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词条 Liver disease
释义

  1. Associated medical conditions (types)

  2. Mechanism

     DNA damage  Other relevant aspects  Air pollutants 

  3. Diagnosis

  4. Treatment

  5. See also

  6. References

  7. Further reading

  8. External links

{{Infobox medical condition (new)
| name = Hepatic disease
| image = Non-alcoholic_fatty_liver_disease1.jpg
| caption = Micrograph of non-alcoholic fatty liver disease
| field = Gastroenterology
| pronounce =
| synonyms =
| symptoms =
| complications =
| onset =
| duration =
| types = Fatty liver disease , Hepatitis(and several more) [1]
| causes =
| risks =
| diagnosis = Liver function tests[2]
| 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.[1]

Associated medical conditions (types)

There are more than a hundred different kinds of liver disease. Symptoms may include jaundice and weight loss. These are some of the most common:[2]

  • Fascioliasis, a parasitic infection of liver caused by a liver fluke of the genus Fasciola, mostly the Fasciola hepatica.[3]
  • Hepatitis, inflammation of the liver, is caused by various viruses (viral hepatitis) also by some liver toxins (e.g. alcoholic hepatitis), autoimmunity (autoimmune hepatitis) or hereditary conditions.[4]
  • Alcoholic liver disease is a hepatic manifestation of alcohol overconsumption, including 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.[5]
  • Fatty liver disease (hepatic steatosis) is a reversible condition where large vacuoles of triglyceride fat accumulate in liver cells.[6] Non-alcoholic fatty liver disease is a spectrum of disease associated with obesity and metabolic syndrome.[7]
  • Hereditary diseases that cause damage to the liver include hemochromatosis,[8] involving accumulation of iron in the body, and Wilson's disease. Liver damage is also a clinical feature of alpha 1-antitrypsin deficiency [9] and glycogen storage disease type II.[10]
  • In transthyretin-related hereditary amyloidosis, the liver produces a mutated transthyretin protein which has severe neurodegenerative and/or cardiopathic effects. Liver transplantation can give a curative treatment option.[11]
  • Gilbert's syndrome, a genetic disorder of bilirubin metabolism found in a small percent of the population, can cause mild jaundice.[12]
  • 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.[13]
  • 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.)[14]
  • Primary biliary cirrhosis is a serious autoimmune disease of the bile capillaries.[15]
  • Primary sclerosing cholangitis is a serious chronic inflammatory disease of the bile duct, which is believed to be autoimmune in origin.[16]
  • Budd–Chiari syndrome is the clinical picture caused by occlusion of the hepatic vein.[17]

Mechanism

Liver disease can occur through several mechanisms.

DNA damage

One general mechanism, increased DNA damage, is shared by some of the major causes of liver disease. These major causes include infection by hepatitis B virus or hepatitis C virus, alcohol abuse, and obesity.[18]

Viral infection by hepatitis B virus (HBV) or hepatitis C virus (HCV) causes an increase of reactive oxygen species (ROS). The increase in intracellular ROS is about 10,000-fold upon chronic HBV infection and 100,000-fold after HCV infection.[19] This increase in ROS causes inflammation and further increase in ROS.[19] ROS cause more than 20 types of DNA damage.[20] Oxidative DNA damage is mutagenic[21] and also causes epigenetic alterations at the sites of DNA repair.[22] Epigenetic alterations and mutations affect the cellular machinery that may cause the cell to replicate at a higher rate and/or result in the cell avoiding apoptosis, and thus contribute to liver disease.[23] 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.[24]

Alcohol consumption in excess causes a build-up of acetaldehyde. Acetaldehyde and free radicals generated by metabolizing alcohol induce DNA damage and oxidative stress.[25][26][27] 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).[28] The level of oxidative stress and acetaldehyde-induced DNA adducts due to alcohol consumption does not appear sufficient to cause increased mutagenesis.[28] However, as reviewed by Nishida et al.,[22] 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.[29]

Obesity is associated with higher risk of primary liver cancer.[30] 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 (DCA), a product of bile acid alteration by certain gut microbes, and these microbes are increased with obesity. The excess DCA causes DNA damage and inflammation in the liver, which, in turn, can lead to liver cancer.[31]

