wikidoc - Changes related to "Category:Needs content" [en]

Non-alcoholic fatty liver disease future or investigational therapies

2026-05-20T02:28:10Z

← Older revision		Revision as of 02:28, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}}		{{CMG}}; {{AE}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]]

	{{PleaseHelp}}		{{PleaseHelp}}

	==Overview==		==Overview==
			Future investigational therapies for MASH include tirzepatide and other dual- or triple-incretin receptor agonists, gliflozins, pan-peroxisome proliferator-activated receptor agonists such as lanifibranor, fibroblast growth factor 21 analogs, fatty acid synthase inhibitors, and genetic target-based therapies such as antisense oligonucleotides targeting PNPLA3.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

			Blood-based biomarkers of fibrosis and vibration-controlled transient elastography are expected to be used more frequently to monitor disease progression and regression, predict long-term liver-related events, and assess treatment response. Polygenic risk scores, metabolic signatures, and microbiome signatures may help identify patients with distinct MASLD trajectories and treatment responses.

	==Future or Investigational Therapies==		==Future or Investigational Therapies==

Non-alcoholic fatty liver disease primary prevention

2026-05-20T02:26:19Z

JAMA article updates

← Older revision		Revision as of 02:26, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	~~Effective measures for the primary prevention of non-alcoholic fatty liver disease~~ include ~~eating~~ a healthy ~~diet~~ and regular ~~exercise~~.		Measures that may reduce MASLD development or progression include maintaining a healthy weight, reducing excess caloric intake, limiting ultraprocessed foods, saturated fats, refined sugars, and sugar-sweetened beverages, engaging in regular physical activity, avoiding alcohol intake, and effectively managing type 2 diabetes, obesity, dyslipidemia, and hypertension.

	==Primary Prevention==		==Primary Prevention==
	Effective measures for the primary prevention of non-alcoholic fatty liver disease include:		Effective measures for the primary prevention of non-alcoholic fatty liver disease include:
	*Eating a healthy [[diet]] that is rich in vegetables, fruits and healthy fats is the first and very important step.<ref name="pmid28573067">{{cite journal \|vauthors=Patil R, Sood GK \|title=Non-alcoholic fatty liver disease and cardiovascular risk \|journal=World J Gastrointest Pathophysiol \|volume=8 \|issue=2 \|pages=51–58 \|year=2017 \|pmid=28573067 \|pmc=5437502 \|doi=10.4291/wjgp.v8.i2.51 \|url=}}</ref>		*Eating a healthy [[diet]] that is rich in vegetables, fruits and healthy fats is the first and very important step.<ref name="pmid28573067">{{cite journal \|vauthors=Patil R, Sood GK \|title=Non-alcoholic fatty liver disease and cardiovascular risk \|journal=World J Gastrointest Pathophysiol \|volume=8 \|issue=2 \|pages=51–58 \|year=2017 \|pmid=28573067 \|pmc=5437502 \|doi=10.4291/wjgp.v8.i2.51 \|url=}}</ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*Regular [[Physical exercise\|exercise]]		*Regular [[Physical exercise\|exercise]]
	*Maintaining a healthy weight		*Maintaining a healthy weight

Non-alcoholic fatty liver disease surgery

2026-05-20T02:24:40Z

JAMA article updates

← Older revision		Revision as of 02:24, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	Surgery is not the first-line treatment option for patients with non- Alcoholic fatty liver disease (NAFLD). However, [[gastric bypass surgery]] is recommended in patients with non-alcoholic fatty liver disease whose [[Body mass index\|BMI]] is greater than ~~40 who psychologically stable and failed medical~~ therapy.		Surgery is not the first-line treatment option for patients with non- Alcoholic fatty liver disease (NAFLD). However, [[gastric bypass surgery]] is recommended in patients with non-alcoholic fatty liver disease whose [[Body mass index\|BMI]] is greater than 35 particularly in those without improvement in imaging-detected hepatic steatosis or fibrosis after behavioral modification or medication therapy.

	== Surgery ==		== Surgery ==

	==== Indications ====		==== Indications ====
	* Patients with NAFLD and [[BMI]] greater than 40 who psychologically stable		* Patients with NAFLD and [[BMI]] greater than 35 who psychologically stable<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	* In patients who failed medical therapy.		* In patients who failed medical therapy.

Non-alcoholic fatty liver disease medical therapy

2026-05-20T02:21:36Z

JAMA article updates

Show changes

Non-alcoholic fatty liver disease other diagnostic studies

2026-05-20T01:52:18Z

JAMA article updates

← Older revision		Revision as of 01:52, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}} ; {{AE}} {{ADG}}		{{CMG}} ; {{AE}} {{ADG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	Liver biopsy may be helpful in the diagnosis of non-alcoholic fatty liver disease. Findings on biopsy include [[Steatosis\|macrovesicular steatosis]], [[inflammation]], ballooning degeneration, zone 3 perivenular/periportal/perisinusoidal fibrosis and, finally, [[mallory bodies]].		Liver biopsy may be helpful in the diagnosis of non-alcoholic fatty liver disease. Findings on biopsy include [[Steatosis\|macrovesicular steatosis]], [[inflammation]], ballooning degeneration, zone 3 perivenular/periportal/perisinusoidal fibrosis and, finally, [[mallory bodies]].
	==Other Diagnostic Studies==		==Other Diagnostic Studies==
	*Liver biopsy is considered as a gold-standard for diagnosing, grading, and staging NAFLD.		*Liver biopsy is considered as a gold-standard for diagnosing, grading, and staging NAFLD, but it is invasive, costly, and associated with rare acute bleeding. Liver biopsy is not typically required to diagnose MASLD, but may be useful when the etiology of liver disease is uncertain, when noninvasive tests are inconclusive, or when MASLD coexists with other liver diseases such as autoimmune hepatitis or viral hepatitis.
	*Invasive test		*Invasive test
	*Associated with significant bleeding risk in patients with [[Clotting\|clotting abnormalities]] due to hepatic disease.		*Associated with significant bleeding risk in patients with [[Clotting\|clotting abnormalities]] due to hepatic disease.
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	\|}		\|}
	===Staging===		===Staging===
	Based on the degree of fibrosis on biospy NASH can be classified into 4 stages.		Based on the degree of fibrosis on biospy NASH can be classified into '''5''' stages.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	{\| ~~border~~=~~"1" cellpadding~~=~~"5" cellspacing~~=~~"0" align~~=~~"center"~~ \|class="wikitable"		{\| class="wikitable"
	~~! colspan="2" style="background:#efefef;"~~ \|~~Staging~~		\|'''Stage'''
			\|'''Histologic description'''
			\|-
			\|F0
			\|Absence of fibrosis
	\|-		\|-
	\|~~Stage 1~~		\|F1
	\|		\|Perisinusoidal or portal fibrosis
	~~Zone 3 [[fibrosis]]<br>~~
	Perisinusoidal ~~fibrosis<br>~~
	~~Portal/ periportal~~ fibrosis
	\|-		\|-
	\|~~Stage 2~~		\|F2
	\|Perisinusoidal and portal/periportal [[fibrosis]]		\|Perisinusoidal and portal or periportal fibrosis
	\|-		\|-
	\|~~Stage 3~~		\|F3
	\|~~Bridging [[~~fibrosis]]		\|Septal and bridging fibrosis
	\|-		\|-
	\|~~Stage 4~~		\|F4
	\|[[Cirrhosis]]		\|Cirrhosis
	\|}		\|}

