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{{Infobox disease |
{{For|Injuries associated with liver|Liver injury}}
Name = Hepatic disease |
{{Infobox medical condition (new)
Image = Non-alcoholic_fatty_liver_disease1.jpg|
| name = Liver disease
Caption = [[Micrograph]] of [[non-alcoholic fatty liver disease]], demonstrating marked [[macrovesicular steatosis]]. [[Trichrome stain]].|
| image = Human liver with metastatic lesions from primary pancreas carcinoma (2).jpg
DiseasesDB = |
| caption = A [[gross pathology]] specimen of [[liver metastases]] caused by [[pancreatic cancer]]
ICD10 = |
ICD9 = |
| field = [[Hepatology]], [[gastroenterology]]
ICDO = |
| pronounce =
OMIM = |
| synonyms = Hepatic disease
MedlinePlus = 000205 |
| symptoms =
| complications =
eMedicineSubj = |
| onset =
eMedicineTopic = |
MeshID = D008107 |
| duration =
| types = [[Fatty liver disease]], [[Hepatitis]] (and several more)<ref name=medl/>
| causes =
| risks =
| diagnosis = [[Liver function tests]]<ref name=web/>
| differential =
| prevention =
| treatment = Depends on type(See types)
| medication =
| prognosis =
| frequency =
| deaths =
}}
}}

'''Liver disease''' (also called '''hepatic disease''') is a type of damage to or [[disease]] of the [[liver]].
'''Liver disease''', or '''hepatic disease''', is any of many [[disease]]s of the [[liver]].<ref name="medl">{{cite web |title=Liver Diseases |url=https://medlineplus.gov/liverdiseases.html |website=MedlinePlus }}</ref> If long-lasting it is termed [[chronic liver disease]].<ref>{{cite web|title=NHS Choices|url=http://www.nhs.uk/conditions/Cirrhosis/Pages/Introduction.aspx|website=Cirrhosis|access-date=6 October 2015}}</ref> Although the diseases differ in detail, liver diseases often have features in common.

==Liver diseases==
{{clear}}
<gallery mode="packed" widths="360px" heights="160">
File:Ground glass hepatocytes high mag cropped 2.jpg|Ground glass hepatocytes
File:Primary biliary cirrhosis intermed mag much cropping.jpg|Primary biliary cirrhosis
File:Buddchiari2.PNG|Budd–Chiari syndrome
File:Non-alcoholic_fatty_liver_disease1.jpg| [[Micrograph]] of [[non-alcoholic fatty liver disease]]
</gallery>
There are more than a hundred different liver diseases. Some of the most common are:<ref>{{Cite web|title = Liver disease – NHS Choices|url = http://www.nhs.uk/Conditions/liver-disease/Pages/Introduction.aspx|website = www.nhs.uk|access-date = 2015-06-20}}</ref>
* [[Fascioliasis]], a parasitic infection of liver caused by a [[liver fluke]] of the genus ''[[Fasciola]]'', mostly ''[[Fasciola hepatica]]''.<ref>{{Cite web|title = CDC – Fasciola|url = https://www.cdc.gov/parasites/fasciola/|website = www.cdc.gov|access-date = 2015-06-20}}</ref>
* [[Hepatitis]], inflammation of the liver, is caused by various viruses ([[viral hepatitis]]) also by some [[hepatotoxicity|liver toxins]] (e.g. [[alcoholic hepatitis]]), autoimmunity ([[autoimmune hepatitis]]) or hereditary conditions.<ref>{{cite web |title=Hepatitis |url=https://medlineplus.gov/hepatitis.html |website=MedlinePlus }}</ref>
* [[Alcoholic liver disease]] is a hepatic manifestation of [[Alcohol abuse|alcohol overconsumption]], including [[fatty liver|fatty liver disease]], alcoholic hepatitis, and [[cirrhosis]]. Analogous terms such as "drug-induced" or "toxic" liver disease are also used to refer to disorders caused by various drugs.<ref>{{MedlinePlusEncyclopedia|000281|Alcoholic liver disease}}</ref>
* [[Fatty liver|Fatty liver disease]] (hepatic [[steatosis]]) is a reversible condition where large vacuoles of [[triglyceride]] fat accumulate in liver cells.<ref>{{Cite web|title = Hepatic steatosis|url = http://medical-dictionary.thefreedictionary.com/Hepatic+steatosis|access-date = 2015-06-20}}</ref> [[Non-alcoholic fatty liver disease]] is a spectrum of disease associated with obesity and [[metabolic syndrome]].<ref>{{Cite web|title = Non-alcoholic fatty liver disease – NHS Choices|url = http://www.nhs.uk/conditions/fatty-liver-disease/Pages/Introduction.aspx|website = www.nhs.uk|access-date = 2015-06-20}}</ref>
* [[Hereditary disease]]s that cause damage to the liver include [[hemochromatosis]],<ref>{{cite web |title=Hemochromatosis |url=https://medlineplus.gov/hemochromatosis.html |website=MedlinePlus }}</ref> involving accumulation of [[iron]] in the body, and [[Wilson's disease]]. Liver damage is also a clinical feature of [[alpha 1-antitrypsin deficiency]]<ref>{{cite web |title=Alpha-1 Antitrypsin Deficiency |url=https://medlineplus.gov/alpha1antitrypsindeficiency.html |website=MedlinePlus }}</ref> and [[glycogen storage disease type II]].<ref>{{Cite book|title = Glycogen Storage Disease Type II (Pompe Disease)|chapter-url = https://www.ncbi.nlm.nih.gov/books/NBK1261/|publisher = University of Washington, Seattle|date = 1993|location = Seattle (WA)|pmid = 20301438|first1 = Nancy|last1 = Leslie|first2 = Brad T.|last2 = Tinkle|editor-first = Roberta A.|editor-last = Pagon|editor-first2 = Margaret P.|editor-last2 = Adam|editor-first3 = Holly H.|editor-last3 = Ardinger|editor-first4 = Stephanie E.|editor-last4 = Wallace|editor-first5 = Anne|editor-last5 = Amemiya|editor-first6 = Lora J.H.|editor-last6 = Bean|editor-first7 = Thomas D.|editor-last7 = Bird|editor-first8 = Cynthia R.|editor-last8 = Dolan|editor-first9 = Chin-To|editor-last9 = Fong|chapter = Pompe Disease}}</ref>
* In [[transthyretin-related hereditary amyloidosis]], the liver produces a mutated transthyretin protein which has severe neurodegenerative or cardiopathic effects. Liver transplantation can be curative.<ref>{{Cite web|title = Transthyretin amyloidosis|url = http://ghr.nlm.nih.gov/condition/transthyretin-amyloidosis|website = Genetics Home Reference|access-date = 2015-06-20}}</ref>
* [[Gilbert's syndrome]], a genetic disorder of [[bilirubin]] metabolism found in a small percent of the population, can cause mild [[jaundice]].<ref>{{Cite web|title = Gilbert syndrome|url = http://ghr.nlm.nih.gov/condition/gilbert-syndrome|website = Genetics Home Reference|access-date = 2015-06-20}}</ref>
* [[Cirrhosis]] is the formation of fibrous tissue ([[fibrosis]]) in the place of liver cells that have died due to a variety of causes, including viral hepatitis, alcohol overconsumption, and other forms of liver toxicity. Cirrhosis causes chronic [[liver failure]].<ref>{{Cite web|title = Cirrhosis: MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000255.htm|website = www.nlm.nih.gov|access-date = 2015-06-20}}</ref>
* Primary [[liver cancer]] most commonly manifests as [[hepatocellular carcinoma]] or [[cholangiocarcinoma]]; rarer forms include [[angiosarcoma]] and [[hemangiosarcoma]] of the liver. (Many liver malignancies are secondary lesions that have metastasized from primary cancers in the gastrointestinal tract and other organs, such as the kidneys, lungs.)<ref>{{Cite web|title = Liver cancer – Hepatocellular carcinoma: MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000280.htm|website = www.nlm.nih.gov|access-date = 2015-06-20}}</ref>
* [[Primary biliary cirrhosis]] is a serious [[autoimmune]] disease of the [[bile canaliculus|bile capillaries]].<ref>{{Cite web|title = Primary biliary cirrhosis: MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000282.htm|website = www.nlm.nih.gov|access-date = 2015-06-20}}</ref>
* [[Primary sclerosing cholangitis]] is a serious chronic [[inflammation|inflammatory]] disease of the [[bile duct]], which is believed to be autoimmune in origin.<ref>{{Cite web|title = Sclerosing cholangitis: MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000285.htm|website = www.nlm.nih.gov|access-date = 2015-06-20}}</ref>
* [[Budd–Chiari syndrome]] is the clinical picture caused by [[Vascular occlusion|occlusion]] of the [[hepatic vein]].<ref>{{Cite web|title = Hepatic vein obstruction (Budd-Chiari): MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000239.htm|website = www.nlm.nih.gov|access-date = 2015-06-20}}</ref>


