Clinical Syndromes of Alcoholic Liver Disease

Abstract

Background and Aims: Alcoholic liver disease continues to be a major health problem with respect to both morbidity and mortality. To understand the clinical syndromes of alcoholic liver disease, this review highlights the papers on both clinical and basic research of alcoholic liver disease, especially on steatosis, alcoholic hepatitis and fibrosis. Methods: The various forms of alcoholic liver disease are described, and knowledge about the clinical and pathophysiological features of different stages of alcoholic liver disease are summarized. Results: Clinical studies combined with basic research have established a spectrum of alcoholic liver disease from steatosis to steatohepatitis, fibrosis, and cirrhosis. New insights into the pathogenesis of alcoholic liver disease include the key roles of the excess production of cytokines, reactive oxygen species, and the shortage of protective mediators, including adiponectin. Conclusion: These new insights will lead to new specific therapies for the treatment of alcoholic hepatitis and alcoholic liver fibrosis.

Inflammation and Hypoglycemia: The Lipid Connection

“…Tabassum, F et al (Tabassum, F et al, 2001) found that the levels of alkaline phosphate, ALT, protein and globulin were significantly increased in alcoholic males compared to control subjects. The AST/ALT ratio is significantly higher in ALD patients sometimes even higher than two (Adachi, M & DA Brenner, 2005).…”

“…Fatty liver, the most common syndrome of ALD, is characterized by the excessive accumulation of fat inside hepatocytes (Adachi, M & DA Brenner, 2005). Indeed the excessive fat accumulation in the hepatocytes is the most common and earliest response of the liver to chronic alcohol consumption (Song, Z et al, 2008).…”

“…They also reported that malnutrition can also occur in early alcoholic liver disease due to the suppression of TCA cycle coupled with decreased gluconeogenesis due to ethanol. Chronic ethanol consumption increases fatty acid synthesis by inducing the expression of lipogenic enzymes which are regulated by transcription factor SREBP (Adachi, M & DA Brenner, 2005). Chronic ethanol consumption significantly inhibits mitochondrial ALDH activity while the rate of ethanol oxidation to acetaldehyde is even enhanced, resulting in striking increase in tissue and plasma levels of acetaldehyde which results in metabolic disturbances, such as hyperlactacidemia, acidosis, hyperglycemia, hyperuricemia and fatty liver (Lieber, CS, 1997).…”

Alcohol and the digestive system – should it always be blamed?

“…Prawie u wszystkich osób uzależnionych rozwija się stłuszczenie wątroby, a u jednej trzeciej stwierdza się alkoholowe zapalenie wątroby, które u czę-ści osób przekształci się w marskość wątroby. Rozwój alkoholowej choroby wątroby jest uwarunkowany wieloczynnikowo, a śmiertelność z tego powodu w Europie i Stanach Zjednoczonych zawiera się w przedziale 5-6%, co daje 9. miejsce wśród najczęstszych przyczyn zgonów w tej populacji [24,77,96].…”

Cirrhosis and mortality risks of biopsy‐verified alcoholic pure steatosis and steatohepatitis: a nationwide registry‐based study

“…Alcoholic fatty liver disease comprises alcoholic pure steatosis characterised by macrovesicular steatosis and alcoholic steatohepatitis characterised by neutrophil infiltration, ballooning degeneration, Mallory bodies and variable fibrosis. 9,10 Both conditions are often asymptomatic and therefore probably under-recognised, and their prognostic impact is unclear, especially regarding the effect of hepatic inflammation. The distinction between the two diseases can only be made by liver biopsy, and the paucity of data based on liver biopsy diagnoses contributes to the prognostic uncertainty.…”