Non-alcoholic fatty liver disease other imaging findings

2026-05-20T01:47:59Z

JAMA article updates

← Older revision		Revision as of 01:47, 20 May 2026
(One intermediate revision by the same user not shown)
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}}		{{CMG}}; {{AE}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]]

	==Overview==		==Overview==
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	==Liver stiffness measurement (LSM) by elastography ==		==Liver stiffness measurement (LSM) by elastography ==

			Vibration-controlled transient elastography is used to noninvasively measure liver stiffness and is commonly used after FIB-4 testing in patients at increased risk for advanced fibrosis. A liver stiffness measurement greater than 8.0 kPa should prompt referral to a hepatologist for further evaluation.

	Two-dimensional shear wave elastography [SWE]) can estimate liver stiffness measurements: "LS of 8 and 12.5 kPa represent generally accepted cut-off values for F3 and F4 fibrosis. LS highly correlates with portal pressure, and esophageal varices are likely at values >20 kPa."<ref name="pmid24367208">{{cite journal\| author=Mueller S, Sandrin L\| title=Liver stiffness: a novel parameter for the diagnosis of liver disease. \| journal=Hepat Med \| year= 2010 \| volume= 2 \| issue= \| pages= 49-67 \| pmid=24367208 \| doi=10.2147/hmer.s7394 \| pmc=3846375 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24367208 }} </ref>		Two-dimensional shear wave elastography [SWE]) can estimate liver stiffness measurements: "LS of 8 and 12.5 kPa represent generally accepted cut-off values for F3 and F4 fibrosis. LS highly correlates with portal pressure, and esophageal varices are likely at values >20 kPa."<ref name="pmid24367208">{{cite journal\| author=Mueller S, Sandrin L\| title=Liver stiffness: a novel parameter for the diagnosis of liver disease. \| journal=Hepat Med \| year= 2010 \| volume= 2 \| issue= \| pages= 49-67 \| pmid=24367208 \| doi=10.2147/hmer.s7394 \| pmc=3846375 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24367208 }} </ref>
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	==Hepatic steatosis==		==Hepatic steatosis==
	Hepattic steatosis can be measured with the Controlled attenuation parameter (CAP).<ref name="pmid33460567">{{cite journal\| author=Petroff D, Blank V, Newsome PN, Voican CS, Thiele M \| display-authors=etal\| title=Assessment of hepatic steatosis by controlled attenuation parameter using the M and XL probes: an individual patient data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2021 \| volume= 6 \| issue= 3 \| pages= 185-198 \| pmid=33460567 \| doi=10.1016/S2468-1253(20)30357-5 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33460567 }} </ref><ref name="pmid30689971">{{cite journal\| author=Eddowes PJ, Sasso M, Allison M, Tsochatzis E, Anstee QM, Sheridan D \| display-authors=etal\| title=Accuracy of FibroScan Controlled Attenuation Parameter and Liver Stiffness Measurement in Assessing Steatosis and Fibrosis in Patients With Nonalcoholic Fatty Liver Disease. \| journal=Gastroenterology \| year= 2019 \| volume= 156 \| issue= 6 \| pages= 1717-1730 \| pmid=30689971 \| doi=10.1053/j.gastro.2019.01.042 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30689971 }} </ref>		Hepattic steatosis can be measured with the Controlled attenuation parameter (CAP).<ref name="pmid33460567">{{cite journal\| author=Petroff D, Blank V, Newsome PN, Voican CS, Thiele M \| display-authors=etal\| title=Assessment of hepatic steatosis by controlled attenuation parameter using the M and XL probes: an individual patient data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2021 \| volume= 6 \| issue= 3 \| pages= 185-198 \| pmid=33460567 \| doi=10.1016/S2468-1253(20)30357-5 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33460567 }} </ref><ref name="pmid30689971">{{cite journal\| author=Eddowes PJ, Sasso M, Allison M, Tsochatzis E, Anstee QM, Sheridan D \| display-authors=etal\| title=Accuracy of FibroScan Controlled Attenuation Parameter and Liver Stiffness Measurement in Assessing Steatosis and Fibrosis in Patients With Nonalcoholic Fatty Liver Disease. \| journal=Gastroenterology \| year= 2019 \| volume= 156 \| issue= 6 \| pages= 1717-1730 \| pmid=30689971 \| doi=10.1053/j.gastro.2019.01.042 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30689971 }} </ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

			The controlled attenuation parameter measures attenuation of ultrasound waves through the liver and is usually performed with vibration-controlled transient elastography. A controlled attenuation parameter value of 248 dB/m or greater is considered diagnostic for hepatic steatosis, and higher values indicate more severe steatosis.

			Compared with conventional ultrasonography, controlled attenuation parameter has similar sensitivity and slightly higher specificity, approximately 90%, for detecting hepatic steatosis.

