SpecialtyGastroenterology, hepatology, infectious diseases, internal medicine, family medicine Edit this on Wikidata

Hepatitis (plural hepatitides) is a medical condition defined by the inflammation of the liver and characterized by the presence of inflammatory cells in the tissue of the organ. The name is from the Greek hepar (ἧπαρ), the root being hepat- (ἡπατ-), meaning liver, and suffix -itis, meaning "inflammation" (c. 1727).[1] The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.

Hepatitis may occur with limited or no symptoms, but often leads to jaundice, anorexia (poor appetite) and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses known as the hepatitis viruses cause most cases of hepatitis worldwide, but it can also be due to toxins (notably alcohol, certain medications, some industrial organic solvents and plants), other infections and autoimmune diseases.

Signs and symptoms


Initial features are of nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis from any cause, are: profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin (i.e., jaundice) and abdominal discomfort. Physical findings are usually minimal, apart from jaundice in a third and tender hepatomegaly (swelling of the liver) in about 10%. Some exhibit lymphadenopathy (enlarged lymph nodes, in 5%) or splenomegaly (enlargement of the spleen, in 5%).[2]

Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.[3]

A small proportion of people with acute hepatitis progress to acute liver failure, in which the liver is unable to clear harmful substances from the circulation (leading to confusion and coma due to hepatic encephalopathy) and produce blood proteins (leading to peripheral edema and bleeding). This may become life-threatening and occasionally requires a liver transplant.


Chronic hepatitis often leads to nonspecific symptoms such as malaise, tiredness and weakness, and often leads to no symptoms at all. It is commonly identified on blood tests performed either for screening or to evaluate nonspecific symptoms. The occurrence of jaundice indicates advanced liver damage. On physical examination there may be enlargement of the liver.[4]

Extensive damage and scarring of liver (i.e. cirrhosis) leads to weight loss, easy bruising and bleeding tendencies, peripheral edema (swelling of the legs) and accumulation of ascites (fluid in the abdominal cavity). Eventually, cirrhosis may lead to various complications: esophageal varices (enlarged veins in the wall of the esophagus that can cause life-threatening bleeding) hepatic encephalopathy (confusion and coma) and hepatorenal syndrome (kidney dysfunction).

Acne, abnormal menstruation, lung scarring, inflammation of the thyroid gland and kidneys may be present in women with autoimmune hepatitis.[4]




Alcoholic hepatitis

Main article: Alcoholic hepatitis

Ethanol, mostly in alcoholic beverages, is a significant cause of hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.

Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C.[citation needed] The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis.

Drug induced

Main article: Hepatotoxicity

A large number of drugs can cause hepatitis:[17]

The clinical course of drug-induced hepatitis is quite variable, depending on the drug and the patient's tendency to react to the drug. For example, halothane hepatitis can range from mild to fatal as can INH-induced hepatitis. Hormonal contraception can cause structural changes in the liver. Amiodarone hepatitis can be untreatable since the long half life of the drug (up to 60 days) means that there is no effective way to stop exposure to the drug. Statins can cause elevations of liver function blood tests normally without indicating an underlying hepatitis. Lastly, human variability is such that any drug can be a cause of hepatitis.

Other toxins

Other Toxins can cause hepatitis:

Metabolic disorders

Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.

Non-alcoholic steatohepatitis (NASH) is effectively a consequence of metabolic syndrome.


"Obstructive jaundice" is the term used to describe jaundice due to obstruction of the bile duct (by gallstones or external obstruction by cancer). If longstanding, it leads to destruction and inflammation of liver tissue.


Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes, possibly due to genetic predisposition or acute liver infection; causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis.

Alpha 1-antitrypsin deficiency

In severe cases of alpha 1-antitrypsin deficiency (A1AD), the accumulated protein in the endoplasmic reticulum causes liver cell damage and inflammation.

Non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is the occurrence of fatty liver in people who have no history of alcohol use. It is most commonly associated with obesity (80% of all obese people have fatty liver). It is more common in women. Severe NAFLD leads to inflammation, a state referred to as non-alcoholic steatohepatitis (NASH), which on biopsy of the liver resembles alcoholic hepatitis (with fat droplets and inflammatory cells, but usually no Mallory bodies).