==Signs and symptoms==
==Signs and symptoms==
Some of the signs and symptoms of a liver disease are the following:
The symptoms<ref>[http://timeshealth.org/early-signs-and-symptoms-of-liver-disease/] related to liver dysfunction include both physical signs and a variety of [[symptom]]s related to digestive problems, [[coagulopathy|coagulopathies]],<ref>{{cite journal|title=Coagulopathy in liver disease|journal=Current Treat Options Gastroenterol|year=2007|pages=464–73|volume=10|issue=6}}</ref> blood sugar problems, [[immune disorder]]s, abnormal absorption of fats, and metabolism problems.{{Citation needed|date=February 2011}}
* [[Jaundice]]<ref>{{Cite web|title=Liver Disease {{!}} NIDDK|url=https://www.niddk.nih.gov/health-information/liver-disease|access-date=2021-11-30|website=National Institute of Diabetes and Digestive and Kidney Diseases|language=en-US}}</ref>
* Confusion and altered consciousness caused by [[hepatic encephalopathy]].<ref>{{cite web |url= https://www.lecturio.com/concepts/alcoholic-liver-disease/ | title= Alcoholic Liver Disease
| website= The Lecturio Medical Concept Library |access-date= 27 June 2021}}</ref>
* [[Thrombocytopenia]] and [[coagulopathy]].<ref name="Blonski Siropaides Reddy 2007 pp. 464–73">{{cite journal | last1=Blonski | first1=W | last2=Siropaides | first2=T | last3=Reddy | first3=KR | s2cid=23396752 | title=Coagulopathy in liver disease. | journal=Current Treatment Options in Gastroenterology | volume=10 | issue=6 | year=2007 | issn=1092-8472 | pmid=18221607 | pages=464–73| doi=10.1007/s11938-007-0046-7 }}</ref>
* Risk of [[hemorrhage|bleeding symptoms]], particularly taking place in the [[gastrointestinal tract]]<ref name="Tripodi Mannucci pp. 147–156">{{cite journal | last1=Tripodi | first1=Armando | last2=Mannucci | first2=Pier Mannuccio | s2cid=198152 | title=The Coagulopathy of Chronic Liver Disease | journal=New England Journal of Medicine | publisher=Massachusetts Medical Society | volume=365 | issue=2 | date=2011-07-14 | issn=0028-4793 | doi=10.1056/nejmra1011170 | pmid=21751907 | pages=147–156}}</ref>


==Mechanisms==
The [[malabsorption]] of fats may lead to symptoms that include indigestion, reflux, deficit of [[fat soluble vitamin]]s, [[hemorrhoid]]s, [[gallstone]]s, intolerance to fatty foods, intolerance to alcohol, nausea and vomiting attacks, abdominal bloating, and [[constipation]].
Liver diseases can develop through several mechanisms:


===DNA damage===
Nervous system disorders include depression, mood changes, especially anger and irritability, poor concentration and "[[foggy brain]]", overheating of the body, especially the face and torso, and recurrent headaches (including migraine) associated with nausea.
One general mechanism, increased [[DNA damage]], is shared by some of the major liver diseases, including infection by ''[[hepatitis B virus]]'' or ''[[hepatitis C virus]]'', [[alcohol use disorder|heavy alcohol consumption]], and [[obesity and cancer#Mechanisms|obesity]].<ref name="urlChronic Liver Disease/Cirrhosis | Johns Hopkins Medicine Health Library">{{cite web |url=https://www.hopkinsmedicine.org/healthlibrary/conditions/liver_biliary_and_pancreatic_disorders/chronic_liver_diseasecirrhosis_85,P00662 |title=Chronic Liver Disease/Cirrhosis &#124; Johns Hopkins Medicine Health Library |date=12 April 2022 }}</ref>


Viral infection by hepatitis B virus, or hepatitis C virus causes an increase of [[reactive oxygen species]]. The increase in [[intracellular]] reactive oxygen species is about 10,000-fold with chronic hepatitis B virus infection and 100,000-fold following hepatitis C virus infection.<ref name="enomoto">{{cite journal |last1= Iida-Ueno |first1= A |last2= Enomoto |first2= M |last3= Tamori |first3= A |last4= Kawada |first4= N |date= 21 April 2017 |title= Hepatitis B virus infection and alcohol consumption |journal= World Journal of Gastroenterology |volume= 23 |issue= 15 |pages= 2651–2659 |doi= 10.3748/wjg.v23.i15.2651 | pmid= 28487602
The blood sugar problems include [[hypoglycaemia]].
|pmc= 5403744 |doi-access= free }}</ref> This increase in reactive oxygen species causes inflammation<ref name=enomoto/> and more than 20 types of DNA damage.<ref name="pmid27989142">{{cite journal | vauthors = Yu Y, Cui Y, Niedernhofer LJ, Wang Y | title = Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage | journal = Chemical Research in Toxicology | volume = 29 | issue = 12 | pages = 2008–2039 | date = December 2016 | pmid = 27989142 | pmc = 5614522 | doi = 10.1021/acs.chemrestox.6b00265 }}</ref> Oxidative DNA damage is mutagenic<ref name="pmid22293091">{{cite journal | vauthors = Dizdaroglu M | title = Oxidatively induced DNA damage: mechanisms, repair and disease | journal = Cancer Letters | volume = 327 | issue = 1–2 | pages = 26–47 | date = December 2012 | pmid = 22293091 | doi = 10.1016/j.canlet.2012.01.016 }}</ref> and also causes epigenetic alterations at the sites of DNA repair.<ref name=Nishida>{{cite journal | vauthors = Nishida N, Kudo M | title = Oxidative stress and epigenetic instability in human hepatocarcinogenesis | journal = Digestive Diseases | volume = 31 | issue = 5–6 | pages = 447–53 | year = 2013 | pmid = 24281019 | doi = 10.1159/000355243 | doi-access = free }}</ref> [[Cancer epigenetics|Epigenetic]] alterations and mutations affect the cellular machinery that may cause the cell to replicate at a higher rate or result in the cell avoiding [[apoptosis]], and thus contribute to liver disease.<ref name="pmid24473361">{{cite journal | vauthors = Shibata T, Aburatani H | s2cid = 8611393 | title = Exploration of liver cancer genomes | journal = Nature Reviews. Gastroenterology & Hepatology | volume = 11 | issue = 6 | pages = 340–9 | date = June 2014 | pmid = 24473361 | doi = 10.1038/nrgastro.2014.6 }}</ref> By the time accumulating epigenetic and mutational changes eventually cause hepatocellular carcinoma, epigenetic alterations appear to have an even larger role in [[carcinogenesis]] than mutations. Only one gene, [[TP53]], is mutated in more than 20% of liver cancers while 41 genes each have hypermethylated promoters (repressing gene expression) in more than 20% of liver cancers.<ref name="pmid23392071">{{cite journal | vauthors = Ozen C, Yildiz G, Dagcan AT, Cevik D, Ors A, Keles U, Topel H, Ozturk M | title = Genetics and epigenetics of liver cancer | journal = New Biotechnology | volume = 30 | issue = 4 | pages = 381–4 | date = May 2013 | pmid = 23392071 | doi = 10.1016/j.nbt.2013.01.007 | hdl = 11693/20956 |hdl-access=free }}</ref>