Other relevant aspects

A common form of liver disease is viral infection. Viral hepatitides such as Hepatitis B virus and Hepatitis C virus can be vertically transmitted during birth via contact with infected blood.[32][33] According to a 2012 NICE publication, "about 85% of hepatitis B infections in newborns become chronic".[34] In occult cases, Hepatitis B virus is present by HBV DNA, but testing for HBsAg is negative.[35] High consumption of alcohol can lead to several forms of liver disease including alcoholic hepatitis, alcoholic fatty liver disease, cirrhosis, and liver cancer.[36] 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.[37] 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.[37] Approximately 3–10% of individuals with cirrhosis develop a form of liver cancer known as hepatocellular carcinoma.[37]

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.[38]

Air pollutants

Particulate matter (PM) or carbon black (CB) are common pollutants. The following factors are the harmful effects of liver exposure under PM or CB. First, they have an obvious direct toxic effect on the liver. Chemicals will affect metabolism and impact liver function. Second, inflammation of liver caused by PM and CB impact lipid metabolism and fatty liver disease. Third, PM and CB can translocate from lung to liver.[39]

PM and CB can easily translocate from lung to liver. Because they are very diverse and each has different toxicodynamics, detailed mechanisms are not clear. Water-soluble fractions of PM is the most important part for PM translocation to liver through extra-pulmonary circulation. When PM goes through blood vessel into blood, it combines with immune cells, that will stimulate innate immune responses. Pro-inflammatory cytokines will be released and cause disease progression.[39]

Diagnosis

A number of liver function tests (LFTs) 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.[40]

Imaging tests such as transient elastography, ultrasound and magnetic resonance imaging can be used to examine 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.[41]

Treatment

Anti-viral medications are available to treat infections such as hepatitis B.[42] Other conditions may be managed by slowing down disease progression, for example:

  • By using steroid-based drugs in autoimmune hepatitis.[43]
  • Regularly removing a quantity of blood from a vein (venesection) in the iron overload condition, hemochromatosis.[44]
  • 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.[45]
  • In cholestatic liver disease, (where the flow of bile is affected due to cystic fibrosis[46]) a medication called ursodeoxycholic acid (URSO, also referred to as UDCA) may be given.[47]

See also

  • Model for end-stage liver disease (MELD)