The diagnosis depends on medical history, physical exam, blood tests, radiological imaging and sometimes a liver biopsy. The initial evaluation to identify the presence of fatty infiltration of the liver is medical imaging, including such ultrasound, computed tomography (CT), or magnetic resonance (MRI). However, imaging cannot readily identify inflammation in the liver. Therefore, the differentiation between steatosis and NASH often requires a liver biopsy. It can also be difficult to distinguish NASH from alcoholic hepatitis when the patient has a history of alcohol consumption. Sometimes in such cases a trial of abstinence from alcohol along with follow-up blood tests and a repeated liver biopsy are required.

NASH is becoming recognized as the most important cause of liver disease second only to hepatitis C in numbers of patients going on to cirrhosis.[citation needed]

Ischemic hepatitis

Main article: Ischemic hepatitis

Ischemic hepatitis is caused by decreased circulation to the liver cells. Usually this is due to decreased blood pressure (or shock), leading to the equivalent term "shock liver". Patients with ischemic hepatitis are usually very ill due to the underlying cause of shock. Rarely, ischemic hepatitis can be caused by local problems with the blood vessels that supply oxygen to the liver (such as thrombosis, or clotting of the hepatic artery which partially supplies blood to liver cells). Blood testing of a person with ischemic hepatitis will show very high levels of transaminase enzymes (AST and ALT), which may exceed 1000 U/L. The elevation in these blood tests is usually transient (lasting 7 to 10 days). It is rare that liver function will be affected by ischemic hepatitis.

Giant cell hepatitis

Giant cell hepatitis is a rare form of hepatitis (~700 cases reported) that predominantly occurs in children. Diagnosis is made on the basis of the presence of hepatocellular multinucleate giant cells.[21][22][23] Cases presenting in adults are rare and tend to be rapidly progressive.[24][25][26][27] The cause is currently unknown but an infectious cause is suspected.[28][29]Hepatitis E[30], hepatitis C[31], paramyxovirus[32][33], papillomavirus[34] and Human herpes virus 6[35][36] have been suggested as causes. A similar condition has been reported in cats.[37] but it is not known if there is any connection between these. The condition tends to improve with the use of ribivirin which suggests a viral origin.[38][39]