Alcohol consumption in excess causes a build-up of acetaldehyde. Acetaldehyde and free radicals generated by metabolizing alcohol induce DNA damage and [[oxidative stress]].<ref name="pmid20813101">{{cite journal | vauthors = Yu HS, Oyama T, Isse T, Kitagawa K, Pham TT, Tanaka M, Kawamoto T | title = Formation of acetaldehyde-derived DNA adducts due to alcohol exposure | journal = Chemico-Biological Interactions | volume = 188 | issue = 3 | pages = 367–75 | date = December 2010 | pmid = 20813101 | doi = 10.1016/j.cbi.2010.08.005 | bibcode = 2010CBI...188..367Y }}</ref><ref name=Lee>{{cite journal | vauthors = Lee SM, Kim-Ha J, Choi WY, Lee J, Kim D, Lee J, Choi E, Kim YJ | title = Interplay of genetic and epigenetic alterations in hepatocellular carcinoma | journal = Epigenomics | volume = 8 | issue = 7 | pages = 993–1005 | date = July 2016 | pmid = 27411963 | doi = 10.2217/epi-2016-0027 | doi-access = free }}</ref><ref name="urlDrinking alcohol causes cancer by damaging DNA - Independent.ie">{{cite web |url=https://www.independent.ie/irish-news/health/drinking-alcohol-causes-cancer-by-damaging-dna-36460586.html |title=Drinking alcohol causes cancer by 'damaging DNA' - Independent.ie |date=5 January 2018 }}</ref> In addition, activation of neutrophils in alcoholic liver disease contributes to the pathogenesis of hepatocellular damage by releasing reactive oxygen species (which can damage DNA).<ref name="pmid22524187">{{cite journal | vauthors = Wang HJ, Gao B, Zakhari S, Nagy LE | title = Inflammation in alcoholic liver disease | journal = Annual Review of Nutrition | volume = 32 | pages = 343–68 | date = August 2012 | pmid = 22524187 | pmc = 3670145 | doi = 10.1146/annurev-nutr-072610-145138 }}</ref> The level of oxidative stress and acetaldehyde-induced DNA adducts due to alcohol consumption does not appear sufficient to cause increased mutagenesis.<ref name="pmid22524187"/> However, as reviewed by Nishida et al.,<ref name=Nishida /> alcohol exposure, causing oxidative DNA damage (which is repairable), can result in epigenetic alterations at the sites of DNA repair. Alcohol-induced epigenetic alterations of gene expression appear to lead to liver injury and ultimately carcinoma.<ref name="pmid24313164">{{cite journal | vauthors = Shukla SD, Lim RW | title = Epigenetic effects of ethanol on the liver and gastrointestinal system | journal = Alcohol Research | volume = 35 | issue = 1 | pages = 47–55 | year = 2013 | pmid = 24313164 | pmc = 3860425 }}</ref>
[[Hypercholesterolemia]]: elevated LDL [[cholesterol]], reduced [[High density lipoprotein|HDL cholesterol]], elevated [[triglyceride]]s, clogged arteries leading to high [[blood pressure]], [[heart attack]]s and [[stroke]]s, buildup of fat in other body organs (fatty degeneration of organs), lumps of fat in the skin (lipomas and other fatty tumors), excessive weight gain (which may lead to obesity), inability to lose weight even while dieting, sluggish metabolism, protuberant abdomen (pot belly), [[cellulite]], fatty liver, and a roll of fat around the upper abdomen (liver roll) etc.{{Citation needed|date=February 2011}} Or too low levels of lipids: [[hypocholesterolemia]]: low total cholesterol, low LDL and VLDL cholesterol, low triglycerides.