	==Other imaging==		==Other imaging==

Non-alcoholic fatty liver disease MRI

2026-05-20T01:44:11Z

JAMA article updates

← Older revision		Revision as of 01:44, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	==MRI==		==MRI==
	*[[Abdominal]] [[MRI]] may be helpful in the diagnosis of NAFLD.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html#afp20130701p35-b13 \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician2">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref>		*[[Abdominal]] [[MRI]] may be helpful in the diagnosis of NAFLD.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html#afp20130701p35-b13 \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician2">{{cite web \|url=http://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*Findings on [[MRI]] suggestive NAFLD include:		*Findings on [[MRI]] suggestive NAFLD include:
	**[[Quantification]] of [[hepatic steatosis]].<ref name="pmid24040614">{{cite journal \|vauthors=Ligabue G, Besutti G, Scaglioni R, Stentarelli C, Guaraldi G \|title=MR quantitative biomarkers of non-alcoholic fatty liver disease: technical evolutions and future trends \|journal=Quant Imaging Med Surg \|volume=3 \|issue=4 \|pages=192–5 \|year=2013 \|pmid=24040614 \|pmc=3759141 \|doi=10.3978/j.issn.2223-4292.2013.08.01 \|url=}}</ref><ref name="pmid24966609">{{cite journal \|vauthors=Lee SS, Park SH \|title=Radiologic evaluation of nonalcoholic fatty liver disease \|journal=World J. Gastroenterol. \|volume=20 \|issue=23 \|pages=7392–402 \|year=2014 \|pmid=24966609 \|pmc=4064084 \|doi=10.3748/wjg.v20.i23.7392 \|url=}}</ref>		**[[Quantification]] of [[hepatic steatosis]].<ref name="pmid24040614">{{cite journal \|vauthors=Ligabue G, Besutti G, Scaglioni R, Stentarelli C, Guaraldi G \|title=MR quantitative biomarkers of non-alcoholic fatty liver disease: technical evolutions and future trends \|journal=Quant Imaging Med Surg \|volume=3 \|issue=4 \|pages=192–5 \|year=2013 \|pmid=24040614 \|pmc=3759141 \|doi=10.3978/j.issn.2223-4292.2013.08.01 \|url=}}</ref><ref name="pmid24966609">{{cite journal \|vauthors=Lee SS, Park SH \|title=Radiologic evaluation of nonalcoholic fatty liver disease \|journal=World J. Gastroenterol. \|volume=20 \|issue=23 \|pages=7392–402 \|year=2014 \|pmid=24966609 \|pmc=4064084 \|doi=10.3748/wjg.v20.i23.7392 \|url=}}</ref>
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	*MRI also helps longitudinal follow-up of patients with non-alcoholic fatty liver disease to check response to therapy		*MRI also helps longitudinal follow-up of patients with non-alcoholic fatty liver disease to check response to therapy
	*Another kind of MRI is magnetic resonance spectroscopy (MRS) which reflects fat in the whole liver like [[Triglyceride\|triglycerides]] in a specific volume; and [[proton]] density fat fraction (PDFF).<ref name="pmid288000872">{{cite journal \|vauthors=Di Martino M, Koryukova K, Bezzi M, Catalano C \|title=Imaging Features of Non-Alcoholic Fatty Liver Disease in Children and Adolescents \|journal=Children (Basel) \|volume=4 \|issue=8 \|pages= \|year=2017 \|pmid=28800087 \|pmc=5575595 \|doi=10.3390/children4080073 \|url=}}</ref>		*Another kind of MRI is magnetic resonance spectroscopy (MRS) which reflects fat in the whole liver like [[Triglyceride\|triglycerides]] in a specific volume; and [[proton]] density fat fraction (PDFF).<ref name="pmid288000872">{{cite journal \|vauthors=Di Martino M, Koryukova K, Bezzi M, Catalano C \|title=Imaging Features of Non-Alcoholic Fatty Liver Disease in Children and Adolescents \|journal=Children (Basel) \|volume=4 \|issue=8 \|pages= \|year=2017 \|pmid=28800087 \|pmc=5575595 \|doi=10.3390/children4080073 \|url=}}</ref>
			*Magnetic resonance imaging-proton density fat fraction has a sensitivity of 77% to 92% and specificity of 87% to 94% for detecting any degree of hepatic steatosis. Magnetic resonance spectroscopy has sensitivity and specificity of approximately 95% to 98%, but these methods are primarily used in clinical trials and specialized centers.<ref name="pmid412125502">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	==References==		==References==

Non-alcoholic fatty liver disease ultrasound

2026-05-20T01:42:12Z

JAMA article updates

← Older revision		Revision as of 01:42, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==

	[[Ultrasound]] ~~may be~~ helpful in the diagnosis of non-alcoholic fatty liver disease. ~~Increased~~ echogenicity ~~and~~ coarsened echotexture of the liver is the ~~most prominent~~ and ~~diagnostic finding on an ultrasound~~ in ~~patients diagnosed non-alcoholic fatty liver disease~~.		[[Ultrasound]] is helpful in the diagnosis of non-alcoholic fatty liver disease and is the first-line imaging test for diagnosis of hepatic steatosis. Sonographic findings include increased hepatic echogenicity compared with the renal cortex, decreased visibility of intrahepatic vessels, coarsened echotexture of the liver and impaired visualization of the diaphragm and deeper liver tissue. Ultrasonography has a sensitivity of 80% to 89% and specificity of 87% to 90% for detecting moderate to severe steatosis, but sensitivity is less than 50% for mild steatosis when hepatic fat content is less than 20%.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	==Ultrasound==		==Ultrasound==

Non-alcoholic fatty liver disease laboratory findings

2026-05-20T01:37:59Z

JAMA article updates

← Older revision		Revision as of 01:37, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
	There are no specific diagnostic laboratory findings associated with non alcoholic fatty liver disease. Laboratory findings include abnormal liver function tests but are unspecific. Other laboratory tests are generally performed to rule out other diagnosis.		There are no specific diagnostic laboratory findings associated with non alcoholic fatty liver disease. Laboratory findings include abnormal liver function tests but are unspecific. Other laboratory tests are generally performed to rule out other diagnosis.
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	**Typical finding include a 2-4 fold elevation of the [[ALT]]		**Typical finding include a 2-4 fold elevation of the [[ALT]]
	**An [[ALT]]/[[AST]] ratio of greater than 1.		**An [[ALT]]/[[AST]] ratio of greater than 1.
			**Normal aminotransferase levels do not exclude MASLD, advanced fibrosis, or cirrhosis. Up to two-thirds of patients with MASLD, including patients with advanced fibrosis or cirrhosis, may have normal serum aminotransferase levels, and serum ALT levels do not correlate well with histological severity.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	* Evaluation for alternative causes of liver disease should be performed.		* Evaluation for alternative causes of liver disease should be performed.
	** These include [[HCV\|HCV serology]], serologies for [[autoimmune hepatitis]], and copper studies including serum [[ceruloplasmin]] and 24-hour urinary copper if [[Wilson's disease\|Wilson disease]] is suspected.		** These include [[HCV\|HCV serology]], serologies for [[autoimmune hepatitis]], and copper studies including serum [[ceruloplasmin]] and 24-hour urinary copper if [[Wilson's disease\|Wilson disease]] is suspected.

	* [[Fasting plasma glucose]] testing following an overnight fast is important to look for [[hyperglycemia]], which is an indicator of [[insulin resistance]].		* Laboratory evaluation should include assessment of metabolic risk factors. [[Fasting plasma glucose]] testing following an overnight fast is important to look for [[hyperglycemia]], which is an indicator of [[insulin resistance]].
	** Fasting [[insulin]] levels can confirm [[hyperinsulinemia]] and [[insulin resistance]]		** Fasting [[insulin]] levels can confirm [[hyperinsulinemia]] and [[insulin resistance]]
	* [[Lipid]] levels ( serum [[cholesterol]] and fasting [[triglycerides]] ) should be evaluated		* [[Lipid]] levels ( serum [[cholesterol]] and fasting [[triglycerides]] ) should be evaluated
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	* Iron studies (in particular elevated [[ferritin]] and transferring saturation) are often abnormal in NAFLD		* Iron studies (in particular elevated [[ferritin]] and transferring saturation) are often abnormal in NAFLD
	* Some patients with NAFLD may have low titers of [[Autoimmune disease\|autoimmune]] [[antibodies]].		* Some patients with NAFLD may have low titers of [[Autoimmune disease\|autoimmune]] [[antibodies]].
			* Noninvasive fibrosis assessment commonly includes the Fibrosis-4 index and the enhanced liver fibrosis test.
			** The Fibrosis-4 index includes age, serum alanine aminotransferase level, serum aspartate aminotransferase level, and platelet count. It estimates the risk of advanced liver fibrosis as low when the score is less than 1.30, indeterminate when the score is 1.30 to 2.67, and high when the score is greater than 2.67. A Fibrosis-4 index less than 1.3 has a negative predictive value of 85% to 90% for detecting advanced liver fibrosis.

