Alcoholic Hepatitis

Author: Leah Farquharson 

Editor: Helia Mansouri Dana


Alcoholic hepatitis (AH) is the inflammation of the liver as a result of heavy alcohol use, resulting in the production of toxic compounds upon alcohol degradation by the liver (Im, 2019). Fatty changes in the liver associated with AH may result in inflammation, fibrosis, and even cirrhosis (Hosseini et al., 2019).

Patients can present from asymptomatic to cirrhotic and even cancerous at the time of diagnosis (Singal et al., 2018). Symptoms include abdominal pain and distention, malnutrition, jaundice and changes in mental status (Hosseini et al., 2019). The primary treatment for AH is alcohol abstinence which may involve psychotherapy (Im, 2019), addiction management programs and pharmaceuticals to manage the addiction (Hosseini et al., 2019).

Generally, females are at higher risk AH compared to males due to a differing alcohol metabolism mechanism and higher percent body fat (Singal et al., 2018). AH is also of higher prevalence in certain races, specifically individuals of Eastern or Southern European descent, as well as United Kingdom descent in comparison to countries with large muslim populations (Hosseini et al., 2019). In the United States, blacks and hispanics have a higher risk of developing AH and increased mortality in comparison to their white counterparts which highlights the socioeconomic and cultural aspects of its prevalence (Hosseini et al., 2019).


AH is caused by excessive alcohol use (Hosseini et al., 2019). Alcohol is quickly absorbed by the Gastrointestinal (GI) system resulting in a quick increase of blood alcohol concentrations which must be metabolized by the liver (Hosseini et al., 2019). High concentrations of alcohol results in the metabolic properties of alcohol to switch from the hepatic enzymes (alcohol dehydrogenase and acetaldehyde dehydrogenase) to the Cytochrome P4502E1 (CYP2E1) system, which is upregulated during chronic high alcohol levels (Hosseini et al., 2019).

Metabolizing alcohol via the Cytochrome P4502E1 (CYP2E1) system results in hepatic cells experiencing high levels of reactive oxygen species (ROS) which lowers concentrations of intracellular endogenous antioxidants (Hosseini et al., 2019). The presence of alcohol in hepatocytes can lead to the accumulation of fat because fatty acid metabolism is  compromised in high alcohol concentrations (Hosseini et al., 2019). Hepatic cells can further become stressed as a result of high alcohol levels, which may activate apoptotic pathways resulting in cell death (Hosseini et al., 2019). Damage to the hepatic cells results in the release of  damage-associated molecular patterns (DAMPs) by the cells  , leading to inflammation (Hosseini et al., 2019).



  • Jaundice (rapid onset or worsening) (Singal et al., 2018),
  • Malnutrition and micronutrient deficiencies,
  • Abdominal pain,
  • Feeling of fullness or distention,
  • Fever (Hosseini et al., 2019),
  • Ascites (fluid containing protein buildup in abdomen) (Singal et al., 2018), 
  • Portal hypertension and associated GI bleeding (Singal et al., 2018), 
  • Hepatic encephalopathy (Singal et al., 2018),which may be seen as changes in mental status (Hosseini et al., 2019)
  • Hepatocellular carcinoma (a type of liver cancer)  (Singal et al., 2018) 


Risk Factors

  • Chronic and heavy alcohol use (over 30-60 mg/ day) (Hosseini et al., 2019)
  • Genetic factors – e.g. gene for patatin-like phospholipase domain containing protein 3 (related to lipid metabolism) (Singal et al., 2018)
  • Sex – females are at higher risk of developing AH (Singal et al., 2018). 
  • Obesity (Singal et al., 2018) 
  • Cigarette smoking (Singal et al., 2018) 
  • Race and ethnicity (Hosseini et al., 2019)
  • Nutrient deficiencies such as Zinc, riboflavin, Vitamin B12, and Vitamin A (Hosseini et al., 2019),
  • Malnutrition (Hosseini et al., 2019),
  • Presence of other liver disease, especially Hepatitis C, is known to act synergistically with alcohol and greatly increase risk of developing AH and severity of AH (Hosseini et al., 2019),



Clinical Diagnosis

A history of chronic heavy alcohol use is a main determinant of AH (Singal et al., 2018), usually over the course of twenty years (Hosseini et al., 2019). Patients with over 30-60g alcohol intake per day are considered to be heavy alcohol users (Hosseini et al., 2019). A major factor of AH diagnosis is ruling out any other possible liver disease of the individual (Singal et al., 2018). Physical examination may be performed to determine if enlarged liver, fever, and abdominal bruit are present (Singal et al., 2018).

