• Clinical science

Alcoholic liver disease


Alcoholic liver disease (ALD) refers to a range of progressive liver conditions caused by chronic and excessive alcohol consumption. One-third of the US population consumes alcohol above the recommended levels, increasing their risk of ALD. There are three stages of ALD, which may or may not occur sequentially. The first stage is typically asymptomatic and involves the development of (potentially) reversible alcoholic fatty liver. Continued alcohol consumption will lead to alcoholic hepatitis, the second stage, which often becomes chronic. Clinical findings in this stage include jaundice, fatigue, and fever. In the third and final stage, the patient develops alcoholic cirrhosis. Patient history, transaminase levels, and imaging studies are crucial for diagnosis and show different patterns of hepatic injury. Nonalcoholic steatohepatitis is a differential diagnosis and is currently regarded as an important cause of cirrhosis. Treatment of ALD requires complete cessation of alcohol use.


  • Second most common cause of liver cirrhosis in the United States
  • 28% of the US population exceeds the recommended limits of alcohol consumption.
  • Lifetime prevalence of alcohol abuse: 18%
  • ∼ 10–20% of heavy drinkers develop cirrhosis.


Epidemiological data refers to the US, unless otherwise specified.


  • Alcoholism is a very important cause of chronic liver diseases.
  • Significant alcohol consumption
    • Men: > 210 g pure alcohol per week
    • Women: > 140 g pure alcohol per week



Clinical features

The stages of ALD may overlap and do not necessarily occur in sequence.

Alcoholic fatty liver (reversible)

  • Mostly asymptomatic
  • Some patients report feeling a sensation of pressure in the upper abdominal area.
  • Hepatomegaly: soft in consistency
  • Regresses after cessation of alcohol consumption
  • Acute exacerbation with risk of hepatic failure is rare.

Alcoholic hepatitis (reversible in mild cases)

Alcohol-related cirrhosis (irreversible)

  • Final stage of ALD
  • See “Clinical features” in cirrhosis.



A history of alcohol abuse that correlates with typical laboratory and imaging findings is diagnostic of alcoholic liver disease.

Alcoholic fatty liver

Imaging and laboratory studies in the case of alcoholic fatty liver will show a reversal of changes within a month if the patient abstains from alcohol!

Alcoholic hepatitis

To remember that AST > ALT in alcoholic hepatitis, think of “Make a toAST with alcohol!

Alcohol-related cirrhosis

  • See cirrhosis.
  • Diagnosis confirmed by biopsy



  1. Alcoholic fatty liver
    • Accumulation of lipid droplets in the hepatocytes with gradual single cell necrosis within the lobules
  2. Alcoholic hepatitis
  3. Alcohol-related cirrhosis
    • Infiltration of lymphocytes
    • Massive accumulation of fat in hepatocytes
    • Formation of fibrous septa and regenerative nodules
    • Perivascular sclerosis of central veins (especially in the early stage)

Alcoholic fatty liver and mild alcoholic hepatitis may be reversible after cessation of alcohol intake. However, severe alcoholic hepatitis and cirrhosis are not reversible!


Differential diagnoses

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH)

NASH is a diagnosis of exclusion! Other causes of chronic liver disease must be ruled out by laboratory studies and/or biopsy.

A distinction between alcoholic and non-alcoholic fatty liver disease can only be drawn based on patient history!

There is more ALT than AST (AST/ALT < 1) if the Liver is infiltrated with Lipids.


The differential diagnoses listed here are not exhaustive.




Decompensated cirrhosis

Mainly characterized by a constellation of clinical features resulting from decreased hepatic function:

Other organ damage following chronic alcohol use

Zieve syndrome

We list the most important complications. The selection is not exhaustive.