	* [[Biomarkers]]		* [[Biomarkers]]
	** CK18 represents a promising [[biomarker]] for evaluation of the presence of NASH.		** CK18 represents a promising [[biomarker]] for evaluation of the presence of NASH.
	** A defining characteristic of NASH is [[cellular]] death, and [[serum]] CK18 levels had been shown to correlate with [[steatohepatitis]].		** A defining characteristic of NASH is [[cellular]] death, and [[serum]] CK18 levels had been shown to correlate with [[steatohepatitis]].

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	** F3. Bridging fibrosis. Numerous septa		** F3. Bridging fibrosis. Numerous septa
	** F4. Cirrhosis		** F4. Cirrhosis
			* The enhanced liver fibrosis test uses tissue inhibitor of metalloproteinase 1, type III procollagen amino terminal peptide, and hyaluronic acid to generate a fibrosis severity score. The enhanced liver fibrosis test has a sensitivity of approximately 98% for detecting advanced liver fibrosis.
			* The Agile 3+ score combines liver stiffness measured by vibration-controlled transient elastography with aspartate aminotransferase to alanine aminotransferase ratio, platelet count, diabetes status, sex, and age. It may identify advanced fibrosis more accurately than the Fibrosis-4 index or liver stiffness measurement alone.
	* Nonivasive serological liver fibrosis score such as AST to platelet ratio (APRI), and proprietary tests such as: FibroTest, FibroSure, Hepascore, and FibroSpect. An example is based on the "serum hyaluronic acid, procollagen type III N-terminal peptide, and tissue inhibitor of metalloproteinase 1"<ref name="pmid33185364">{{cite journal\| author=Newsome PN, Buchholtz K, Cusi K, Linder M, Okanoue T, Ratziu V \| display-authors=etal\| title=A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. \| journal=N Engl J Med \| year= 2021 \| volume= 384 \| issue= 12 \| pages= 1113-1124 \| pmid=33185364 \| doi=10.1056/NEJMoa2028395 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33185364 }} </ref>.		* Nonivasive serological liver fibrosis score such as AST to platelet ratio (APRI), and proprietary tests such as: FibroTest, FibroSure, Hepascore, and FibroSpect. An example is based on the "serum hyaluronic acid, procollagen type III N-terminal peptide, and tissue inhibitor of metalloproteinase 1"<ref name="pmid33185364">{{cite journal\| author=Newsome PN, Buchholtz K, Cusi K, Linder M, Okanoue T, Ratziu V \| display-authors=etal\| title=A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. \| journal=N Engl J Med \| year= 2021 \| volume= 384 \| issue= 12 \| pages= 1113-1124 \| pmid=33185364 \| doi=10.1056/NEJMoa2028395 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33185364 }} </ref>.
	** A score > "9.8 indicates a moderate risk of advanced fibrosis"<ref name="pmid33185364">/		** A score > "9.8 indicates a moderate risk of advanced fibrosis"<nowiki><ref name="pmid33185364">/</nowiki>
	** A score > "11.3 denotes a high risk of advanced fibrosis"<ref name="pmid33185364"/>		** A score > "11.3 denotes a high risk of advanced fibrosis"<ref name="pmid33185364" />
	* Noninvasive imaging scores such as the Fibroscan.		* Noninvasive imaging scores such as the Fibroscan.

Non-alcoholic fatty liver disease physical examination

2026-05-20T01:31:29Z

JAMA article updates

← Older revision		Revision as of 01:31, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
Line 8:		Line 8:
	==Physical Examination==		==Physical Examination==
	Patients with NAFLD usually appear [[asymptomatic]]. Physical examination of patients with NAFLD is usually unremarkable.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=https://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref>		Patients with NAFLD usually appear [[asymptomatic]]. Physical examination of patients with NAFLD is usually unremarkable.<ref name="urlNonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician">{{cite web \|url=https://www.aafp.org/afp/2013/0701/p35.html \|title=Nonalcoholic Fatty Liver Disease: Diagnosis and Management - American Family Physician \|format= \|work= \|accessdate=}}</ref>

			Approximately 50% to 60% of patients with MASLD have mild to moderate hepatomegaly, while less than 5% have splenomegaly. More than 80% of patients are overweight or obese, 60% to 70% have atherogenic dyslipidemia, approximately 60% have prediabetes or type 2 diabetes, and up to 50% have hypertension.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>

	==References==		==References==

Non-alcoholic fatty liver disease history and symptoms

2026-05-20T01:29:18Z

JAMA article updates

← Older revision		Revision as of 01:29, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
Line 7:		Line 7:

	==History==		==History==
	There is no significant history associated in patients with the non-alcoholic fatty liver disease. However, history of alcohol consumption and family history of non-alcoholic fatty liver disease must be obtained.		There is no significant history associated in patients with the non-alcoholic fatty liver disease. MASLD is often detected incidentally when hepatic steatosis is identified on abdominal ultrasonography performed for another indication or when mild to moderate elevations in serum aminotransferase levels are found. However, history of alcohol consumption and family history of non-alcoholic fatty liver disease must be obtained.

	==Symptoms==		==Symptoms==
	Usually, nonalcoholic fatty liver disease presents with no or few symptoms and sighs but when it does it shows the following<ref>{{Cite web\|url=https://www.mayoclinic.org/diseases-conditions/nonalcoholic-fatty-liver-disease/symptoms-causes/syc-20354567\|title=Nafld\|last=\|first=\|date=\|website=\|publisher=\|access-date=}}</ref><ref name="pmid28507929">{{cite journal \|vauthors=Vizuete J, Camero A, Malakouti M, Garapati K, Gutierrez J \|title=Perspectives on Nonalcoholic Fatty Liver Disease: An Overview of Present and Future Therapies \|journal=J Clin Transl Hepatol \|volume=5 \|issue=1 \|pages=67–75 \|year=2017 \|pmid=28507929 \|pmc=5411359 \|doi=10.14218/JCTH.2016.00061 \|url=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease">{{cite web \|url=http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/nonalcoholic-fatty-liver-disease/ \|title=Nonalcoholic Fatty Liver Disease \|format= \|work= \|accessdate=}}</ref>		Usually, nonalcoholic fatty liver disease presents with no or few symptoms and sighs but when it does it shows the following<ref>{{Cite web\|url=https://www.mayoclinic.org/diseases-conditions/nonalcoholic-fatty-liver-disease/symptoms-causes/syc-20354567\|title=Nafld\|last=\|first=\|date=\|website=\|publisher=\|access-date=}}</ref><ref name="pmid28507929">{{cite journal \|vauthors=Vizuete J, Camero A, Malakouti M, Garapati K, Gutierrez J \|title=Perspectives on Nonalcoholic Fatty Liver Disease: An Overview of Present and Future Therapies \|journal=J Clin Transl Hepatol \|volume=5 \|issue=1 \|pages=67–75 \|year=2017 \|pmid=28507929 \|pmc=5411359 \|doi=10.14218/JCTH.2016.00061 \|url=}}</ref><ref name="urlNonalcoholic Fatty Liver Disease">{{cite web \|url=http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/nonalcoholic-fatty-liver-disease/ \|title=Nonalcoholic Fatty Liver Disease \|format= \|work= \|accessdate=}}</ref><ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*[[Hepatomegaly]]		*[[Hepatomegaly]]
			*Malaise
	*[[Fatigue]]		*[[Fatigue]]
	*[[Ascites]]		*[[Ascites]]