Obesity is associated with a higher risk of primary liver cancer.<ref name="pmid27909908">{{Cite book | vauthors = Aleksandrova K, Stelmach-Mardas M, Schlesinger S | title = Obesity and Cancer | chapter = Obesity and Liver Cancer | journal = Recent Results in Cancer Research. Fortschritte der Krebsforschung. Progres dans les Recherches Sur le Cancer | volume = 208 | pages = 177–198 | year = 2016 | pmid = 27909908 | doi = 10.1007/978-3-319-42542-9_10 | series = Recent Results in Cancer Research | isbn = 978-3-319-42540-5 }}</ref> As shown with mice, obese mice are prone to liver cancer, likely due to two factors. Obese mice have increased pro-inflammatory cytokines. Obese mice also have higher levels of deoxycholic acid, a product of bile acid alteration by certain gut microbes, and these microbes are increased with obesity. The excess deoxycholic acid causes DNA damage and inflammation in the liver, which, in turn, can lead to liver cancer.<ref name="urlGut Bugs Could Explain Obesity-Cancer Link | Science | AAAS">{{cite web |url=https://www.science.org/content/article/gut-bugs-could-explain-obesity-cancer-link |title=Gut Bugs Could Explain Obesity-Cancer Link &#124; Science &#124; AAAS |date=2013-06-26 }}</ref>
==Types==
There are more than a hundred kinds of liver disease.<ref>[http://timeshealth.org/early-signs-and-symptoms-of-liver-disease/|Early signs and symptoms of LIVER disease]</ref> The most widely spread are as follows:
* [[Fascioliasis]], a parasitic infection of the liver caused by a [[Liver fluke]] of the ''[[Fasciola]]'' genus, mostly the ''[[Fasciola hepatica]]''.
* [[Hepatitis]], inflammation of the liver, is caused mainly by various viruses ([[viral hepatitis]]) but also by some [[hepatotoxicity|liver toxins]] (e.g. [[alcoholic hepatitis]]), autoimmunity ([[autoimmune hepatitis]]) or hereditary conditions.
* [[Alcoholic liver disease]] is any hepatic manifestation of [[Alcohol abuse|alcohol overconsumption]], including [[fatty liver|fatty liver disease]], alcoholic hepatitis, and [[cirrhosis]]. Analogous terms such as "drug-induced" or "toxic" liver disease are also used to refer to the range of disorders caused by various drugs and environmental chemicals.
* Fatty liver disease (hepatic [[steatosis]]) is a reversible condition where large vacuoles of [[triglyceride]] fat accumulate in liver cells. [[Non-alcoholic fatty liver disease]] is a spectrum of disease associated with obesity and [[metabolic syndrome]], among other causes. Fatty liver may lead to inflammatory disease (i.e. [[steatohepatitis]]) and, eventually, cirrhosis.
* [[Cirrhosis]] is the formation of fibrous tissue ([[fibrosis]]) in the place of liver cells that have died due to a variety of causes, including viral hepatitis, alcohol overconsumption, and other forms of liver toxicity. Cirrhosis causes chronic [[liver failure]].
* Primary [[liver cancer]] most commonly manifests as [[hepatocellular carcinoma]] and/or [[cholangiocarcinoma]]; rarer forms include [[angiosarcoma]] and [[hemangiosarcoma]] of the liver. (Many liver malignancies are secondary lesions that have metastasized from primary cancers in the gastrointestinal tract and other organs, such as the kidneys, lungs, breast, or prostate.)
* [[Primary biliary cirrhosis]] is a serious [[autoimmune]] disease of the [[bile canaliculus|bile capillaries]].
* [[Primary sclerosing cholangitis]] is a serious chronic [[inflammation|inflammatory]] disease of the [[bile duct]], which is believed to be autoimmune in origin.
* Centrilobular necrosis of liver can be caused by leakage of enteric toxins into circulation. Salmonella toxins in ileum have been shown to cause severe damage to liver hepatic cells <ref>YashRoy R.C. (2000) Salmonella 3,10:r:- toxicity in rabbit ileum and liver by light and electron microscopy Indian Journal of Pathology and Microbiology, vol. 43(1), pp. 17-22.https://www.researchgate.net/publication/10904218_Salmonella_3_10r_toxicity_in_rabbit_ileum_and_liver_by_light_and_electron_microscopy?ev=prf_pub</ref>
* [[Budd–Chiari syndrome]] is the clinical picture caused by [[Vascular occlusion|occlusion]] of the [[hepatic vein]], which in some cases may lead to cirrhosis.
* [[Hereditary disease]]s that cause damage to the liver include [[hemochromatosis]], involving accumulation of [[iron]] in the body, and [[Wilson's disease]], which causes the body to retain [[copper]]. Liver damage is also a clinical feature of [[alpha 1-antitrypsin deficiency]] and [[glycogen storage disease type II]].
* In [[transthyretin-related hereditary amyloidosis]], the liver produces a mutated transthyretin protein which has severe neurodegenerative and/or cardiopathic effects. Liver transplantation can provide a curative treatment option.
* [[Gilbert's syndrome]], a genetic disorder of [[bilirubin]] metabolism found in about 5% of the population, can cause mild [[jaundice]].


===Other relevant aspects===
There are also many pediatric liver diseases including: [[biliary atresia]], [[alpha-1 antitrypsin deficiency]], [[Alagille syndrome]], and [[progressive familial intrahepatic cholestasis]].
Several liver diseases are due to viral infection. [[Viral hepatitis#Hepatitis viruses|Viral hepatitides]] such as [[Hepatitis B virus]] and [[Hepatitis C virus]] can be vertically transmitted during birth via contact with infected blood.<ref name=Benova2014>{{cite journal | vauthors = Benova L, Mohamoud YA, Calvert C, Abu-Raddad LJ | title = Vertical transmission of hepatitis C virus: systematic review and meta-analysis | journal = Clinical Infectious Diseases | volume = 59 | issue = 6 | pages = 765–73 | date = September 2014 | pmid = 24928290 | pmc = 4144266 | doi = 10.1093/cid/ciu447 }}</ref><ref name=Komatsu2014>{{cite journal | vauthors = Komatsu H | title = Hepatitis B virus: where do we stand and what is the next step for eradication? | journal = World Journal of Gastroenterology | volume = 20 | issue = 27 | pages = 8998–9016 | date = July 2014 | pmid = 25083074 | pmc = 4112872 |doi = 10.3748/wjg.v20.i27.8998 |doi-broken-date = 1 November 2024 |doi-access=free}}</ref> According to a 2012 [[NICE]] publication, "about 85% of hepatitis B infections in newborns become chronic".<ref>{{Cite web|title = Hepatitis B and C: ways to promote and offer testing to people at increased risk of infection {{!}} Guidance and guidelines {{!}} NICE|url = http://www.nice.org.uk/guidance/ph43|website = www.nice.org.uk| date=12 December 2012 |access-date = 2015-06-24}}</ref> In occult cases, Hepatitis B virus is present by hepatitis B virus [[DNA]], but testing for [[HBsAg]] is negative.<ref>{{cite journal | vauthors = Samal J, Kandpal M, Vivekanandan P | title = Molecular mechanisms underlying occult hepatitis B virus infection | journal = Clinical Microbiology Reviews | volume = 25 | issue = 1 | pages = 142–63 | date = January 2012 | pmid = 22232374 | pmc = 3255968 | doi = 10.1128/CMR.00018-11 }}</ref> High consumption of [[alcoholic beverage|alcohol]] can lead to several forms of liver disease including [[alcoholic hepatitis]], [[Fatty liver|alcoholic fatty liver disease]], [[cirrhosis]], and [[liver cancer]].<ref name=Suk2014>{{cite journal | vauthors = Suk KT, Kim MY, Baik SK | title = Alcoholic liver disease: treatment | journal = World Journal of Gastroenterology | volume = 20 | issue = 36 | pages = 12934–44 | date = September 2014 | pmid = 25278689 | pmc = 4177474 | doi = 10.3748/wjg.v20.i36.12934 | doi-access = free }}</ref> In the earlier stages of alcoholic liver disease, [[adipose tissue|fat]] builds up in the liver's cells due to increased [[Fatty acid synthesis|creation of]] [[triglyceride]]s and [[fatty acid]]s and a decreased ability to [[Beta oxidation|break down fatty acids]].<ref name=Williams2014>{{cite journal | vauthors = Williams JA, Manley S, Ding WX | title = New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases | journal = World Journal of Gastroenterology | volume = 20 | issue = 36 | pages = 12908–33 | date = September 2014 | pmid = 25278688 | pmc = 4177473 | doi = 10.3748/wjg.v20.i36.12908 | doi-access = free }}</ref> Progression of the disease can lead to [[Steatohepatitis|liver inflammation from the excess fat in the liver]]. [[Fibrosis|Scarring]] in the liver often occurs as the body attempts to heal and extensive scarring can lead to the development of cirrhosis in more advanced stages of the disease.<ref name=Williams2014/> Approximately 3–10% of individuals with cirrhosis develop a form of liver cancer known as [[hepatocellular carcinoma]].<ref name=Williams2014/> According to Tilg, et al., gut microbiome could very well have an effect, be involved in the pathophysiology, on the various types of liver disease which an individual may encounter.<ref>{{cite journal | vauthors = Tilg H, Cani PD, Mayer EA | title = Gut microbiome and liver diseases | journal = Gut | volume = 65 | issue = 12 | pages = 2035–2044 | date = December 2016 | pmid = 27802157 | doi = 10.1136/gutjnl-2016-312729 | doi-access = free }}</ref> Insight into the exact causes and mechanisms mediating pathophysiology of the liver is quickly progressing due to the introduction new technological approaches like [[Single cell sequencing]] and kinome profiling <ref>{{cite journal | vauthors = Yu B, Mamedov R, Fuhler GM, Peppelenbosch MP | title = Drug Discovery in Liver Disease Using Kinome Profiling | journal = International Journal of Molecular Sciences | volume = 22 | issue = 5 | pages = 2623 | date = March 2021 | pmid = 33807722 | pmc = 7961955| doi = 10.3390/ijms22052623| doi-access = free }}</ref>