References

1. ^1 {{Cite web|title = Liver Diseases: MedlinePlus|url = https://www.nlm.nih.gov/medlineplus/liverdiseases.html|website = www.nlm.nih.gov|access-date = 2015-06-20}}
2. ^{{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}}
3. ^{{Cite web|title = CDC – Fasciola|url = https://www.cdc.gov/parasites/fasciola/|website = www.cdc.gov|access-date = 2015-06-20}}
4. ^{{Cite web|title = Hepatitis: MedlinePlus|url = https://www.nlm.nih.gov/medlineplus/hepatitis.html|website = www.nlm.nih.gov|access-date = 2015-06-20}}
5. ^{{Cite web|title = Alcoholic liver disease: MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000281.htm|website = www.nlm.nih.gov|access-date = 2015-06-20}}
6. ^{{Cite web|title = Hepatic steatosis|url = http://medical-dictionary.thefreedictionary.com/Hepatic+steatosis|access-date = 2015-06-20}}
7. ^{{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}}
8. ^{{Cite web|title = Hemochromatosis: MedlinePlus|url = https://www.nlm.nih.gov/medlineplus/hemochromatosis.html|website = www.nlm.nih.gov|access-date = 2015-06-20}}
9. ^{{Cite web|title = Alpha-1 Antitrypsin Deficiency: MedlinePlus|url = https://www.nlm.nih.gov/medlineplus/alpha1antitrypsindeficiency.html|website = www.nlm.nih.gov|access-date = 2015-06-20}}
10. ^{{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|first = Nancy|last = 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 JH|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}}
11. ^{{Cite web|title = Transthyretin amyloidosis|url = http://ghr.nlm.nih.gov/condition/transthyretin-amyloidosis|website = Genetics Home Reference|access-date = 2015-06-20}}
12. ^{{Cite web|title = Gilbert syndrome|url = http://ghr.nlm.nih.gov/condition/gilbert-syndrome|website = Genetics Home Reference|access-date = 2015-06-20}}
13. ^{{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}}
14. ^{{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}}
15. ^{{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}}
16. ^{{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}}
17. ^{{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}}
18. ^{{cite web |url=https://www.hopkinsmedicine.org/healthlibrary/conditions/liver_biliary_and_pancreatic_disorders/chronic_liver_diseasecirrhosis_85,P00662 |title=Chronic Liver Disease/Cirrhosis | Johns Hopkins Medicine Health Library |format= |website= |access-date=}}
19. ^1 {{cite journal | vauthors = Ivanov AV, Valuev-Elliston VT, Tyurina DA, Ivanova ON, Kochetkov SN, Bartosch B, Isaguliants MG | title = Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis | journal = Oncotarget | volume = 8 | issue = 3 | pages = 3895–3932 | date = January 2017 | pmid = 27965466 | pmc = 5354803 | doi = 10.18632/oncotarget.13904 }}
20. ^{{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 }}
21. ^{{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 }}
22. ^1 {{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 }}
23. ^{{cite journal | vauthors = Shibata T, Aburatani H | 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 }}
24. ^{{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 }}
25. ^{{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 }}
26. ^{{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 }}
27. ^{{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 |website= |access-date=}}
28. ^1 {{cite journal | vauthors = Wang HJ, Gao B, Zakhari S, Nagy LE | title = Inflammation in alcoholic liver disease | journal = Annual Review of Nutrition | volume = 32 | issue = | pages = 343–68 | date = August 2012 | pmid = 22524187 | pmc = 3670145 | doi = 10.1146/annurev-nutr-072610-145138 }}
29. ^{{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 | doi = }}
30. ^{{Cite book | vauthors = Aleksandrova K, Stelmach-Mardas M, Schlesinger S | title = Obesity and Liver Cancer | journal = Recent Results in Cancer Research. Fortschritte der Krebsforschung. Progres dans les Recherches Sur le Cancer | volume = 208 | issue = | 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 }}
31. ^{{cite web |url=http://www.sciencemag.org/news/2013/06/gut-bugs-could-explain-obesity-cancer-link |title=Gut Bugs Could Explain Obesity-Cancer Link | Science | AAAS |format= |website= |access-date=|date=2013-06-26 }}
32. ^{{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 }}
33. ^{{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 = 2019-03-16 }}
34. ^{{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|access-date = 2015-06-24}}
35. ^{{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 }}
36. ^{{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 }}
37. ^1 2 {{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 }}
38. ^{{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 | url = http://gut.bmj.com/content/65/12/2035.full }}
39. ^1 {{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 }}
40. ^1 {{Cite web|title = Liver function tests: MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/003436.htm|website = www.nlm.nih.gov|access-date = 2015-06-20}}
41. ^{{cite journal | vauthors = Tapper EB, Lok AS | 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 }}
42. ^{{cite journal | vauthors = De Clercq E, Férir G, Kaptein S, Neyts J | title = Antiviral treatment of chronic hepatitis B virus (HBV) infections | journal = Viruses | volume = 2 | issue = 6 | pages = 1279–305 | date = June 2010 | pmid = 21994680 | pmc = 3185710 | doi = 10.3390/v2061279 }}
43. ^{{Cite book|title = Autoimmune Hepatitis: A Guide for Practicing Clinicians|url = https://books.google.com/?id=e-SsnIOHDrIC&pg=PA198&dq=autoimmune+hepatitis+++steroid+drugs#v=onepage&q=autoimmune%2520hepatitis%2520%2520%2520steroid%2520drugs&f=false|publisher = Springer Science & Business Media|date = 2011-12-02|isbn = 9781607615699|language = en|first = Gideon M.|last = Hirschfield|first2 = E. Jenny|last2 = Heathcote}}
44. ^{{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}}
45. ^{{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}}
46. ^{{Cite book|title = Liver Disease in Children|url = https://books.google.com/?id=A4LBAgAAQBAJ&pg=PA114&lpg=PA114&dq=cholestatic+liver+disease++cystic+fibrosis#v=onepage&q=cholestatic%2520liver%2520disease%2520%2520cystic%2520fibrosis&f=false|publisher = Cambridge University Press|date = 2014-02-20|isbn = 9781107729094|language = en|first = Frederick J.|last = Suchy|first2 = Ronald J.|last2 = Sokol|first3 = William F.|last3 = Balistreri}}
47. ^{{Cite journal|title = Ursodeoxycholic acid for liver disease related to cystic fibrosis {{!}} Cochrane|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|year = 2017|last1 = Cheng|first1 = Katharine|last2 = Ashby|first2 = Deborah|last3 = Smyth|first3 = Rosalind L.}}

Further reading

  • {{Cite book|title = Handbook of Liver Disease|url = https://books.google.com/?id=uyKht3EwjA0C&printsec=frontcover&dq=liver+disease#v=onepage&q=liver%2520disease&f=false|publisher = Elsevier Health Sciences|date = 2011-08-03|isbn = 978-1455723164|language = en|first = Lawrence S.|last = Friedman|first2 = Emmet B.|last2 = Keeffe}}

External links

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