See also


  1. ^ Online Etymology Dictionary
  2. ^ Ryder S, Beckingham I (2001). "Acute hepatitis". BMJ. 322 (7279): 151–153. doi:10.1136/bmj.322.7279.151. PMC 1119417. PMID 11159575.
  3. ^ a b V.G. Bain and M. Ma, Acute Viral Hepatitis, Chapter 14, First principle of gastroenterology (an online text book)
  4. ^ a b Chronic hepatitis at Merck Manual of Diagnosis and Therapy Home Edition
  5. ^ Miguet JP, Coaquette A, Bresson-Hadni S, Lab M (1990) The other types of viral hepatitis. Rev Prat 40(18):1656-1659
  6. ^ Chau TN, Lee KC, Yao H, Tsang TY, Chow TC, Yeung YC, Choi KW, Tso YK, Lau T, Lai ST, Lai CL (2004) SARS-associated viral hepatitis caused by a novel coronavirus: report of three cases. Hepatology 39(2):302-310
  7. ^ Naides SJ (1998). "Rheumatic manifestations of parvovirus B19 infection". Rheum. Dis. Clin. North Am. 24 (2): 375–401. doi:10.1016/S0889-857X(05)70014-4. PMID 9606764. ((cite journal)): Unknown parameter |month= ignored (help)
  8. ^ Xiong W (2010) Clinical efficacy of treating infant cytomegalovirus hepatitis with ganciclovir and impact on cytokines. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 26(11):1130-2
  9. ^ Okano M, Gross TG (2011) Acute or chronic life-threatening diseases associated with Epstein-Barr virus infection. Am J Med Sci.
  10. ^ Gallegos-Orozco JF, Rakela-Brödner J (2010) Hepatitis viruses: not always what it seems to be. Rev Med Chil 138(10):1302-1311
  11. ^ Papic N, Pangercic A, Vargovic M, Barsic B, Vince A, Kuzman I (2011) Liver involvement during influenza infection: perspective on the 2009 influenza pandemic. Influenza Other Respi Viruses doi: 10.1111/j.1750-2659.2011.00287.x.
  12. ^ Figure 7.12 (Some causes of acute parenchymal damage), Parveen, M.D. Kumar (Editor), Michael, M.d. Clark (Editor) (2005). Clinical Medicine. Philadelphia, PA: W.B. Saunders Company. ISBN 0-7020-2763-4. ((cite book)): |author= has generic name (help)CS1 maint: multiple names: authors list (link)
  13. ^ Scott Moses, MD, Acute Hepatitis causes, Family practice notebook.com
  14. ^ Chan JC, Jeffers LJ, Gould EW, Hutson D, Martinez OV, Reddy KR, Hassan F, Schiff ER (1990) Visceral protothecosis mimicking sclerosing cholangitis in an immunocompetent host: successful antifungal therapy. Rev Infect Dis 12(5):802-807
  15. ^ Mathew LG, Pulimood S, Thomas M, Acharya MA, Raj PM, Mathews MS (2010) Disseminated protothecosis. Indian J Pediatr 77(2):198-199
  16. ^ Lanotte P, Baty G, Senecal D, Dartigeas C, Bailly E, Duong TH, Chandenier J, Goudeau A (2009) Fatal algaemia in patient with chronic lymphocytic leukemia. Emerg Infect Dis 15(7):1129-1130
  17. ^ "Hepatitis as a result of chemicals and drugs". HealthAtoZ. Archived from the original on 2006-06-23. Retrieved 2006-07-01.
  18. ^ Lim JR, Faught PR, Chalasani NP, Molleston JP (2006). "Severe liver injury after initiating therapy with atomoxetine in two children". J. Pediatr. 148 (6): 831–4. doi:10.1016/j.jpeds.2006.01.035. PMID 16769398.((cite journal)): CS1 maint: multiple names: authors list (link)
  19. ^ Bastida G, Nos P, Aguas M, Beltrán B, Rubín A, Dasí F, Ponce J (2005). "Incidence, risk factors and clinical course of thiopurine-induced liver injury in patients with inflammatory bowel disease". Aliment Pharmacol Ther. 22 (9): 775–82. doi:10.1111/j.1365-2036.2005.02636.x. PMID 16225485.((cite journal)): CS1 maint: multiple names: authors list (link)
  20. ^ Nadir A, Reddy D, Van Thiel DH (2000). "Cascara sagrada-induced intrahepatic cholestasis causing portal hypertension: case report and review of herbal hepatotoxicity". Am. J. Gastroenterol. 95 (12): 3634–7. doi:10.1111/j.1572-0241.2000.03386.x. PMID 11151906.((cite journal)): CS1 maint: multiple names: authors list (link)
  21. ^ Torbenson M, Hart J, Westerhoff M, Azzam RK, Elgendi A, Mziray-Andrew HC, Kim GE, Scheimann A (2010) Neonatal giant cell hepatitis: histological and etiological findings. Am J Surg Pathol 34(10):1498-1503