===Air pollutants===
==Diagnostics==
[[Particulates|Particulate matter]] or carbon black are common pollutants. They have a direct toxic effect on the liver; cause inflammation of liver caused by and thereby impact lipid metabolism and fatty liver disease; and can translocate from the lungs to the liver.<ref name="kim">{{cite journal | vauthors = Kim JW, Park S, Lim CW, Lee K, Kim B | title = The role of air pollutants in initiating liver disease | journal = Toxicological Research | volume = 30 | issue = 2 | pages = 65–70 | date = June 2014 | pmid = 25071914 | pmc = 4112066 | doi = 10.5487/TR.2014.30.2.065 }}</ref>
A number of [[liver function tests]] (LFTs) are available to test the proper function of the liver. These test for the presence of [[enzyme]]s in blood that are normally most abundant in liver tissue, metabolites or products. [[Blood proteins|serum proteins]], [[serum albumin]], [[Globulin|serum globulin]], A/G Ratio,
[[alanine transaminase]], [[aspartate transaminase]], [[prothrombin time]], [[partial thromboplastin time]], [[platelet count]].


Because particulate matter and carbon black are very diverse and each has different toxicodynamics, detailed mechanisms of translocation are not clear. Water-soluble fractions of particulate matter are the most important part of translocation to the liver, through extrapulmonary circulation. When particulate matter gets into the bloodstream, it combines with immune cells and stimulates innate immune responses. [[Proinflammatory cytokine|Pro-inflammatory cytokines]] are released and cause disease progression.<ref name=kim/>
==Treatment==
The most effective way to treat alcoholic liver disease and non-alcoholic fatty liver disease is to make lifestyle changes, such as:
* Cutting out alcohol
* Improving the diet
* Engaging in regular exercise
Anti-viral medications are available to treat infections such as [[Hepatitis B]] and [[Hepatitis C]]. This is an area of active research and drug development and today many treatments offer improved outcomes, by clearing or controlling the virus to slow any decline in the condition of your liver.


==Diagnosis==
Other conditions may be managed by slowing down disease progression, for example:
A number of [[liver function tests]] are available to test the proper function of the liver. These test for the presence of [[enzyme]]s in blood that are normally most abundant in liver tissue, metabolites or products. [[Blood proteins|serum proteins]], [[serum albumin]], [[Globulin|serum globulin]], [[alanine transaminase]], [[aspartate transaminase]], [[prothrombin time]], [[partial thromboplastin time]].<ref name="web">{{MedlinePlusEncyclopedia|003436|Liver function tests}}</ref>


Imaging tests such as [[transient elastography]], [[medical ultrasonography|ultrasound]] and [[magnetic resonance imaging]] can be used to show the liver tissue and the bile ducts. [[Liver biopsy]] can be performed to examine liver tissue to distinguish between various conditions; tests such as [[elastography]] may reduce the need for biopsy in some situations.<ref>{{cite journal | vauthors = Tapper EB, Lok AS | s2cid = 205117722 | title = Use of Liver Imaging and Biopsy in Clinical Practice | journal = The New England Journal of Medicine | volume = 377 | issue = 8 | pages = 756–768 | date = August 2017 | pmid = 28834467 | doi = 10.1056/NEJMra1610570 }}</ref>
* By using steroid-based drugs in autoimmune hepatitis.
* Regularly removing a quantity of blood from a vein (venesection) in the iron overload condition, [[hemochromatosis]].
* Wilson’s disease, a condition where copper builds up in the body, can be managed with drugs which bind copper allowing it to be passed from your body in urine.
* In cholestatic liver disease (where the flow of bile is affected) a medication called [[ursodeoxycholic acid]] (URSO, also referred to as UDCA) may be given. Made from naturally occurring bile acid, it may offer some protection for the liver from the harmful chemicals in the bile, slowing damage.


In liver disease, [[prothrombin time]] is longer than usual.<ref name="Blonski Siropaides Reddy 2007 pp. 464–73"/> In addition, the amounts of both [[coagulation factor]]s and [[anticoagulation factor]]s are reduced as a diseased liver cannot productively synthesize them as it did when healthy.<ref name="Barton 2016 pp. 1927–1933">{{cite journal | last=Barton | first=Cassie A. | title=Treatment of Coagulopathy Related to Hepatic Insufficiency | journal=Critical Care Medicine | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=44 | issue=10 | year=2016 | issn=0090-3493 | doi=10.1097/ccm.0000000000001998 | pmid=27635482 | pages=1927–1933| s2cid=11457839 }}</ref> Nonetheless, there are two exceptions in this falling tendency: coagulation factor VIII and [[von Willebrand factor]], a [[platelet adhesive protein]].<ref name="Barton 2016 pp. 1927–1933"/> Both inversely rise in the setting of hepatic insufficiency, thanks to the drop of [[hepatic clearance]] and compensatory productions from other sites of the body.<ref name="Barton 2016 pp. 1927–1933"/> [[Fibrinolysis]] generally proceeds faster with acute liver failure and advanced stage liver disease, unlike [[chronic liver disease]] in which concentration of [[fibrinogen]] remains unchanged.<ref name="Barton 2016 pp. 1927–1933"/>
==See also==
* [[Hepato-biliary diseases]]


A previously undiagnosed liver disease may become evident first after [[autopsy]].{{citation needed|date=January 2021}} Following are [[gross pathology]] images:
==References==
<gallery mode="packed" widths="360px" heights="220">
{{reflist}}
File:Gross pathology of alcoholic liver cirrhosis.jpg|Diffuse [[cirrhosis]]
File:Wątroba marska (Ultima Thule).jpg|Macronodular cirrhosis
File:Nutmeg liver (crop).jpg|Nutmeg texture of [[congestive hepatopathy]]
</gallery>