Non-alcoholic fatty liver disease natural history, complications and prognosis

2026-05-20T01:10:03Z

JAMA article updates

← Older revision		Revision as of 01:10, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{MKK}}		{{CMG}}; {{AE}} {{MKK}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
Line 14:		Line 14:
	**1) Patients with [[Non-alcoholic fatty liver disease\|NAFLD]] has overall high [[morbidity]] and [[mortality]] rate and the common cause of death in NAFLD patients is cardiovascular disease.		**1) Patients with [[Non-alcoholic fatty liver disease\|NAFLD]] has overall high [[morbidity]] and [[mortality]] rate and the common cause of death in NAFLD patients is cardiovascular disease.
	**2) Patients with [[NASH]] has more liver-related mortality rate		**2) Patients with [[NASH]] has more liver-related mortality rate
			* Approximately 15% to 40% of patients with isolated hepatic steatosis progress to MASH. Fibrosis progression is usually slow, with progression of approximately 1 fibrosis stage over 14 years among patients with isolated steatosis and approximately 1 fibrosis stage over 7 years among patients with MASH. More advanced fibrosis is the strongest risk factor for progression to cirrhosis, hepatic decompensation, and liver-related mortality.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
			* In a systematic review and meta-analysis of patients with histologically confirmed MASLD, 2% to 3% of patients with isolated steatosis developed advanced fibrosis over 15 to 20 years, while approximately 25% to 30% of patients with MASH developed advanced fibrosis within 8 to 10 years. Among patients with biopsy-confirmed MASH and F3 fibrosis, 22% progressed to cirrhosis over 2 years.
			* Cirrhosis is associated with hepatic decompensation events, including ascites, hepatic encephalopathy, and variceal bleeding, which occur at rates of about 10% annually. Up to nearly 2.5% of patients with cirrhosis develop incident hepatocellular carcinoma annually.
	* If left untreated, patients with NAFLD may progress to develop hepato-cellular carcinoma ([[HCC]]). But it is directly propotional to the degree of [[fibrosis]] and advanced [[cirrhosis]]		* If left untreated, patients with NAFLD may progress to develop hepato-cellular carcinoma ([[HCC]]). But it is directly propotional to the degree of [[fibrosis]] and advanced [[cirrhosis]]
	* Children who are positive with NAFLD are also prone to short lifespan when compared to general population.<ref name="pmid27213358">{{cite journal\| author=Calzadilla Bertot L, Adams LA\| title=The Natural Course of Non-Alcoholic Fatty Liver Disease. \| journal=Int J Mol Sci \| year= 2016 \| volume= 17 \| issue= 5 \| pages= \| pmid=27213358 \| doi=10.3390/ijms17050774 \| pmc=4881593 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27213358 }} </ref>		* Children who are positive with NAFLD are also prone to short lifespan when compared to general population.<ref name="pmid27213358">{{cite journal\| author=Calzadilla Bertot L, Adams LA\| title=The Natural Course of Non-Alcoholic Fatty Liver Disease. \| journal=Int J Mol Sci \| year= 2016 \| volume= 17 \| issue= 5 \| pages= \| pmid=27213358 \| doi=10.3390/ijms17050774 \| pmc=4881593 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27213358 }} </ref>
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	**[[Cirrhosis]]. Amon patients with both [[hepatic steatosis]] and elevated [[liver function tests]], the incidence rate of cirrhosis is 3.37 (95% CI: 2.34-4.86) per 1000 1000 person-years.		**[[Cirrhosis]]. Amon patients with both [[hepatic steatosis]] and elevated [[liver function tests]], the incidence rate of cirrhosis is 3.37 (95% CI: 2.34-4.86) per 1000 1000 person-years.
	**[[Internal bleeding]]		**[[Internal bleeding]]
	**~~Encepholopathy~~		**Hepatic decompensation events include ascites, hepatic encephalopathy, and variceal bleeding.

			* Other complications of MASLD include hepatocellular carcinoma, cardiovascular disease, chronic kidney disease, heart failure, atrial fibrillation, incident type 2 diabetes, and certain extrahepatic cancers.

	[[Non-alcoholic fatty liver disease]], especially if with cirrhosis, may be associated with [[thrombocytopenia]]<ref name="pmid34312112">{{cite journal\| author=Rivera-Álvarez M, Córdova-Ramírez AC, Elías-De-La-Cruz GD, Murrieta-Álvarez I, León-Peña AA, Cantero-Fortiz Y \| display-authors=etal\| title=Non-alcoholic fatty liver disease and thrombocytopenia IV: its association with granulocytopenia. \| journal=Hematol Transfus Cell Ther \| year= 2021 \| volume= \| issue= \| pages= \| pmid=34312112 \| doi=10.1016/j.htct.2021.06.004 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34312112 }} </ref><ref name="pmid31575467">{{cite journal\| author=Panke CL, Tovo CV, Villela-Nogueira CA, Cravo CM, Ferreira FC, Rezende GFM \| display-authors=etal\| title=Evaluation of thrombocytopenia in patients with non-alcoholic fatty liver disease without cirrhosis. \| journal=Ann Hepatol \| year= 2020 \| volume= 19 \| issue= 1 \| pages= 88-91 \| pmid=31575467 \| doi=10.1016/j.aohep.2019.05.011 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31575467 }} </ref>.		[[Non-alcoholic fatty liver disease]], especially if with cirrhosis, may be associated with [[thrombocytopenia]]<ref name="pmid34312112">{{cite journal\| author=Rivera-Álvarez M, Córdova-Ramírez AC, Elías-De-La-Cruz GD, Murrieta-Álvarez I, León-Peña AA, Cantero-Fortiz Y \| display-authors=etal\| title=Non-alcoholic fatty liver disease and thrombocytopenia IV: its association with granulocytopenia. \| journal=Hematol Transfus Cell Ther \| year= 2021 \| volume= \| issue= \| pages= \| pmid=34312112 \| doi=10.1016/j.htct.2021.06.004 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34312112 }} </ref><ref name="pmid31575467">{{cite journal\| author=Panke CL, Tovo CV, Villela-Nogueira CA, Cravo CM, Ferreira FC, Rezende GFM \| display-authors=etal\| title=Evaluation of thrombocytopenia in patients with non-alcoholic fatty liver disease without cirrhosis. \| journal=Ann Hepatol \| year= 2020 \| volume= 19 \| issue= 1 \| pages= 88-91 \| pmid=31575467 \| doi=10.1016/j.aohep.2019.05.011 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31575467 }} </ref>.

