Alcoholic liver disease diagnosis is suggested by an established history of habitual alcohol intake of sufficient length and intensity.
Toxic daily threshold of alcohol consumption is 40-80 g for males and 20-40 g for females for 10-12 years.
Signs of alcohol abuse and hepatic injury include malnutrition and muscle wasting, cutaneous telangiectasia, palmar erythema, finger clubbing, Dupuytren's contracture, peripheral neuropathy, parotid gland enlargement and signs of gynecomastia and hypogonadism may also be present.


  • Signs, symptoms and severity of liver disease can be variable between individuals and histological stages

Cofactors in the Development of Alcoholic Liver Disease (ALD)

  • The amount (>30 g/day) and type of alcohol ingested and drinking pattern (eg binge drinking)
  • Genetic factors
    • Rate of alcohol metabolism plays a role
  • Gender
    • Women are more susceptible with a tendency towards disease progression despite abstinence
  • Diet and nutrition
    • Undernutrition
    • Overnutrition and obesity are established independent risk factors for hepatic steatosis and steatohepatitis
  • Concomitant hepatitis B virus (HBV) infection accelerates the progression of ALD and may hasten mortality
  • Hepatitis C virus (HCV) infection increases probability of development of cirrhosis by 8- to 10-fold and HCV infection accelerates progression of ALD

Laboratory Tests

  • Liver function tests (LFTs)
    • Elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); AST>ALT usually >2x upper limit of normal 
    • AST:ALT ratio >1.5 gives a likely diagnosis of ALD; if ratio ≥3, this is strongly suggestive of ALD
    • Alkaline phosphatase and gamma-glutamyl transpeptidase (>100 U/mL) are both usually elevated; the latter is a marker for detection of previous alcohol consumption
    • Total bilirubin >3 mg/dL and albumin <3 g/L
  • Metabolic alterations that may be present:
    • Hyperglycemia, hypertriglyceridemia, hyperuricemia, electrolyte abnormalities
  • Hematological abnormalities
    • Macrocytic anemia may be seen in 75% of patients
    • Thrombocytopenia that may be transitory only; but if with progression to cirrhosis, it may persist
    • Leukocytosis (leukemoid reaction in the absence of infection)
  • May utilize Child-Pugh classification which is a scoring system that uses albumin level, PT, international normalized ratio (INR) bilirubin level, presence of ascites and encephalopathy severity to determine evidence of hepatic dysfunction

Liver Biopsy

  • Liver biopsy is rarely needed to establish the diagnosis
  • May be used to:
    • Clarify atypical cases or uncertain diagnosis
    • If concomitant disease is present
    • Establish stage and severity of the disease and define the prognosis
    • Aid in therapeutic decisions

Infectious Disease Work-up  

  • Eg Blood tests, sputum cultures, urinalysis and urine culture, ascitic fluid cell counts and culture


  • Eg Ultrasound, CT scan, or MRI cannot document alcohol as the etiology of the liver disease but can help in ruling out other causes of abnormal test results such as biliary obstruction, infiltrative and neoplastic liver diseases


  • Diagnosis of alcoholic liver disease (ALD) is suggested by an established history of habitual alcohol intake of sufficient length and intensity
    • Historical data that may also be suggestive include injuries, previous trauma, or visits to the emergency room
  • Patients tend to under report alcohol consumption or deny alcohol abuse
  • Tool most often used to assess alcohol dependency is “CAGE” questionnaire which refers to lifetime occurrence of the following:
    • Cutting down on drinking
    • Annoyance at others’ concerns about drinking
    • Feeling Guilty about drinking
    • Use of alcohol as an Eye opener in the morning
  • Other screening tools include the Michigan Alcoholism Screening Test (MAST), Alcohol Use Disorders Identification Test (AUDIT), and the Lifetime Drinking History
    • The AUDIT is a validated tool to recognize alcohol consumption; an AUDIT score of >8 indicates alcohol use disorder or abuse while a score of >20 indicates alcohol dependence
  • Toxic daily threshold of alcohol consumption is 40-80 g for males and 20-40 g for females x 10-12 years (≥5 drinks/ day for males and ≥4 drinks/day for females)
    • Heavy alcohol use for >5 years, ie >3 drinks/day for males and >2 drinks/day for females, increases risk for ALD


Fatty Liver

  • Develops in about 90% of individuals with an alcoholic intake of 60 g/day
  • Uncomplicated disease is commonly asymptomatic and self-limited
  • May be reversible following abstinence after 4-6 weeks, though a few may lead to progression to fibrosis and cirrhosis despite being abstinent

Alcoholic Hepatitis

  • May be asymptomatic or may present with tender hepatomegaly, jaundice, fever, ascites, hepatic encephalopathy, anorexia, malaise and leukemoid reactions
    • Portal hypertension may be present, even in the absence of cirrhosis
  • Subtypes of alcoholic hepatitis include the following:  
    • Possible: Clinical diagnosis undetermined because of another confounding cause of hepatic disease or ambiguous history of alcohol intake
    • Probable: Clinical diagnosis from heavy alcohol use of >5 years with active use 4 weeks before onset of symptoms, rapid development or worsening of jaundice, AST/ALT ratio of >1.5:1 with levels <400 IU/L and without other causes of hepatic disease  
    • Definite: Features of alcoholic hepatitis histologically confirmed


  • Once a patient has alcoholic hepatitis, the probability of developing cirrhosis is 10-20% per year and up to 70% of patients will eventually develop cirrhosis (especially those who continue drinking, those with severe alcoholic hepatitis and females)

Well-compensated Cirrhosis

  • May be asymptomatic with normal physical exam
  • Steatosis or steatohepatitis are often coexistent and patient may have hepatomegaly and/or splenomegaly
  • Signs of portal hypertension may dominate
  • In more advanced disease, the liver decreases in size and the left hepatic lobe becomes more prominent
    • Entire liver has hard and nodular consistency
  • Splenomegaly of various degrees is frequent

Decompensated Cirrhosis

  • Muscle wasting
  • Ascites and venous collateral circulation
  • Spider angiomata, palmar erythema and Dupuytren’s palmar contracture
  • Parotid and lacrimal gland enlargement
  • If with hypoalbuminemia, patient may have Muehrcke’s nails or white nails
  • Clubbing of fingers in patients with arteriovenous pulmonary shunting
  • Hepatic encephalopathy may be present
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