==Treatment==
{{Medical conditions}}
[[File:Ursodeoxycholic acid acsv.svg|thumb|Ursodeoxycholic acid]]
{{Digestive system diseases}}
Anti-viral medications are available to treat infections such as [[hepatitis B]].<ref>{{cite journal | vauthors = De Clercq E, Férir G, Kaptein S, Neyts J | title = Antiviral treatment of chronic hepatitis B virus infections | journal = Viruses | volume = 2 | issue = 6 | pages = 1279–305 | date = June 2010 | pmid = 21994680 | pmc = 3185710 | doi = 10.3390/v2061279 | doi-access = free }}</ref> Other conditions may be managed by slowing down disease progression, for example:
{{Congenital malformations and deformations of digestive system}}
* By using steroid-based drugs in autoimmune hepatitis.<ref>{{Cite book|title = Autoimmune Hepatitis: A Guide for Practicing Clinicians|url = https://books.google.com/books?id=e-SsnIOHDrIC&q=autoimmune+hepatitis+++steroid+drugs&pg=PA198|publisher = Springer Science & Business Media|date = 2011-12-02|isbn = 978-1-60761-569-9|language = en|first1 = Gideon M.|last1 = Hirschfield|first2 = E. Jenny|last2 = Heathcote}}</ref>
* Regularly removing a quantity of blood from a vein (venesection) in the iron overload condition, [[hemochromatosis]].<ref>{{Cite web|title = Phlebotomy Treatment {{!}} Treatment and Management {{!}} Training & Education {{!}} Hemochromatosis (Iron Storage Disease) {{!}} NCBDDD {{!}} CDC|url = https://www.cdc.gov/ncbddd/hemochromatosis/training/treatment/phlebotomy_treatment.html|website = www.cdc.gov|access-date = 2015-06-20}}</ref>
* [[Wilson's disease]], a condition where copper builds up in the body, can be managed with drugs that bind copper, allowing it to be passed from the body in urine.<ref>{{Cite web|title = Wilson Disease|url = http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/wilson-disease/Pages/facts.aspx|website = www.niddk.nih.gov|access-date = 2015-06-20|archive-date = 2015-06-21|archive-url = https://web.archive.org/web/20150621034922/http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/wilson-disease/Pages/facts.aspx|url-status = dead}}</ref>
* In cholestatic liver disease, (where the flow of bile is affected due to cystic fibrosis<ref>{{Cite book|title = Liver Disease in Children|url = https://books.google.com/books?id=A4LBAgAAQBAJ&q=cholestatic+liver+disease++cystic+fibrosis&pg=PA114|publisher = Cambridge University Press|date = 2014-02-20|isbn = 978-1-107-72909-4|language = en|first1 = Frederick J.|last1 = Suchy|first2 = Ronald J.|last2 = Sokol|first3 = William F.|last3 = Balistreri}}</ref>) a medication called [[ursodeoxycholic acid]] may be given.<ref>{{Cite journal|title = Ursodeoxycholic acid for liver disease related to cystic fibrosis|url = http://www.cochrane.org/CD000222/CF_ursodeoxycholic-acid-for-liver-disease-related-to-cystic-fibrosis|journal = Cochrane Database of Systematic Reviews|volume = 9|pages = CD000222|access-date = 2015-06-20|doi = 10.1002/14651858.CD000222.pub4|pmid = 28891588|pmc = 6483662|year = 2017|last1 = Cheng|first1 = Katharine|last2 = Ashby|first2 = Deborah|last3 = Smyth|first3 = Rosalind L.| issue=9 }}</ref>

== See also ==
* [[Model for end-stage liver disease]] (MELD)

== References ==
{{Reflist}}

== Further reading ==
* {{Cite book|title = Handbook of Liver Disease|url = https://books.google.com/books?id=uyKht3EwjA0C&q=liver+disease|publisher = Elsevier Health Sciences|date = 2011-08-03|isbn = 978-1-4557-2316-4|language = en|first1 = Lawrence S.|last1 = Friedman|first2 = Emmet B.|last2 = Keeffe}}

==External links==
{{Medical resources
| DiseasesDB =
| ICD11 = {{ICD11|5C90}}
| ICD10 =
| ICD9 =
| ICDO =
| OMIM =
| MedlinePlus = 000205
| eMedicineSubj =
| eMedicineTopic =
| MeshID =
}}
{{Scholia|topic}}
{{Medicine}}
{{Authority control}}


[[Category:Diseases of liver|*]]
{{DEFAULTSORT:Liver Disease}}
[[Category:Diseases of liver]]
[[Category:Health effects of alcohol]]
[[Category:Hepatology]]

Latest revision as of 10:34, 2 November 2024

For Injuries associated with liver, see Liver injury.
Liver disease
Other namesHepatic disease
A gross pathology specimen of liver metastases caused by pancreatic cancer
SpecialtyHepatology, gastroenterology
TypesFatty liver disease, Hepatitis (and several more)[1]
Diagnostic methodLiver function tests[2]
TreatmentDepends on type(See types)

Liver disease, or hepatic disease, is any of many diseases of the liver.[1] If long-lasting it is termed chronic liver disease.[3] Although the diseases differ in detail, liver diseases often have features in common.

Liver diseases

[edit]

There are more than a hundred different liver diseases. Some of the most common are:[4]

Signs and symptoms

[edit]

Some of the signs and symptoms of a liver disease are the following:

Mechanisms

[edit]

Liver diseases can develop through several mechanisms:

DNA damage

[edit]

One general mechanism, increased DNA damage, is shared by some of the major liver diseases, including infection by hepatitis B virus or hepatitis C virus, heavy alcohol consumption, and obesity.[24]

Viral infection by hepatitis B virus, or hepatitis C virus causes an increase of reactive oxygen species. The increase in intracellular reactive oxygen species is about 10,000-fold with chronic hepatitis B virus infection and 100,000-fold following hepatitis C virus infection.[25] This increase in reactive oxygen species causes inflammation[25] and more than 20 types of DNA damage.[26] Oxidative DNA damage is mutagenic[27] and also causes epigenetic alterations at the sites of DNA repair.[28] Epigenetic alterations and mutations affect the cellular machinery that may cause the cell to replicate at a higher rate or result in the cell avoiding apoptosis, and thus contribute to liver disease.[29] By the time accumulating epigenetic and mutational changes eventually cause hepatocellular carcinoma, epigenetic alterations appear to have an even larger role in carcinogenesis than mutations. Only one gene, TP53, is mutated in more than 20% of liver cancers while 41 genes each have hypermethylated promoters (repressing gene expression) in more than 20% of liver cancers.[30]

Alcohol consumption in excess causes a build-up of acetaldehyde. Acetaldehyde and free radicals generated by metabolizing alcohol induce DNA damage and oxidative stress.[31][32][33] In addition, activation of neutrophils in alcoholic liver disease contributes to the pathogenesis of hepatocellular damage by releasing reactive oxygen species (which can damage DNA).[34] The level of oxidative stress and acetaldehyde-induced DNA adducts due to alcohol consumption does not appear sufficient to cause increased mutagenesis.[34] However, as reviewed by Nishida et al.,[28] alcohol exposure, causing oxidative DNA damage (which is repairable), can result in epigenetic alterations at the sites of DNA repair. Alcohol-induced epigenetic alterations of gene expression appear to lead to liver injury and ultimately carcinoma.[35]

Obesity is associated with a higher risk of primary liver cancer.[36] As shown with mice, obese mice are prone to liver cancer, likely due to two factors. Obese mice have increased pro-inflammatory cytokines. Obese mice also have higher levels of deoxycholic acid, a product of bile acid alteration by certain gut microbes, and these microbes are increased with obesity. The excess deoxycholic acid causes DNA damage and inflammation in the liver, which, in turn, can lead to liver cancer.[37]

Other relevant aspects

[edit]