	===Prognosis===		===Prognosis===
			* Cardiovascular disease is the leading cause of death in patients with noncirrhotic MASLD, followed by extrahepatic cancer and liver-related complications. In patients with MASLD-related cirrhosis, liver-related and cardiovascular disease-related deaths are the predominant causes of mortality.<ref name="pmid412125502">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	* In a cohort study of patient who had biopsy-proven NAFLD, 6% developed death, hepatocellular carcinoma, or death with 5 years<ref name="pmid37290471">{{cite journal\| author=Mózes FE, Lee JA, Vali Y, Alzoubi O, Staufer K, Trauner M \| display-authors=etal\| title=Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with non-alcoholic fatty liver disease: an individual participant data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37290471 \| doi=10.1016/S2468-1253(23)00141-3 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37290471 }} </ref>.		* In a cohort study of patient who had biopsy-proven NAFLD, 6% developed death, hepatocellular carcinoma, or death with 5 years<ref name="pmid37290471">{{cite journal\| author=Mózes FE, Lee JA, Vali Y, Alzoubi O, Staufer K, Trauner M \| display-authors=etal\| title=Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with non-alcoholic fatty liver disease: an individual participant data meta-analysis. \| journal=Lancet Gastroenterol Hepatol \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37290471 \| doi=10.1016/S2468-1253(23)00141-3 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37290471 }} </ref>.

Line 83:		Line 89:
	** 25% (4 of 16) (Supplementary table 1)		** 25% (4 of 16) (Supplementary table 1)
	* Histology is the most reliable means to grade the severity of the disease and thus estimate prognosis.		* Histology is the most reliable means to grade the severity of the disease and thus estimate prognosis.
			** Fibrosis stage is the strongest prognostic factor for liver-related morbidity and mortality. Compared with patients with no fibrosis, patients with cirrhosis have substantially higher risks of liver-related events, liver-related mortality, liver transplantation, and all-cause mortality.
	** The presence of [[fibrosis]] and [[cirrhosis]] is associated with a particularly poor prognosis among patients with NAFLD. <ref name="pmid22102440">{{cite journal\| author=Jepsen P, Grønbæk H\| title=Prognosis and staging of non-alcoholic fatty liver disease. \| journal=BMJ \| year= 2011 \| volume= 343 \| issue= \| pages= d7302 \| pmid=22102440 \| doi=10.1136/bmj.d7302 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22102440 }} </ref>		** The presence of [[fibrosis]] and [[cirrhosis]] is associated with a particularly poor prognosis among patients with NAFLD. <ref name="pmid22102440">{{cite journal\| author=Jepsen P, Grønbæk H\| title=Prognosis and staging of non-alcoholic fatty liver disease. \| journal=BMJ \| year= 2011 \| volume= 343 \| issue= \| pages= d7302 \| pmid=22102440 \| doi=10.1136/bmj.d7302 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22102440 }} </ref>
	** Depending on the extent of the [[fibrosis]] and [[cirrhosis]] at the time of diagnosis, the prognosis may vary.<ref name="SumanKhullar2016">{{cite journal\|last1=Suman\|first1=A.\|last2=Khullar\|first2=V.\|last3=Limaye\|first3=A.\|title=Complications of Non-Alcoholic Fatty Liver Disease\|journal=Journal of Hepatology\|volume=64\|issue=2\|year=2016\|pages=S473\|issn=01688278\|doi=10.1016/S0168-8278(16)00798-4}}</ref>		** Depending on the extent of the [[fibrosis]] and [[cirrhosis]] at the time of diagnosis, the prognosis may vary.<ref name="SumanKhullar2016">{{cite journal\|last1=Suman\|first1=A.\|last2=Khullar\|first2=V.\|last3=Limaye\|first3=A.\|title=Complications of Non-Alcoholic Fatty Liver Disease\|journal=Journal of Hepatology\|volume=64\|issue=2\|year=2016\|pages=S473\|issn=01688278\|doi=10.1016/S0168-8278(16)00798-4}}</ref>

Non-alcoholic fatty liver disease screening

2026-05-20T01:01:48Z

JAMA article updates

← Older revision		Revision as of 01:01, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}[[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
Line 10:		Line 10:
	* However, American Gastroenterological Association Technical Review recommends screening for non-alcoholic fatty liver disease in population at high risk such as [[obesity]], [[insulin resistance]], and [[metabolic syndrome]].		* However, American Gastroenterological Association Technical Review recommends screening for non-alcoholic fatty liver disease in population at high risk such as [[obesity]], [[insulin resistance]], and [[metabolic syndrome]].
	* Screening is however complicated by the lack of accurate, noninvasive diagnostic tools for NAFLD and the lack of clear treatment that can be proposed to the patient.		* Screening is however complicated by the lack of accurate, noninvasive diagnostic tools for NAFLD and the lack of clear treatment that can be proposed to the patient.
			* Current guidelines summarized in the JAMA review<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref> recommend a 2-tier testing approach to screen for advanced liver fibrosis in high-risk populations, including individuals with prediabetes or type 2 diabetes, obesity, 2 or more cardiometabolic risk factors, imaging-detected hepatic steatosis, or persistently elevated serum aminotransferase levels.
	~~However~~, the AGA ~~recommend~~ screening<ref name="pmid37542503">{{cite journal\| author=Wattacheril JJ, Abdelmalek MF, Lim JK, Sanyal AJ\| title=AGA Clinical Practice Update on the Role of Noninvasive Biomarkers in the Evaluation and Management of Nonalcoholic Fatty Liver Disease: Expert Review. \| journal=Gastroenterology \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37542503 \| doi=10.1053/j.gastro.2023.06.013 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37542503 }} </ref>.		** The first step is calculation of the Fibrosis-4 index, usually performed in primary care. Patients with a Fibrosis-4 index greater than 1.3 should undergo vibration-controlled transient elastography or another noninvasive test, such as the enhanced liver fibrosis test. Patients with liver stiffness greater than 8.0 kPa or an enhanced liver fibrosis test score greater than 9.8 should be referred to a hepatologist.
			** Patients with a FIB-4 score less than 1.3 should undergo lifestyle modification, avoidance of alcohol intake, and treatment of type 2 diabetes, obesity, dyslipidemia, and hypertension. Repeat FIB-4 testing may be performed every 1 to 3 years. Patients with indeterminate or high-risk findings should undergo additional noninvasive fibrosis assessment and may require hepatology referral.
			{\| class="wikitable"
			\|'''FIB-4 score'''
			\|'''Interpretation'''
			\|-
			\|<1.30
			\|Low risk of advanced fibrosis
			\|-
			\|1.30-2.67
			\|Indeterminate risk of advanced fibrosis
			\|-
			\|>2.67
			\|High risk of advanced fibrosis
			\|}
			The AGA also recommends screening<ref name="pmid37542503">{{cite journal\| author=Wattacheril JJ, Abdelmalek MF, Lim JK, Sanyal AJ\| title=AGA Clinical Practice Update on the Role of Noninvasive Biomarkers in the Evaluation and Management of Nonalcoholic Fatty Liver Disease: Expert Review. \| journal=Gastroenterology \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37542503 \| doi=10.1053/j.gastro.2023.06.013 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37542503 }} </ref>.