  • 1. Wolf DC. Cirrhosis. In: Anand BS. Cirrhosis. New York, NY: WebMD. http://emedicine.medscape.com/article/185856. Updated January 8, 2017. Accessed March 25, 2017.
  • 2. Mauriello LM, Gökbayrak NS, Van Marter DF, Paiva AL, Prochaska JM. An internet-based computer-tailored intervention to promote responsible drinking: findings from a pilot test with employed adults. Alcohol Treat Q. 2012; 30(1): pp. 91–108. doi: 10.1080/07347324.2012.635528.
  • 3. Hasin D, Keyes K. The epidemiology of alcohol and drug disorders. Springer New York; 2010: pp. 23–49.
  • 4. Mathurin P, Bataller R. Trends in the management and burden of alcoholic liver disease. J Hepatol. 2015; 62(1): pp. S38–S46. doi: 10.1016/j.jhep.2015.03.006.
  • 5. Flegel K, MacDonald N, Hebert PC. Binge drinking: all too prevalent and hazardous. Can Med Assoc J. 2011; 183(4): p. 411. doi: 10.1503/cmaj.110029.
  • 6. O'Shea RS, Dasarathy S, McCullough AJ et al. Alcoholic liver disease. Am J Gastroenterol. 2009; 105(1): pp. 14–32. doi: 10.1038/ajg.2009.593.
  • 7. Heuman DM. Alcoholic Hepatitis. In: Anand BS. Alcoholic Hepatitis. New York, NY: WebMD. http://emedicine.medscape.com/article/170539. Updated December 30, 2016. Accessed March 25, 2017.
  • 8. Robert T Means. Hematologic complications of alcohol use. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/hematologic-complications-of-alcohol-use. Last updated January 22, 2020. Accessed August 17, 2020.
  • 9. Akunjee M, Akunjee N. CSA book: MRCGP CSA Symptom Solver: Clinical frameworks for the MRCGP CSA exam. London, United Kingdom: Clinical Prep; 2014.
  • 10. Gaillard F et al. Diffuse Hepatic Steatosis. https://radiopaedia.org/articles/diffuse-hepatic-steatosis. Updated January 1, 2017. Accessed March 25, 2017.
  • 11. Goljan EF. Rapid Review Pathology. Philadelphia, PA: Elsevier Saunders; 2013.
  • 12. Tommolino E. Fatty Liver. In: Anand BS. Fatty Liver. New York, NY: WebMD. http://emedicine.medscape.com/article/175472. Updated January 25, 2017. Accessed March 25, 2017.
  • 13. Sakhuja P. Pathology of alcoholic liver disease, can it be differentiated from nonalcoholic steatohepatitis?. World J Gastroenterol. 2014; 20(44): pp. 16474–16479. doi: 10.3748/wjg.v20.i44.16474.
  • 14. Orman ES, Odena G, Bataller R. Alcoholic liver disease: Pathogenesis, management, and novel targets for therapy. J Gastroenterol Hepatol. 2013; 28(S1): pp. 77–84. doi: 10.1111/jgh.12030.
  • 15. Torruellas C. Diagnosis of alcoholic liver disease. World J Gastroenterol. 2014; 20(33): pp. 11684–11699. doi: 10.3748/wjg.v20.i33.11684.
  • 16. Bayard M, Holt J, Boroughs E. Nonalcoholic fatty liver disease. Am Fam Physician. 2006; 73(11): pp. 1961–1968. pmid: 16770927.
  • 17. Adams LA, Feldstein AE. Nonalcoholic steatohepatitis: risk factors and diagnosis. Expert Rev Gastroenterol Hepatol. 2010; 4(5): pp. 623–635. doi: 10.1586/egh.10.56.
  • Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014.
  • Le T, Bhushan V, Chen V, King M. First Aid for the USMLE Step 2 CK. McGraw-Hill Education; 2015.
last updated 11/03/2020
{{uncollapseSections(['jA0_ji', 'kA0mPi', 'OA0IPi', 'Dxc1Ae0', 'mA0V4i', 'nA074i', 'LA0w4i', 'oA00ki', 'KA0Uki', '6A0jki'])}}