{"doi":"10.1002/cld.920","title":"Alcohol‐Associated Liver Disease: East Versus West","abstract":"Watch a video presentation of this article Watch an interview with the author Alcohol-associated liver disease (ALD) is one of the major causes of chronic liver diseases worldwide. ALD represents a spectrum of histopathological changes in patients with excessive alcohol use ranging from alcohol-induced steatosis, alcoholic steatohepatitis, and cirrhosis.1 Alcoholic steatosis can occur in patients who consumed 120 to 150 g of alcohol per day for 2 to 3 weeks.2 Alcoholic hepatitis (AH) is a severe form of ALD with high morbidity and mortality.3 Approximately 8% to 20% of patients who drink alcohol excessively will progress to cirrhosis in their lifetime4 (Fig. 1). Approximately 27% of liver-related deaths worldwide are attributed to alcohol consumption, with the highest in Europe and levels increasing globally.5 The overall mortality rates from ALD vary across countries in the Eastern and Western Hemispheres, and are closely correlated with the per capita alcohol consumption.6 Total alcohol per capita consumption is highest in the developed world, notably Eastern Europe, which has the highest per capita consumption.7 Although the per capita alcohol consumption is lower in several countries in Asia when compared with the West, there has been a rapid rise in per capita alcohol consumption in countries such as Indian and China with recent changes in the economies and increase in average incomes.1 For instance, the percentage of regular alcohol drinkers among the general population in different areas in China increased from 27.0% in 2000 to 66.2% in 2015, and the percentage of excessive drinkers increased from 0.21% in 1982 to 14.8% in 2000.8 Several factors place patients at risk for ALD among excessive drinkers.1 Overweight and obesity were found to increase the risk for ALD based on studies in the United States, Europe, and Asia.1 Variants in genes encoding members of the alcohol dehydrogenase (ADH) family affect their ability to metabolize alcohol and determine the risk for alcohol dependence and ALD.1, 9 Patients with variants encoding for high levels of enzyme activity (ADH1B*2 and ADH1C*1 alleles) are believed to be at risk for ALD because of the accumulation of a toxic alcohol metabolite, acetaldehyde. A recent meta-analysis confirmed this association in Asian populations but found no association in Western populations.10 The explanation in the difference between East and West populations is likely due to the low allele frequency for ADH1B*2 in Caucasians. Approximately 40% to 50% of Chinese people are homozygous or heterozygous for the ALDH2*2 allele with low ALDH2 activity.11 These individuals have high blood concentrations of acetaldehyde after alcohol consumption because of the inability to convert acetaldehyde to acetate, which makes them more susceptible to liver injury.1 The patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene is located on the long arm of chromosome 22.12 Patients with PNPLA3 variant rs738409 have a 2.25-fold increased risk for alcoholic cirrhosis13; the results were confirmed in a recent meta-analysis, especially in the European cohort. A small study from India found that the rs738409 polymorphism increased the risk for ALD 2.1-fold.14 However, further studies are needed to determine the association between PNPLA3 and ALD in Asian populations. The range of clinical features of ALD varies, from asymptomatic to end-stage liver disease with portal hypertension (Fig. 1). Acute deterioration in patients with ALD, presenting as AH or acute-on-chronic liver failure manifesting as jaundice, ascites, and encephalopathy, is often the consequence of recent alcohol use. Many patients in Eastern and Western countries at the time of initial presentation of AH already have underlying alcoholic cirrhosis. Compared with Western populations, individuals with alcohol use disorders in Asia-Pacific countries have increased rates of viral hepatitis infection, which might exacerbate the progression of unde","journal":"Clinical Liver Disease","year":2020,"id":87887,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":11,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9591,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":242909,"name":"Suthat Liangpunsakul","orcid":"0000-0002-6504-8123","position":1,"is_corresponding":false},{"id":446090,"name":"Teerha Piratvisuth","orcid":"0000-0002-5249-9208","position":2,"is_corresponding":false},{"id":446089,"name":"Phunchai Charatcharoenwitthaya","orcid":"0000-0002-8334-0267","position":0,"is_corresponding":true}],"reference_count":39,"raw_metadata":null,"created_at":"2026-07-18T22:00:29.831859Z","pmid":"33489093","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}