) |
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| ==Signs and symptoms== | | ==[[Non-alcoholic fatty liver disease overview|Overview]]== |
| ===Symptoms and associations===
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| By definition, alcohol consumption of over 20 g/day excludes the condition.<ref name=Adams/> Most patients with NAFLD have no or few symptoms. Infrequently patients may complain of fatigue, [[malaise]] and dull right upper quadrant [[abdominal pain|abdominal discomfort]]. Mild [[jaundice]] can rarely be noticed. More commonly it is diagnosed as a result of abnormal [[liver function tests]] during routine blood tests. Often following an asymptomatic course, the disease may present first with cirrhosis and/or the complication of portal hypertension. In that respect, NASH is becoming an increasingly common indication for liver transplantation. <ref>Choudhury J, Sanyal A. Clinical Aspects of Fatty Liver Disease. Semin Liver Dis 2004; 24: 349-362.</ref> As awareness of this condition spreads, it has been regarded as a major cause of cryptogenic [[cirrhosis]] of the liver.<ref name=Clark>Clark JM, Diehl AM. Nonalcoholic fatty liver disease: an underrecognized cause of cryptogenic cirrhosis. ''JAMA'' 2003;289:3000-4. PMID 12799409.</ref>
| | ==[[Non-alcoholic fatty liver disease historical perspective|Historical Perspective]]== |
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| ===Secondary causes=== | | ==[[Non-alcoholic fatty liver disease classification|Classification]]== |
| NAFLD can also be caused by the following medications (termed ''secondary'' NAFLD):
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| * [[Amiodarone]]
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| * [[Antiviral drug]]s ([[nucleoside analogues]])
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| * [[Aspirin]] / [[NSAID]]S
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| * [[Corticosteroid]]s
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| * [[Methotrexate]]
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| * [[Nifedipine]]
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| * [[Perhexiline]]
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| * [[Tamoxifen]]
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| * [[Tetracycline]]
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| * [[Valproic acid]]
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| ==Diagnosis== | | ==[[Non-alcoholic fatty liver disease pathophysiology|Pathophysiology]]== |
| Disturbed [[liver enzyme]]s are common, and liver [[medical ultrasonography|ultrasound]] may show [[steatosis]]; it may also be used to exclude [[gallstone]] problems ([[cholelithiasis]]). A [[biopsy]] (tissue examination) of the [[liver]] is the only widely accepted test which can distinguish NASH from other forms of liver disease, and can be used to assess the severity of the inflammation and resultant fibrosis.<ref name=Adams/>
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| | ==[[Non-alcoholic fatty liver disease causes|Causes]]== |
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| | ==[[Non-alcoholic fatty liver disease differential diagnosis|Differentiating Non-Alcoholic Fatty Liver Disease from other Diseases]]== |
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| | ==[[Non-alcoholic fatty liver disease epidemiology and demographics|Epidemiology and Demographics]]== |
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| | ==[[Non-alcoholic fatty liver disease risk factors|Risk Factors]]== |
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| Other tests generally performed are other blood tests ([[erythrocyte sedimentation rate]], [[glucose]], [[human serum albumin|albumin]], [[renal function]] etc.) As the liver is important in [[coagulation]], some coagulation studies will generally be done, especially the INR (international normalized ratio). To distinguish this disease from viral [[hepatitis]], blood tests ([[serology]]) are generally done (hepatitis A, B, C, [[Epstein-Barr virus|EBV]], [[CMV]] and [[herpes]] viruses, as well as [[rubella]]) to ensure these are not playing a role. Additionally, autoimmune causes are ruled out with serology. [[Thyroid-stimulating hormone|TSH]] is warranted, as [[hypothyroidism]] is more prevalent in NASH patients.<ref>Liangpunsakul S, Chalasani N. Is hypothyroidism a risk factor for non-alcoholic steatohepatitis? ''J Clin Gastroenterol'' 2003;37:340-3. PMID 14506393</ref>
| | ==[[Non-alcoholic fatty liver disease screening|Screening]]== |
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| ==Pathophysiology== | | ==[[Non-alcoholic fatty liver disease natural history, complications and prognosis|Natural History, Complications, and Prognosis]]== |
| NAFLD is considered a spectrum of disease activity. This spectrum begins as fatty accumulation in the liver (hepatic [[steatosis]]). A fatty liver can remain without disturbing the function of the liver, but by varying mechanisms and possible insults to the liver, may progress to outright [[inflammation]] of the liver. Whhttp://wikidoc.org/index.php?title=Non-alcoholic_fatty_liver_disease&action=editen inflammation occurs in this setting, the condition is then called NASH. Over time, up to 20 percent of patients with NASH may develop [[cirrhosis]].