Several liver diseases are due to viral infection. Viral hepatitides such as Hepatitis B virus and Hepatitis C virus can be vertically transmitted during birth via contact with infected blood.[38][39] According to a 2012 NICE publication, "about 85% of hepatitis B infections in newborns become chronic".[40] In occult cases, Hepatitis B virus is present by hepatitis B virus DNA, but testing for HBsAg is negative.[41] High consumption of alcohol can lead to several forms of liver disease including alcoholic hepatitis, alcoholic fatty liver disease, cirrhosis, and liver cancer.[42] In the earlier stages of alcoholic liver disease, fat builds up in the liver's cells due to increased creation of triglycerides and fatty acids and a decreased ability to break down fatty acids.[43] Progression of the disease can lead to liver inflammation from the excess fat in the liver. Scarring in the liver often occurs as the body attempts to heal and extensive scarring can lead to the development of cirrhosis in more advanced stages of the disease.[43] Approximately 3–10% of individuals with cirrhosis develop a form of liver cancer known as hepatocellular carcinoma.[43] According to Tilg, et al., gut microbiome could very well have an effect, be involved in the pathophysiology, on the various types of liver disease which an individual may encounter.[44] Insight into the exact causes and mechanisms mediating pathophysiology of the liver is quickly progressing due to the introduction new technological approaches like Single cell sequencing and kinome profiling [45]

Air pollutants

[edit]

Particulate matter or carbon black are common pollutants. They have a direct toxic effect on the liver; cause inflammation of liver caused by and thereby impact lipid metabolism and fatty liver disease; and can translocate from the lungs to the liver.[46]

Because particulate matter and carbon black are very diverse and each has different toxicodynamics, detailed mechanisms of translocation are not clear. Water-soluble fractions of particulate matter are the most important part of translocation to the liver, through extrapulmonary circulation. When particulate matter gets into the bloodstream, it combines with immune cells and stimulates innate immune responses. Pro-inflammatory cytokines are released and cause disease progression.[46]

Diagnosis

[edit]

A number of liver function tests are available to test the proper function of the liver. These test for the presence of enzymes in blood that are normally most abundant in liver tissue, metabolites or products. serum proteins, serum albumin, serum globulin, alanine transaminase, aspartate transaminase, prothrombin time, partial thromboplastin time.[2]

Imaging tests such as transient elastography, ultrasound and magnetic resonance imaging can be used to show the liver tissue and the bile ducts. Liver biopsy can be performed to examine liver tissue to distinguish between various conditions; tests such as elastography may reduce the need for biopsy in some situations.[47]

In liver disease, prothrombin time is longer than usual.[22] In addition, the amounts of both coagulation factors and anticoagulation factors are reduced as a diseased liver cannot productively synthesize them as it did when healthy.[48] Nonetheless, there are two exceptions in this falling tendency: coagulation factor VIII and von Willebrand factor, a platelet adhesive protein.[48] Both inversely rise in the setting of hepatic insufficiency, thanks to the drop of hepatic clearance and compensatory productions from other sites of the body.[48] Fibrinolysis generally proceeds faster with acute liver failure and advanced stage liver disease, unlike chronic liver disease in which concentration of fibrinogen remains unchanged.[48]

A previously undiagnosed liver disease may become evident first after autopsy.[citation needed] Following are gross pathology images:

Treatment

[edit]
Ursodeoxycholic acid

Anti-viral medications are available to treat infections such as hepatitis B.[49] Other conditions may be managed by slowing down disease progression, for example:

  • By using steroid-based drugs in autoimmune hepatitis.[50]
  • Regularly removing a quantity of blood from a vein (venesection) in the iron overload condition, hemochromatosis.[51]
  • Wilson's disease, a condition where copper builds up in the body, can be managed with drugs that bind copper, allowing it to be passed from the body in urine.[52]
  • In cholestatic liver disease, (where the flow of bile is affected due to cystic fibrosis[53]) a medication called ursodeoxycholic acid may be given.[54]

See also

[edit]

