Alcohol-associated liver disease, one of the most common types of liver disease worldwide, is associated with tremendous morbidity, mortality, and financial costs. Although significant progress has been made in screening and management of patients with early, or nonadvanced, ALD, there remain unmet clinical needs and areas of future prospects in the management.
ALD is caused by alcohol use disorder (AUD)—harmful alcohol consumption (=2 drinks per day or >7 per week in females and =3 drinks daily or >14 weekly in males) despite negative physical, social, and interpersonal consequences accompanied by dependence, withdrawal, and tolerance of alcohol.1
Manifestation of ALD varies from nonadvanced disease (steatosis with or without steatohepatitis and fibrosis stage =2 or periportal fibrosis) to advanced disease (advanced or stage 3 fibrosis and cirrhosis).1 Steatosis is defined as more than 5% of hepatocytes containing fat droplets. Ultrasound examination accurately identifies patients with fat droplets in more than 33% of hepatocytes (moderate or severe steatosis). Controlled attenuation parameter and magnetic resonance–proton density fat fraction can detect mild steatosis, but high cost and lack of availability—as the technology is often only at tertiary centers—limit their widespread use. Steatohepatitis is identified on liver histology with features such as neutrophilic lobular infiltration, hepatocyte ballooning, Mallory hyaline, and steatosis.