  22. ^ Krokhina NB, Ushakova RA, Kobeleva IaM (2010) Significance of hepatic biopsy specimens in the diagnosis of liver disease in babies of the first year of life. Arkh Patol 72(1):19-23
  23. ^ Kirsch R, Yap J, Roberts EA, Cutz E (2009) Clinicopathologic spectrum of massive and submassive hepatic necrosis in infants and children. Hum Pathol 40(4):516-526
  24. ^ Hayashi H, Narita R, Hiura M, Abe S, Tabaru A, Tanimoto A, Sasaguri Y, Harada M (2011) A case of adult autoimmune hepatitis with histological features of giant cell hepatitis. Intern Med 50(4):315-319
  25. ^ Hartl J, Buettner R, Rockmann F, Farkas S, Holstege A, Vogel C, Schnitzbauer A, Schlitt HJ, Schoelmerich J, Kirchner G (2010) Giant cell hepatitis: an unusual cause of fulminant liver failure. Z Gastroenterol 48(11):1293-1266
  26. ^ Gábor L, Pál K, Zsuzsa S (1997) Giant cell hepatitis in adults. Pathol Oncol Res 3(3):215-218
  27. ^ Alexopoulou A, Deutsch M, Ageletopoulou J, Delladetsima JK, Marinos E, Kapranos N, Dourakis SP (2003) A fatal case of postinfantile giant cell hepatitis in a patient with chronic lymphocytic leukaemia. Eur J Gastroenterol Hepatol 15(5):551-555
  28. ^ Duhaut P, Bosshard S, Ducroix JP (2004) Is giant cell arteritis an infectious disease? Biological and epidemiological evidence. Presse Med 33(19 Pt 2):1403-1408
  29. ^ Shet TM, Kandalkar BM, Vora IM (1998) Neonatal hepatitis--an autopsy study of 14 cases. Indian J Pathol Microbiol 41(1):77-84
  30. ^ Harmanci O, Onal IK, Ersoy O, Gürel B, Sökmensüer C, Bayraktar Y (2007) Postinfantile giant cell hepatitis due to hepatitis E virus along with the presence of autoantibodies. Dig Dis Sci 52(12):3521-3523
  31. ^ Moreno A, Moreno A, Pérez-Elías MJ, Quereda C, Fernández-Muñoz R, Antela A, Moreno L, Bárcena R, López-San Román A, Celma ML, García-Martos M, Moreno S. Syncytial giant cell hepatitis in human immunodeficiency virus-infected patients with chronic hepatitis C: 2 cases and review of the literature (2006) Hum Pathol 37(10):1344-1349
  32. ^ Fimmel CJ, Guo L, Compans RW, Brunt EM, Hickman S, Perrillo RR, Mason AL (1993) A case of syncytial giant cell hepatitis with features of a paramyxoviral infection. Am J Gastroenterol 93(10):1931-1937
  33. ^ Krech RH, Geenen V, Maschek H, Högemann B (1998) Adult giant cell hepatitis with fatal outcome. Clinicopathologic case report and reflections on pathogenesis. Pathologe 19(3):221-225
  34. ^ Drut R, Gómez MA, Drut RM, Cueto RE, Lojo M (1998) Human papillomavirus, neonatal giant cell hepatitis and biliary duct atresia. Acta Gastroenterol Latinoam 28(1):27-31
  35. ^ Potenza L, Luppi M, Barozzi P, Rossi G, Cocchi S, Codeluppi M, Pecorari M, Masetti M, Di Benedetto F, Gennari W, Portolani M, Gerunda GE, Lazzarotto T, Landini MP, Schulz TF, Torelli G, Guaraldi G (2008) HHV-6A in syncytial giant-cell hepatitis. N Engl J Med 359(6):593-602
  36. ^ Kuntzen T, Friedrichs N, Fischer HP, Eis-Hübinger AM, Sauerbruch T, Spengler U (2005) Postinfantile giant cell hepatitis with autoimmune features following a human herpesvirus 6-induced adverse drug reaction. Eur J Gastroenterol Hepatol 17(10):1131-1134
  37. ^ Suzuki K, Nakayama H, Doi K (2001) Giant cell hepatitis in two young cats. J Vet Med Sci. 2001 Feb;63(2):199-201
  38. ^ Hassoun Z, N'Guyen B, Cote J, Marleau D, Willems B, Roy A, Dagenais M, Lapointe R, Letourneau R, Villeneuve JP (2000) A case of giant cell hepatitis recurring after liver transplantation and treated with ribavirin. Can J Gastroenterol 14(8):729-731
  39. ^ Durand F, Degott C, Sauvanet A, Molas G, Sicot C, Marcellin P, Belghiti J, Erlinger S, Benhamou JP, Bernuau J (1997) Subfulminant syncytial giant cell hepatitis: recurrence after liver transplantation treated with ribavirin. J Hepatol 26(3):722-776