Liver alcohol damage

Another common liver disease, alcoholic liver damage produced by moderate to heavy alcoholic intake, is also reflected by an elevation of the serum GOT and GPT activities. The serim glutamyl transferase activity is reported to be a sensitive index of alcoholic intake and can serve to monitor persons on alcoholic withdrawal programs (60). The LD-5 isoenzyme arises mainly from liver tissue, but has a short half-life (61), which is about 1/5 and 1/2 of the half life of the transaminases, GPT and GOT respectively. Some authors consider that a normal LD-5 isoenzyme activity in a jaundiced patient is sufficient evidence to exclude primary liver disease and that obstruction is probably responsible for the jaundice (62). In hemolytic jaundice the LDH-1 and 2 isoenzymes are elevated. 

Hepatocellular damage manifests as elevated serum aminotransferases [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)]. The degree of transaminase elevation does not correlate with the remaining functional metabolic capacity of the liver. An AST level two-fold higher than ALT is indicative of alcoholic liver damage. 

In adults, excessive alcohol consumption reduces liver reserves of vitamin A, both as a result of alcoholic liver damage and also by induction of cytochrome P450 enzymes that catalyze the oxidation of retinol to retinoic acid (as also occurs with chronic use of barbiturates). However, chronic consumption of alcohol can also potentiate the toxicity of retinol (Section 2.5.1). 

Studies in twins have suggested that genetic factors may be important in the development of alcoholic liver damage. While there are differences in the various enzymes involved with alcohol metabolism, some of the differences are not consistent or large enough to account for differences in susceptibility. Genetic differences in protective mechanisms and genes involved with inflammation have also been linked to susceptibility to alcohol-induced liver disease. 

Liver diseases severe acute (necrotic) hepatitis, chronic hepatitis, chronic alcoholic liver damage, liver cirrhosis, cardiac liver, liver abscess, liver tumours and liver metastases, toxic liver damage, etc. A severe and, above all, constant reduction in ChE activity (e. g. < 500 U/1) is usually suggestive of an unfavourable prognosis and the foreseeable moment of liver death . 

The diagnosis of acute viral hepatitis C is based on the following parameters, whereby especially alcoholic liver damage must first be ruled out (353, 377) ... 

Addiction to alcohol 520 5 Clinical features of alcoholic liver damage 529... 

Fig. 28.11 Chronic moderate periportal and portal inflammatory reaction with septal fibrosis and centrilobular steatosis in chronic alcoholic liver damage (DD mild chronic viral hepatitis C ) (van Gieson)...

Morgan, K., French, S. W., and Morgan, T. R. (2002) Production of a cytochrome P450 2E1 transgenic mouse and initial evaluation of alcoholic liver damage. Hepatology 36, 122-134. 

Precautions Some studies have indicated that small quantities (four ounces per day) have been found to be beneficial in lowering cholesterol. Large quantities over extended periods can lead to alcoholism, liver damage, numbness of the extremities, brain damage, gastritis, and heart muscle damage. Pregnant women should avoid alcohol entirely because of the disastrous effects on the unborn. 

Allopurinol has been shown to attenuate lipid peroxidation in ethanol-fed rats (Kato etal., 1990). However, this was not correlated with any possible effect on histological damage and, as discussed previously, the significance of lipid peroxidation is unclear. Despite the evidence suggesting that oxidative stress and increased oxidative metabolism may play a role in the pathogenesis of human alcoholic liver disease, it remains to be shown that treatment with specific antioxidants will modify this process. 

Ward. R. J. and Peters, T.J. (1992). The antioxidant status of patients with either alcohol-induced liver damage of myopathy. Alcohol and Alcoholism 27, 359-365. 

Outline the progression of liver damage from excessive alcohol intake. 

Cirrhosis is the result of long-term insult to the liver, so damage is typically not evident clinically until the fourth decade of life. Chronic liver disease and cirrhosis combined were the 12th leading cause of death in the United States in 2002. In patients between the ages of 25 and 64, damage from excessive alcohol use accounted for over one-half of the deaths.2 Alcoholic liver disease and viral hepatitis are the most common causes of cirrhosis in the United States and worldwide. 

Lifestyle modifications can limit disease complications and slow further liver damage. Avoidance of additional hepatic insult is critical for successful cirrhosis treatment. The only proven treatment for alcoholic liver disease is the immediate cessation of alcohol consumption. Patients who have cirrhosis from etiologies other than alcoholic liver disease should also abstain from alcohol consumption to prevent further liver damage. 

Acetaminophen is usually well tolerated, but potentially fatal hepatotoxicity with overdose is well documented. It should be used with caution in patients with liver disease and those who chronically abuse alcohol. Chronic alcohol users (three or more drinks daily) should be warned about an increased risk of liver damage or GI bleeding with acetaminophen. Other individuals do not appear to be at increased risk for GI bleeding. Renal toxicity occurs less frequently than with NSAIDs. 

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