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Alcoholic Liver Disease Postgrad Med J: First Published As 10.1136/Pmj.76.895.280 on 1 May 2000 280 Postgrad Med J 2000;76:280–286 Alcoholic liver disease Postgrad Med J: first published as 10.1136/pmj.76.895.280 on 1 May 2000. Downloaded from Kevin Walsh, Graeme Alexander Abstract Alcohol is a major cause of liver cirrhosis Box 1: Safe limits for alcohol intake in the Western world and accounts for the x Males = 21 units per week (1 unit = majority of cases of liver cirrhosis seen in glass or half pint) district general hospitals in the UK. The x Females = 14 units per week three most widely recognised forms of alcoholic liver disease are alcoholic fatty liver (steatosis), acute alcoholic hepatitis, and alcoholic cirrhosis. The exact patho- genesis of alcoholic liver injury is still not Box 2: Factors increasing susceptibility clear but immune mediated and free to ALD radical hepatic injury are thought to be x Lifetime intake of alcohol important. There is increasing interest in genetic factors predisposing to hepatic x Female sex injury in susceptible individuals. Diagno- x Genetic factors sis is based on accurate history, raised x Drinking without food serum markers such as ã-glutamyl- Binge drinking transferase, mean corpuscular volume, x and IgA and liver histology when x High concentration alcoholic drinks—for obtainable. Abstinence is the most example, spirits important aspect of treatment. Newer x Drinking multiple diVerent alcoholic drugs such as acamprosate and naltrex- beverages one are used to reduce alcohol craving. Vitamin supplements and nutrition are vital while corticosteroids have a role in acute alcoholic hepatitis where there Danish subjects found that ALD was increased is no evidence of gastrointestinal above a threshold of 7–13 drinks per week in haemorrhage or sepsis. Liver transplan- females and 14–27 drinks in males.2 There was tation has excellent results in abstinent a steep dose dependent increase in ALD risk patients with end stage liver disease but above this threshold with increasing alcohol there are concerns about recidivism after intake. Women had greater susceptibility to http://pmj.bmj.com/ transplant. ALD at any given level of intake. Kwo have (Postgrad Med J 2000;76:280–286) et al recently shown that men and women have 3 Keywords: cirrhosis; liver disease; alcohol equivalent alcohol elimination rates. The gen- der diVerences in susceptibility to liver injury Epidemiology may be due to pharmacokinetic reasons such as Alcoholic liver disease (ALD) is one of the diVerences in ethanol absorption or alterna- major medical complications of alcohol abuse. tively diVerences in the response of the liver to Alcohol is the major cause of liver cirrhosis in alcohol induced injury such as that caused by on September 25, 2021 by guest. Protected copyright. the Western world, with schistosomial infec- oxidative by-products of ethanol metabolism in tion being the major cause of portal hyper- the liver. tension in the developing countries. Alcohol The pattern of drinking was also important as accounts for 80% of all liver cirrhosis cases ALD is increased in those who drink without seen in district general hospitals in the UK. accompanying food and also in those who drink Alcoholic cirrhosis is increasingly seen in multiple diVerent alcoholic beverages.1 It is well countries such as Japan and India which known that food delays gastric emptying and traditionally had a low prevalence of the intestinal absorption of alcohol and thus intake disease. of food before drinking will decrease the rise of The safe limits for alcohol intake are contro- blood alcohol concentrations. The absorption of versial. Guidelines recommended by the Royal alcohol is lower when consuming low concentra- Department of College of Physicians advise a weekly limit of tion beverages such as beer compared with high Medicine, University 21 units (210 g) of alcohol in men and 14 units concentration spirits. of Cambridge, Box in women. The 1994 OYce of Population A recent study in 12 687 subjects showed 157, Addenbrooke’s Censuses and Surveys’ General Household that coVee consumption protected males from Hospital, Cambridge Survey found that 27% of men and 13% of the induction of ã-glutamyltransferase by alco- CB2 2QQ, UK women in the UK were exceeding these limits. hol and may possibly protect against liver cell K Walsh 4 G Alexander A recent prospective Italian study in 6534 sub- damage caused by alcohol. jects showed the risk threshold for developing Correspondence to: ALD is 30 g ethanol/day and this risk increases Spectrum of liver disease Dr Alexander with increasing daily intake.1 Women had The three most widely recognised forms Submitted 3 June 1999 greater susceptibility to ALD in the range of of ALD are alcoholic fatty liver (steatosis), Accepted 6 September 1999 3–8 drinks daily. A previous study in 13 285 acute alcoholic hepatitis, and alcoholic Alcoholic liver disease 281 cirrhosis. At least 80% of heavy drinkers Postgrad Med J: first published as 10.1136/pmj.76.895.280 on 1 May 2000. Downloaded from develop steatosis, 10%–35% develop alcoholic Box 3: Major classification of ALD hepatitis, and approximately 10% will