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Abstract
A study conducted 15-year ago showed that only 13.5% of chronic alcoholics developed alcohol-induced liver damage, which misled some people to believe a lack of relationship between the amount of alcohol and the oc-currence of liver disease. However, it is true that a significant correlation exists between per capita consumption and the prevalence of cirrhosis. Alcoholic fatty liver is observed in most of chronic alcoholics even though the severity is not uniform. Abstinence remains the cornerstone of therapy for alcoholic liver disease (ALD). There is also consensus for the use of corticosteroids and pentoxifylline in severe alcoholic hepatitis maintaining good nutritional status to treat comorbidities in all forms of ALD, and liver transplantation in the end-stage ALD patients who can stop drinking for 6 months pre-transplantation period. Several clinical trials targeting tumor necrosis factor (TNF-α) and reducing oxidative stress have not been successful at this time. There is still a large field of alcohol research to explore in order to go farther in the area of pathophysiology. We need to understand a role of various cytokines and immune cells in the development of ALD to have more treatment tools to cope with ALD.
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Fig. 1.
Current view of pathogenesis of alcohol-induced liver inflammation and a role of the innate immune system. ADH, alcohol dehydrogenase; CYP2E1, cytochrome P4502E1; TLR, toll- like receptor; TNF, tumor necrosis factor; IL, inter-leukin. From Tilg H, Day CP. Management of strategies in alcoholic liver disease. Nat Clin Prac Gastroenterol Hepatol 2007;4:24- 34.
Table 1.
Ethanol Metabolizing Enzymes in Humans
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