	Workflows to promote screening may increase treatment<ref name="pmid37549979">{{cite journal\| author=Zhang X, Yip TC, Wong GL, Leow WX, Liang LY, Lim LL \| display-authors=etal\| title=Clinical care pathway to detect advanced liver disease in patients with type 2 diabetes through automated fibrosis score calculation and electronic reminder messages: a randomised controlled trial. \| journal=Gut \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37549979 \| doi=10.1136/gutjnl-2023-330269 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37549979 }} </ref>.		Workflows to promote screening may increase treatment<ref name="pmid37549979">{{cite journal\| author=Zhang X, Yip TC, Wong GL, Leow WX, Liang LY, Lim LL \| display-authors=etal\| title=Clinical care pathway to detect advanced liver disease in patients with type 2 diabetes through automated fibrosis score calculation and electronic reminder messages: a randomised controlled trial. \| journal=Gut \| year= 2023 \| volume= \| issue= \| pages= \| pmid=37549979 \| doi=10.1136/gutjnl-2023-330269 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=37549979 }} </ref>.

Non-alcoholic fatty liver disease risk factors

2026-05-20T00:56:27Z

JAMA article updates

← Older revision		Revision as of 00:56, 20 May 2026
Line 1:		Line 1:
	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	==Risk Factors==		==Risk Factors==
	Risk factors in the development of non-alcoholic fatty liver disease include:<ref name="pmid25892859">{{cite journal\| author=Streba LA, Vere CC, Rogoveanu I, Streba CT\| title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question. \| journal=World J Gastroenterol \| year= 2015 \| volume= 21 \| issue= 14 \| pages= 4103-10 \| pmid=25892859 \| doi=10.3748/wjg.v21.i14.4103 \| pmc=4394070 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25892859 }} </ref><ref name="pmid22319959">{{cite journal\| author=He S, Bao W, Shao M, Wang W, Wang C, Sun J et al.\| title=Risk factors for non-alcoholic fatty liver disease in a Chinese population. \| journal=Acta Gastroenterol Belg \| year= 2011 \| volume= 74 \| issue= 4 \| pages= 503-8 \| pmid=22319959 \| doi= \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22319959 }} </ref><ref name="pmid258928592">{{cite journal \|vauthors=Streba LA, Vere CC, Rogoveanu I, Streba CT \|title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question \|journal=World J. Gastroenterol. \|volume=21 \|issue=14 \|pages=4103–10 \|year=2015 \|pmid=25892859 \|pmc=4394070 \|doi=10.3748/wjg.v21.i14.4103 \|url=}}</ref>		Risk factors in the development of non-alcoholic fatty liver disease include:<ref name="pmid25892859">{{cite journal\| author=Streba LA, Vere CC, Rogoveanu I, Streba CT\| title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question. \| journal=World J Gastroenterol \| year= 2015 \| volume= 21 \| issue= 14 \| pages= 4103-10 \| pmid=25892859 \| doi=10.3748/wjg.v21.i14.4103 \| pmc=4394070 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25892859 }} </ref><ref name="pmid22319959">{{cite journal\| author=He S, Bao W, Shao M, Wang W, Wang C, Sun J et al.\| title=Risk factors for non-alcoholic fatty liver disease in a Chinese population. \| journal=Acta Gastroenterol Belg \| year= 2011 \| volume= 74 \| issue= 4 \| pages= 503-8 \| pmid=22319959 \| doi= \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22319959 }} </ref><ref name="pmid258928592">{{cite journal \|vauthors=Streba LA, Vere CC, Rogoveanu I, Streba CT \|title=Nonalcoholic fatty liver disease, metabolic risk factors, and hepatocellular carcinoma: an open question \|journal=World J. Gastroenterol. \|volume=21 \|issue=14 \|pages=4103–10 \|year=2015 \|pmid=25892859 \|pmc=4394070 \|doi=10.3748/wjg.v21.i14.4103 \|url=}}</ref><ref name="pmid412125502">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
	*[[Viral hepatitis]]		*[[Viral hepatitis]]
	*Rapid [[weight loss]]		*Rapid [[weight loss]]
	*[[Malnutrition]]		*[[Malnutrition]]
	*[[Hypertriglyceridemia]]		*[[Hypertriglyceridemia]]
			*Low HDL cholesterol
	*[[Sleep apnea]]		*[[Sleep apnea]]
	*[[Hypothyroidism]]		*[[Hypothyroidism]]
	*[[Obesity]]		*Abdominal overweight or [[Obesity]]
	*[[Hypopituitarism]]		*[[Hypopituitarism]]
	*[[Diabetes mellitus type 2]]		*Prediabetes or [[Diabetes mellitus type 2]]
			*Insulin resistance
			*Hypertension
	*[[Polycystic ovary syndrome\|PCOS]] ([[polycystic ovarian syndrome]])		*[[Polycystic ovary syndrome\|PCOS]] ([[polycystic ovarian syndrome]])
			*Older age
			*Male sex
			*Postmenopausal status
			*PNPLA3 and TM6SF2 genetic variants
			*Sedentary lifestyle
			*Smoking
			*High intake of fructose, especially from sugar-sweetened beverages
			*High-calorie diets rich in saturated fats, sugars, and processed foods
			*Alcohol intake above MASLD thresholds
	*Medications like [[tamoxifen]], [[corticosteriods]], [[methotrexate]]		*Medications like [[tamoxifen]], [[corticosteriods]], [[methotrexate]]


			Cardiometabolic risk factors used in the classification of MASLD include body mass index of 25 or greater, or 23 or greater in Asian individuals; waist circumference of 80 cm or greater in women and 94 cm or greater in men; fasting glucose level of 5.6 mmol/L or greater, 2-hour postload glucose level of 7.8 mmol/L or greater, hemoglobin A1c level of 5.7% or greater, established type 2 diabetes, or use of glucose-lowering medication; blood pressure of 130/85 mm Hg or greater or use of antihypertensive medication; plasma triglyceride level of 1.70 mmol/L or greater or use of triglyceride-lowering medication; and low HDL cholesterol.

	==References==		==References==
	{{reflist\|2}}		{{reflist\|2}}

Non-alcoholic fatty liver disease epidemiology and demographics

2026-05-20T00:49:32Z

JAMA article updates

← Older revision		Revision as of 00:49, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	===Prevalance===		===Prevalance===
			* MASLD is the most common chronic liver disease worldwide. Approximately 30% to 40% of adults worldwide have MASLD. The prevalence is substantially higher among individuals with type 2 diabetes and obesity, affecting approximately 60% to 70% of individuals with type 2 diabetes and approximately 70% to 80% of individuals with obesity.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
			* In a systematic review of 92 population-based studies from 1990 to 2019, the highest prevalence of ultrasound-detected MASLD was observed in Latin America and the lowest in Western Europe. By 2040, the global prevalence of MASLD among adults is projected to exceed 55%. In 2021, the global age-standardized prevalence of MASLD was 15,018 per 100,000 population, and the annual incidence was 608 per 100,000 population. The prevalence was higher in men than women and peaked at 45 to 49 years of age in men and 50 to 54 years of age in women.
			* Among individuals with type 2 diabetes, the global pooled prevalence of MASLD based on ultrasonography was 65.3%. Among individuals with type 2 diabetes who had liver biopsy data, the global histological prevalence of MASH was 66.4%, stage F2 fibrosis was present in 40.8%, and advanced fibrosis, defined as stage F3 or F4, was present in 15.5%.
	* The prevalence of non-alcoholic liver disease in the United States is estimated to be 10,000 to 24,000 cases per 100,000 individuals annually.		* The prevalence of non-alcoholic liver disease in the United States is estimated to be 10,000 to 24,000 cases per 100,000 individuals annually.