References

[edit]
  1. ^ a b "Liver Diseases". MedlinePlus.
  2. ^ a b MedlinePlus Encyclopedia: Liver function tests
  3. ^ "NHS Choices". Cirrhosis. Retrieved 6 October 2015.
  4. ^ "Liver disease – NHS Choices". www.nhs.uk. Retrieved 2015-06-20.
  5. ^ "CDC – Fasciola". www.cdc.gov. Retrieved 2015-06-20.
  6. ^ "Hepatitis". MedlinePlus.
  7. ^ MedlinePlus Encyclopedia: Alcoholic liver disease
  8. ^ "Hepatic steatosis". Retrieved 2015-06-20.
  9. ^ "Non-alcoholic fatty liver disease – NHS Choices". www.nhs.uk. Retrieved 2015-06-20.
  10. ^ "Hemochromatosis". MedlinePlus.
  11. ^ "Alpha-1 Antitrypsin Deficiency". MedlinePlus.
  12. ^ Leslie N, Tinkle BT (1993). "Pompe Disease". In Pagon RA, Adam MP, Ardinger HH, Wallace SE, Amemiya A, Bean LJ, Bird TD, Dolan CR, Fong CT (eds.). Glycogen Storage Disease Type II (Pompe Disease). Seattle (WA): University of Washington, Seattle. PMID 20301438.
  13. ^ "Transthyretin amyloidosis". Genetics Home Reference. Retrieved 2015-06-20.
  14. ^ "Gilbert syndrome". Genetics Home Reference. Retrieved 2015-06-20.
  15. ^ "Cirrhosis: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  16. ^ "Liver cancer – Hepatocellular carcinoma: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  17. ^ "Primary biliary cirrhosis: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  18. ^ "Sclerosing cholangitis: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  19. ^ "Hepatic vein obstruction (Budd-Chiari): MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  20. ^ "Liver Disease | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 2021-11-30.
  21. ^ "Alcoholic Liver Disease". The Lecturio Medical Concept Library. Retrieved 27 June 2021.
  22. ^ a b Blonski W, Siropaides T, Reddy KR (2007). "Coagulopathy in liver disease". Current Treatment Options in Gastroenterology. 10 (6): 464–73. doi:10.1007/s11938-007-0046-7. ISSN 1092-8472. PMID 18221607. S2CID 23396752.
  23. ^ Tripodi A, Mannucci PM (2011-07-14). "The Coagulopathy of Chronic Liver Disease". New England Journal of Medicine. 365 (2). Massachusetts Medical Society: 147–156. doi:10.1056/nejmra1011170. ISSN 0028-4793. PMID 21751907. S2CID 198152.
  24. ^ "Chronic Liver Disease/Cirrhosis | Johns Hopkins Medicine Health Library". 12 April 2022.
  25. ^ a b Iida-Ueno A, Enomoto M, Tamori A, Kawada N (21 April 2017). "Hepatitis B virus infection and alcohol consumption". World Journal of Gastroenterology. 23 (15): 2651–2659. doi:10.3748/wjg.v23.i15.2651. PMC 5403744. PMID 28487602.
  26. ^ Yu Y, Cui Y, Niedernhofer LJ, Wang Y (December 2016). "Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage". Chemical Research in Toxicology. 29 (12): 2008–2039. doi:10.1021/acs.chemrestox.6b00265. PMC 5614522. PMID 27989142.
  27. ^ Dizdaroglu M (December 2012). "Oxidatively induced DNA damage: mechanisms, repair and disease". Cancer Letters. 327 (1–2): 26–47. doi:10.1016/j.canlet.2012.01.016. PMID 22293091.
  28. ^ a b Nishida N, Kudo M (2013). "Oxidative stress and epigenetic instability in human hepatocarcinogenesis". Digestive Diseases. 31 (5–6): 447–53. doi:10.1159/000355243. PMID 24281019.
  29. ^ Shibata T, Aburatani H (June 2014). "Exploration of liver cancer genomes". Nature Reviews. Gastroenterology & Hepatology. 11 (6): 340–9. doi:10.1038/nrgastro.2014.6. PMID 24473361. S2CID 8611393.
  30. ^ Ozen C, Yildiz G, Dagcan AT, Cevik D, Ors A, Keles U, Topel H, Ozturk M (May 2013). "Genetics and epigenetics of liver cancer". New Biotechnology. 30 (4): 381–4. doi:10.1016/j.nbt.2013.01.007. hdl:11693/20956. PMID 23392071.
  31. ^ Yu HS, Oyama T, Isse T, Kitagawa K, Pham TT, Tanaka M, Kawamoto T (December 2010). "Formation of acetaldehyde-derived DNA adducts due to alcohol exposure". Chemico-Biological Interactions. 188 (3): 367–75. Bibcode:2010CBI...188..367Y. doi:10.1016/j.cbi.2010.08.005. PMID 20813101.
  32. ^ Lee SM, Kim-Ha J, Choi WY, Lee J, Kim D, Lee J, Choi E, Kim YJ (July 2016). "Interplay of genetic and epigenetic alterations in hepatocellular carcinoma". Epigenomics. 8 (7): 993–1005. doi:10.2217/epi-2016-0027. PMID 27411963.
  33. ^ "Drinking alcohol causes cancer by 'damaging DNA' - Independent.ie". 5 January 2018.
  34. ^ a b Wang HJ, Gao B, Zakhari S, Nagy LE (August 2012). "Inflammation in alcoholic liver disease". Annual Review of Nutrition. 32: 343–68. doi:10.1146/annurev-nutr-072610-145138. PMC 3670145. PMID 22524187.
  35. ^ Shukla SD, Lim RW (2013). "Epigenetic effects of ethanol on the liver and gastrointestinal system". Alcohol Research. 35 (1): 47–55. PMC 3860425. PMID 24313164.
  36. ^ Aleksandrova K, Stelmach-Mardas M, Schlesinger S (2016). "Obesity and Liver Cancer". Obesity and Cancer. Recent Results in Cancer Research. Vol. 208. pp. 177–198. doi:10.1007/978-3-319-42542-9_10. ISBN 978-3-319-42540-5. PMID 27909908. {{cite book}}: |journal= ignored (help)
  37. ^ Benova L, Mohamoud YA, Calvert C, Abu-Raddad LJ (September 2014). "Vertical transmission of hepatitis C virus: systematic review and meta-analysis". Clinical Infectious Diseases. 59 (6): 765–73. doi:10.1093/cid/ciu447. PMC 4144266. PMID 24928290.
  38. ^ Komatsu H (July 2014). "Hepatitis B virus: where do we stand and what is the next step for eradication?". World Journal of Gastroenterology. 20 (27): 8998–9016. doi:10.3748/wjg.v20.i27.8998 (inactive 1 November 2024). PMC 4112872. PMID 25083074.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  39. ^ "Hepatitis B and C: ways to promote and offer testing to people at increased risk of infection | Guidance and guidelines | NICE". www.nice.org.uk. 12 December 2012. Retrieved 2015-06-24.
  40. ^ Samal J, Kandpal M, Vivekanandan P (January 2012). "Molecular mechanisms underlying occult hepatitis B virus infection". Clinical Microbiology Reviews. 25 (1): 142–63. doi:10.1128/CMR.00018-11. PMC 3255968. PMID 22232374.
  41. ^ Suk KT, Kim MY, Baik SK (September 2014). "Alcoholic liver disease: treatment". World Journal of Gastroenterology. 20 (36): 12934–44. doi:10.3748/wjg.v20.i36.12934. PMC 4177474. PMID 25278689.
  42. ^ a b c Williams JA, Manley S, Ding WX (September 2014). "New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases". World Journal of Gastroenterology. 20 (36): 12908–33. doi:10.3748/wjg.v20.i36.12908. PMC 4177473. PMID 25278688.
  43. ^ Tilg H, Cani PD, Mayer EA (December 2016). "Gut microbiome and liver diseases". Gut. 65 (12): 2035–2044. doi:10.1136/gutjnl-2016-312729. PMID 27802157.
  44. ^ Yu B, Mamedov R, Fuhler GM, Peppelenbosch MP (March 2021). "Drug Discovery in Liver Disease Using Kinome Profiling". International Journal of Molecular Sciences. 22 (5): 2623. doi:10.3390/ijms22052623. PMC 7961955. PMID 33807722.
  45. ^ a b Kim JW, Park S, Lim CW, Lee K, Kim B (June 2014). "The role of air pollutants in initiating liver disease". Toxicological Research. 30 (2): 65–70. doi:10.5487/TR.2014.30.2.065. PMC 4112066. PMID 25071914.
  46. ^ Tapper EB, Lok AS (August 2017). "Use of Liver Imaging and Biopsy in Clinical Practice". The New England Journal of Medicine. 377 (8): 756–768. doi:10.1056/NEJMra1610570. PMID 28834467. S2CID 205117722.
  47. ^ a b c d Barton CA (2016). "Treatment of Coagulopathy Related to Hepatic Insufficiency". Critical Care Medicine. 44 (10). Ovid Technologies (Wolters Kluwer Health): 1927–1933. doi:10.1097/ccm.0000000000001998. ISSN 0090-3493. PMID 27635482. S2CID 11457839.
  48. ^ De Clercq E, Férir G, Kaptein S, Neyts J (June 2010). "Antiviral treatment of chronic hepatitis B virus infections". Viruses. 2 (6): 1279–305. doi:10.3390/v2061279. PMC 3185710. PMID 21994680.
  49. ^ Hirschfield GM, Heathcote EJ (2011-12-02). Autoimmune Hepatitis: A Guide for Practicing Clinicians. Springer Science & Business Media. ISBN 978-1-60761-569-9.
  50. ^ "Phlebotomy Treatment | Treatment and Management | Training & Education | Hemochromatosis (Iron Storage Disease) | NCBDDD | CDC". www.cdc.gov. Retrieved 2015-06-20.
  51. ^ "Wilson Disease". www.niddk.nih.gov. Archived from the original on 2015-06-21. Retrieved 2015-06-20.
  52. ^ Suchy FJ, Sokol RJ, Balistreri WF (2014-02-20). Liver Disease in Children. Cambridge University Press. ISBN 978-1-107-72909-4.
  53. ^ Cheng K, Ashby D, Smyth RL (2017). "Ursodeoxycholic acid for liver disease related to cystic fibrosis". Cochrane Database of Systematic Reviews. 9 (9): CD000222. doi:10.1002/14651858.CD000222.pub4. PMC 6483662. PMID 28891588. Retrieved 2015-06-20.

Further reading

[edit]
[edit]
Scholia has a topic profile for Liver disease.
Retrieved from "https://en.wikipedia.org/enwiki/w/index.php?title=Liver_disease&oldid=1254929169"