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| The exact cause is still ''unknown''. However both [[obesity]] and [[insulin resistance]] likely play a strong role in this disease process. The exact reasons and mechanisms by which this disease progresses from one entity to the next is a subject of much research and debate.
| | ==Diagnosis== |
| One such debated mechanisim proposes a "second hit", or further injury, enough to cause change that leads from hepatic steatosis to [[hepatic]] inflammation. [[Oxidative stress]], hormonal imbalances and [[Mitochondrion|mitochondrial]] abnormalities may be potential causes for this "second hit" phenomenon.<ref name=Adams/>
| | [[Non-alcoholic fatty liver disease history and symptoms|History and Symptoms]] | [[Non-alcoholic fatty liver disease physical examination|Physical Examination]] | [[Non-alcoholic fatty liver disease laboratory findings|Laboratory Findings]] | [[Non-alcoholic fatty liver disease electrocardiogram|Electrocardiogram]] | [[Non-alcoholic fatty liver disease x ray|X Ray]] | [[Non-alcoholic fatty liver disease CT|CT]] | [[Non-alcoholic fatty liver disease MRI|MRI]] | [[Non-alcoholic fatty liver disease ultrasound|Ultrasound]] | [[Non-alcoholic fatty liver disease other imaging findings|Other Imaging Findings]] | [[Non-alcoholic fatty liver disease other diagnostic studies|Other Diagnostic Studies]] | [[Non-alcoholic fatty liver disease Noninvasive scores| Noninvasive scores]] |
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| ==Treatment== | | ==Treatment== |
| Trials are presently being conducted to optimise treatment of NASH. No standard treatment has yet emerged as the "gold standard". General recommendations include improving metabolic risk factors and reducing alcohol intake.<ref name=Adams/>
| | [[Non-alcoholic fatty liver disease medical therapy|Medical Therapy]] | [[Non-alcoholic fatty liver disease surgery|Surgery]] | [[Non-alcoholic fatty liver disease primary prevention|Primary Prevention]] | [[Non-alcoholic fatty liver disease secondary prevention|Secondary Prevention]] | [[Non-alcoholic fatty liver disease cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Non-alcoholic fatty liver disease future or investigational therapies|Future or Investigational Therapies]] |
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| A large number of treatments have been studied for NAFLD. While many may improve biochemical markers, such as [[alanine transaminase]] levels, most have not been shown to reverse the histological abnormalities or reduce clinical endpoints:<ref name=Adams/>
| | ==Case Studies== |
| * Weight loss: gradual weight loss, and possibly [[bariatric surgery]], may improve the process in obese patients.
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| * Insulin sensitisers ([[metformin]] and [[rosiglitazone]] but more markedly [[pioglitazone]]) have shown efficacy in some studies.
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| * [[Antioxidants]] and [[Ursodiol|ursodeoxycholic acid]], as well as lipid-lowering drugs, have little benefit.
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| | [[Non-alcoholic fatty liver disease case study one|Case #1]] |
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| == References == | | ==External Links== |
| <references/>
| | * [http://digestive.niddk.nih.gov/ddiseases/pubs/nash/ NIH] page on Nonalcoholic Steatohepatitis |
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| ==External links==
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| * [http://www.medscape.com/viewarticle/458509_1 Medscape] article on NASH.
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| * [http://www.medicinenet.com/fatty_liver/article.htm MEDICINENET] article on Steatosis.
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| * [http://digestive.niddk.nih.gov/ddiseases/pubs/nash/ NIH] page on Nonalcoholic Steatohepatitis
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| {{SIB}}
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| {{Gastroenterology}} | | {{Gastroenterology}} |
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| [[Category:Gastroenterology]] | | [[Category:Gastroenterology]] |
| [[Category:Hepatitis]] | | [[Category:Hepatology]] |
| | [[Category:Disease]] |
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| [[es:Esteatohepatitis no alcohólica]] | | [[es:Esteatohepatitis no alcohólica]] |
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