Pathological Diagnosis

Further tests such as blood tests, imaging such as MRI, CT and ultrasound, may be necessary to confirm diagnosis and severity of the AH (Singal et al., 2018). Blood tests in AH patients may show an increase in circulating inflammatory white blood cells and increased circulating pro-inflammatory cytokines due to the activation of the inflammatory response associated with AH (Hosseini et al., 2019). Patients may also have increased levels of serum bilirubin and creatinine (Hosseini et al., 2019).

Since AH involves chronic heavy alcohol use, patients with AH often have high levels of alcohol biomarkers (Singal et al., 2018). Patients with AH may also have nutritional deficiencies such as riboflavin, B12, vitamin A and zinc (Hosseini et al., 2019).  Furthermore, imaging may show collagen deposits and fibrosis, and in severe cases bridging fibrosis and cirrhosis (Hosseini et al., 2019). Liver biopsy is usually performed in uncertain cases to confirm diagnoses (Im et al., 2019). Fat accumulation in hepatic cells is an indicator of AH (Hosseini et al., 2019). 

Other tests such as a Maddrey test, Gah test or Lille test may be administered to categorize the severity of the disease (Hosseini et al., 2019). A prothrombin time test may be administered to determine blood clotting time with a longer time indicating higher risk or greater severity of AH (Hosseini et al., 2019).



Non-Pharmaceutical Treatment

The first step in treatment for individuals with AH is prolonged abstinence of alcohol to prevent further development of the disease (Singal et al., 2018). As a result, psychosocial treatment may be necessary to address the alcohol addiction (Im, 2019). Patients may enroll in abstinence programs such as Alcoholics Anonymous, motivational counselling, and cognitive behavioural therapy to help manage their addiction (Hosseini et al., 2019). However, addiction management therapy is difficult in some patients due to possible hepatic encephalopathy, and hospitalization time results in absence from program meetings (Singal et al., 2018). The most important treatment approach to individuals with AH is a personalized treatment plan involving both pharmaceuticals and psychosocial interventions (Singal et al., 2018).

Pharmaceutical Treatment

Pharmaceuticals such as Acomprosate and Naltrexone may help decrease alcohol cravings to aid in patients’ addiction management (Hosseini et al., 2019). Corticosteroids may be administered as a short term relief (Singal et al., 2018) but  are generally less effective and have a worse prognosis if the individual has greater degrees of inflammation (Hosseini et al., 2019). In cases of severe AH and cirrhosis, hospitalization may be necessary (Singal et al., 2018). To aid with abstinence, baclofen (γ-amino butyric acid-B receptor agonist) may be used (Singal et al., 2018). Furthermore, “gut decontamination” using antibodies has been shown to decrease the effects and damage of alcohol related liver inflammation and steatosis (Hosseini et al., 2019). 


Articles on Misdiagnosis

Amini, M., & B.A. Runyon. (2010). Alcoholic hepatitis 2010: a clinician’s guide to diagnosis and therapy. World Journal of Gastroenterology, 16(39), 4905-4912. DOI: 10.3748/wjg.v16.i39.4905.

O’Beirne, J., Patch, D., Holt, S., Hamilton, M., & A.K. Burroughs. (2000). Alcoholic hepatitis–the case for intensive management. Postgraduate Medical Journal, 76, 504-507. DOI: 10.1136/pmj.76.898.504.

Roth, C.N., et al. (2017). Prediction of histologic alcoholic hepatitis based on clinical presentation limits the need for liver biopsy. Hepatology Communications, 1(10), 1070-1084. DOI 10.1002/hep4.1119. 



Hosseini, N., Shor, J., & Szabo, G. (2019). Alcoholic Hepatitis: A Review. Alcohol and Alcoholism, 54(4), 408–416. DOI: 10.1093/alcalc/agz036.

Im, G. Y. (2019). Acute Alcoholic Hepatitis. Clinics in Liver Disease, 23(1), 81–98. DOI: 10.1016/j.cld.2018.09.005.

Im, G. Y., Cameron, A. M., & Lucey, M. R. (2019). Liver transplantation for alcoholic hepatitis. Journal of Hepatology, 70(2), 328–334. DOI: 10.1016/j.jhep.2018.11.007.

Singal, A. K., Bataller, R., Ahn, J., Kamath, P. S., & Shah, V. H. (2018). ACG Clinical Guideline: Alcoholic Liver Disease. American Journal of Gastroenterology, 113(2), 175–194. DOI: 10.1038/ajg.2017.469.

Singal, A. K., Louvet, A., Shah, V. H., & Kamath, P. S. (2018). Grand Rounds: Alcoholic Hepatitis. Journal of Hepatology, 69(2), 534–543. DOI: 10.1016/j.jhep.2018.05.001.


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