ALD diagnosis

In contrast to non-alcoholic fatty liver disease patients, those with ALD mostly present for medical care very late due to jaundice or from cirrhosis complications. No specific laboratory tests exist that diagnose liver disease connected to alcohol use.

1. Patients with alcohol abuse and dependence can be identified with the alcohol use disorders inventory test (AUDIT) validated tool.
2. Non-invasive tools such as transient elastography in early ALD patients presenting with fatty liver or minor derangements in transaminases still need more data to be considered.
3. The mean corpuscular volume, aminotransferases, and γ-glutamyl transferase are sensitive biochemical tests, but lack specificity in cirrhosis patients. About 75–90% sensitivity is seen with carbohydrate-deficient transferrin combined with γ-glutamyl transferase.

After excluding other causes of liver diseases in someone with documented persistent heavy alcohol use 8 weeks before symptoms onset, a clinical diagnosis of AH can be made if:

• There is rapid development or worsening of jaundice and liver-related complications
• The serum total bilirubin is greater than 3 mg/dL
• ALT and AST is elevated more than 1.5 times the upper normal limit but less than 400 U/L
• AST/ALT ratio is greater than 1.5

If alcohol usage history is uncertain, or the clinical diagnosis is confusing with another liver disease etiology, a transjugular liver biopsy is recommended in patients with suspected AH.

Non-pharmacological therapies

Behavioral interventions such as motivational enhancement therapy, cognitive behavioral therapy, motivational interviewing, supportive therapy, and psychoeducation are some major approaches to induce or to maintain alcohol abstinence in ALD patients.

The five “A” model contains the following minimum components that every brief intervention must have:

• Ask about use
• Advice to quit or reduce
• Assess willingness
• Assist to quit or reduce
• Arrange follow-up

Patients educate themselves about how their thought processes contribute to their behavior during structured goal-directed cognitive behavior therapy. Brief motivational interventions are better than no intervention for reducing alcohol relapses.

Pharmacological therapies

Disulfiram, acamprosate, gabapentin, naltrexone, topiramate, sertraline, and baclofen have been used for AUD. Among these, only baclofen is safe in patients with ALD and cirrhosis.

Baclofen 5 mg three times a day is the usual starting dose which can be raised to a maximum of 15 mg three times a day after every 3–5 days intervals based on patient tolerance. Increase in abstinence rates cause the efficacy of baclofen to improve.

Even in advanced liver disease and AH patients, baclofen has a very good safety profile and can be monitored by hepatologists or addiction specialists. Baclofen may also be effective in preventing alcohol relapse.

Management of liver disease

Alcoholic cirrhosis

Decompensated cirrhotic patients are managed as per the problems faced.

1. Symptomatic relief of tense ascites is done via a therapeutic paracentesis.
2. Antibiotics, along with albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 is given if there is spontaneous bacterial peritonitis.
3. Lactulose and rifaximin therapy, as well as control of infection is sought in hepatic encephalopathy patients as per current guidelines.
4. In some patients imaging of the head and CSF studies may help.
5. A drug screen is also suggested.
6. Acute variceal bleeding episodes can be managed with terlipressin or octreotide (vasoactive agents), antibiotics, and endoscopic therapy. After starting vasoactive therapy, wait for at least 30 minutes before endoscopy.

Alcoholic hepatitis

1. Corticosteroids and nutritional supplementation are therapies that have proven efficacy and should be offered to affected patients.
2. Pentoxifylline, n-acetyl cysteine and granulocyte colony-stimulating factor have potential efficacy and can also be used.
3. Therapies with no efficacy include tumor necrosis factor-α inhibitors, antioxidant cocktail and vitamin E, the hepatic mitogens: insulin and glucagon, anabolic steroids and propylthiouracil.