develop x Alcoholic fatty liver (steatosis) 5 cirrhosis. x Acute alcoholic hepatitis x Alcoholic cirrhosis ALCOHOLIC FATTY LIVER (STEATOSIS) Steatosis is invariable if consumption exceeds 80 g of alcohol per day. A large proportion of the cytoplasm of aVected hepatocytes is Box 4: Histological features of ALD occupied by a single large triglyceride occlu- sion but liver function is often normal. It is x Steatosis (fatty liver) reversible with abstinence but may progress to x Mallory’s hyaline bodies cirrhosis if excess alcohol intake persists.6 x Cholestasis Deaths due directly to fatty liver are rare and x Liver fibrosis are usually caused by acute liver failure or fat embolism. x Micronodular cirrhosis ACUTE ALCOHOLIC HEPATITIS system, is increased by enzyme induction and In alcoholic hepatitis, hepatocyte ballooning is also responsible for production of acetalde- occurs due to increased intracellular water hyde. accumulation. Mallory’s hyaline bodies are Acetaldehyde is increased in zone 3 (also the perinuclear eosinophilic inclusion bodies and maximal site of action of alcohol dehydro- are probably condensed and disorganised genase). This is also the site of the terminal fragments of the cytoskeletal framework of the veins making this zone the most hypoxic hepatocyte. They are not specific for alcoholic and therefore highly susceptible to hypoxic hepatitis as they are also seen in Wilson’s injury. Oxygen derived free radicals may disease and primary biliary cirrhosis. It has cause direct hepatocyte injury by lipid peroxi- been estimated that 15–20 years of excessive dation. drinking is necessary to develop alcoholic Acetaldehyde binds covalently to proteins hepatitis. There is prominent cholestasis. forming adducts that are antigenic. Humans It is more severe in females and also in and animals exposed to long term alcohol Northern Europeans and is unrelated to excess develop persistent circulating antibod- pattern of drinking or type of alcohol drink. ies that recognise acetaldehyde protein High mortality rates are seen (30%–60%). adducts.7 Acetaldehyde modified self proteins Patients often deteriorate after hospital may serve as neoantigens, initiating harmful admission despite abstinence. This latter phe- humoral and/or cellular immune responses, nomenon may be due to reperfusion liver which leads to tissue injury.8 The expression of injury. the proinflammatory cytokines, tumour necro- http://pmj.bmj.com/ sis factor-alpha (TNF-á), transforming ALCOHOLIC CIRRHOSIS growth factor-beta (TGF-â), interleukin (IL)- Cirrhosis is the most severe form of alcoholic 1â, and IL-6 are increased in alcoholic liver liver injury and is usually of the micronodular injury while the anti-inflammatory cytokine, type. The risk is increased in continuous IL-4 is decreased.9 These cytokines stimulate drinkers compared to binge drinkers. Collagen stellate cells which produce collagen leading to deposition can be pericellular, in the space of liver fibrosis. A study by Neuman et al suggests Disse, and around central veins (central hyaline that it is TNF-á that is the main candidate on September 25, 2021 by guest. Protected copyright. sclerosis). The latter is often associated with accounting for toxicity as addition of an rapid progression to cirrhosis and commoner equivalent amount of IL-6 seen in ALD did and more severe in women. Collagen bridges not produce injury in a normal rat liver eventually develop between central veins and whereas equivalent amounts of TNF-á did portal tracts isolating groups of hepatocytes produce injury.10 Removal of toxic reactive which form the regeneration nodules. Survival oxygen species is achieved via three major for patients is 60%–70% at one year and 35%– antioxidant enzymes: catalase, superoxide dis- 50% at five years. mutase, and glutathione peroxidase. The gen- eration of high concentrations of free radicals Pathogenesis during the metabolism of alcohol may exceed There are a number of hypotheses regarding the capacity of the antioxidant defence mecha- the pathogenesis of alcoholic liver injury. nisms and contribute to the development of Ethanol metabolism usually takes place in alcohol induced liver injury. Polavarapu et al the mitochondria. Ethanol is oxidised to have shown that in rats with alcohol induced acetaldehyde by alcohol dehydrogenase, which injury, these antioxidant enzymes are reduced in turn is oxidised to acetate by acetaldehyde and levels are inversely correlated with severity dehydrogenase. These oxidation reactions are of liver injury.11 Alcohol reduces alkaline associated with the formation of NADH and protease activity in rats resulting in failure to NAD and alter the redox state of the cell. This clear hepatocytes of oxidatively damaged has harmful eVects on lipid and carbohydrate proteins.12 This results in oxidative liver metabolism—for example, steatosis. In ha- damage. bitual drinkers, a microsomal mixed function Soluble fatty acid synthase (FAS) and oxidase, the microsomal ethanol oxidising FAS ligand are increased in patients with 282 Walsh,Alexander acute alcoholic hepatitis and alcoholic Postgrad Med J: first published as 10.1136/pmj.76.895.280 on 1 May 2000.
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