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	=== Gender ===		=== Gender ===
	* Men are more commonly affected by non-alcoholic liver disease than women.		* Men are more commonly affected by non-alcoholic liver disease than women. In global 2021 estimates, prevalence peaked at 45 to 49 years of age in men and at 50 to 54 years of age in women.
	* Among women it is more common in post-menopausal women than pre-menopausal.		* Among women it is more common in post-menopausal women than pre-menopausal.

Non-alcoholic fatty liver disease causes

2026-05-20T00:33:03Z

JAMA article updates

← Older revision		Revision as of 00:33, 20 May 2026
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}} [[User:Parth Vikram Singh\|Parth Vikram Singh, MBBS]][3]

	==Overview==		==Overview==
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	*Less common causes of non-alcoholic fatty liver disease include [[hypertension]] and [[dyslipidemia]].		*Less common causes of non-alcoholic fatty liver disease include [[hypertension]] and [[dyslipidemia]].
			*The risk of developing MASLD and progressing to MASH increases with the number of metabolic syndrome features, including abdominal obesity, hypertension, hypertriglyceridemia, low HDL cholesterol, and elevated blood glucose.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref> Cardiometabolic risk factors used in the classification of MASLD include body mass index of 25 or greater, or 23 or greater in Asian individuals; waist circumference of 80 cm or greater in women and 94 cm or greater in men; fasting glucose level of 5.6 mmol/L or greater, 2-hour postload glucose level of 7.8 mmol/L or greater, hemoglobin A1c level of 5.7% or greater, established type 2 diabetes, or use of glucose-lowering medication; blood pressure of 130/85 mm Hg or greater or use of antihypertensive medication; plasma triglyceride level of 1.70 mmol/L or greater or use of triglyceride-lowering medication; and low HDL cholesterol.
			*Other contributors include older age, male sex, postmenopausal status, PNPLA3 and TM6SF2 genetic variants, sedentary lifestyle, smoking, high fructose intake, alcohol consumption above MASLD thresholds, and high-calorie diets rich in saturated fats, sugars, and processed foods.
			*Other known causes of hepatic steatosis that should be excluded include use of corticosteroids, methotrexate, or tamoxifen; hepatitis C virus infection; iron overload; celiac disease; HIV infection; malnutrition; Wilson disease; lysosomal acid lipase deficiency; hypobetalipoproteinemia; and inborn errors of metabolism.

	===Secondary NAFLD===		===Secondary NAFLD===

Non-alcoholic fatty liver disease classification

2026-05-20T00:22:39Z

← Older revision		Revision as of 00:22, 20 May 2026
(2 intermediate revisions by the same user not shown)
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	__NOTOC__		__NOTOC__
	{{Non alcoholic fatty liver disease}}		{{Non alcoholic fatty liver disease}}
	{{CMG}}; {{AE}} {{VKG}}		{{CMG}}; {{AE}} {{VKG}}{{PVS}}

	==Overview==		==Overview==
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	** Conditions such as [[abetalipoproteinemia]] or [[Wilson's disease\|Wilson’s disease]]		** Conditions such as [[abetalipoproteinemia]] or [[Wilson's disease\|Wilson’s disease]]
	\|}		\|}


			Steatotic liver disease may be subclassified according to the presence of cardiometabolic risk factors, alcohol intake, and other causes of hepatic steatosis.<ref name="pmid41212550">{{cite journal\|vauthors=Tilg H, Petta S, Stefan N, Targher G\|title=Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review\|journal=JAMA\|volume=335\|issue=2\|pages=163–174\|date=January 2026\|pmid=41212550\|doi=10.1001/jama.2025.19615\|url=}}</ref>
			{\| class="wikitable"
			!Category
			!Definition
			\|-
			\|MASLD
			\|Hepatic steatosis with at least 1 cardiometabolic risk factor, alcohol intake less than 140 g/week in women and less than 210 g/week in men, and no other known cause of hepatic steatosis
			\|-
			\|Metabolic dysfunction and alcohol-related liver disease (MetALD)
			\|Hepatic steatosis with metabolic dysfunction and alcohol intake of 140-350 g/week in women or 210-420 g/week in men
			\|-
			\|Alcohol-associated liver disease
			\|Alcohol intake greater than 350 g/week in women or greater than 420 g/week in men
			\|-
			\|Cryptogenic steatotic liver disease
			\|Hepatic steatosis without cardiometabolic risk factors and without an identifiable cause
			\|-
			\|Specific-etiology steatotic liver disease
			\|Hepatic steatosis due to another identifiable cause, such as drug-induced liver injury, iron overload, genotype 3 hepatitis C, Wilson disease, lysosomal acid lipase deficiency, hypobetalipoproteinemia, inborn errors of metabolism, celiac disease, malnutrition, or HIV infection
			\|}
			One standard drink is approximately equivalent to 10 g of alcohol, corresponding approximately to 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof distilled spirits.

	==Histopathological classification==		==Histopathological classification==
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	\|}		\|}
	===Staging===		===Staging===
	Based on ~~the degree of [[~~fibrosis~~]] on [[biopsy]] non~~-~~alochoic fatty liver disease can be classified into 4 stages.~~
	{~~\| border="1" cellpadding="5" cellspacing="0" align="center"~~ \|class="wikitable"		Based on liver biopsy histology, liver fibrosis in MASLD is scored using a '''5-stage scale:'''
	~~! colspan="2" style="background:#efefef;"~~ \|~~Staging~~		{\| class="wikitable"
			\|'''Stage'''
			\|'''Histologic description'''
			\|-
			\|F0
			\|Absence of fibrosis
	\|-		\|-
	\|~~Stage 1~~		\|F1
	\|		\|Perisinusoidal or portal fibrosis
	~~Zone 3 [[fibrosis]]<br>~~
	Perisinusoidal ~~[[fibrosis]]<br>~~
	~~Portal/ periportal [[~~fibrosis]]
	\|-		\|-
	\|~~Stage 2~~		\|F2
	\|Perisinusoidal and portal/periportal fibrosis		\|Perisinusoidal and portal or periportal fibrosis
	\|-		\|-
	\|~~Stage 3~~		\|F3
	\|~~Bridging [[~~fibrosis]]		\|Septal and bridging fibrosis
	\|-		\|-
	\|~~Stage 4~~		\|F4
	\|[[Cirrhosis]]		\|Cirrhosis
	\|}		\|}