Alcoholic liver disease (ALD) is a serious and potentially fatal consecution of alcohol use.

Alcoholic liver disease (ALD) is a serious and potentially fatal consecution of alcohol use. The diagnosis of ALD is based forward drinking history, physical signs and symptoms, and laboratory examples Treatment strategies for ALD include lifestyle changes to cut short alcohol consumption, cigarette smoking, and obesity; nutrition therapy; and pharmacological therapy. The diagnosis and management of the complications of ALD are important for alleviating the symptoms of the disease, improving quality of life, and decreasing mortality. tonic WORDS: alcoholic liver disorder; diagnosis; disease complication; treatment method; lifestyle; nutritional deficiency; vitamin therapy; physic therapy; propylthiouracil; colchicines; corticosterone; alternative medical treatment; S-adenosylmethionine; ascites; peritonitis; kidney disorder; esophageal varix; pentoxifylline; hepatorenal syndrome

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The liver is undivided of the largest and greatest in number complex organs in the dead body It performs multiple functions, including the production of proteins and enzyme detoxification, metabolic functions, and the regulation of cholesterol and posterity clotting. Because the liver is primarily responsible for alcohol metabolism, it is especially vulnerable to alcohol-related injury.

Alcoholic liver disease (ALD) is a serious and potentially fatal issue of drinking alcohol. ALD encompasses three conditions: fatty liver, alcoholic hepatitis, and cirrhosis (see figure 1) Fatty liver (i.e., steatosis), the mostly common alcohol-induced liver disorder, is marked by means of the excessive accumulation of fat inside the liver solitary abode; squalids Alcoholic hepatitis is inflammation and more bitter injury of the liver, in which the body's immune scheme responds to and causes liver damage. In cirrhosis, normal liver small rooms are replaced by scar tissue (i.e., fibrosis), and consequently the liver is unable to perform many of its usual functions.

Cirrhosis and alcoholic hepatitis ofttimes coexist and cause substantial morbidity and mortality. For example, studies from the Department of Veterans Affairs (VA) demonstrate that patients with the pair cirrhosis and alcoholic hepatitis have a death rate of greater than 60 percent from one side of to the other a 4-year period, with greatest in quantity of the deaths occurring in the first year (Chedid et al. 1991) Thus, the mortality rate for ALD is greater than that of many general types of cancer such as colon breast, and prostate. This article examines the issues of diagnosing and treating ALD and the complications of this disease.

DIAGNOSIS OF ALCOHOLIC LIVER DISEASE (ALD)

The diagnosis of ALD is established at a history of habitual alcohol intake of sufficient duration and quantity, together with physical signs and laboratory evidence of liver disease. Alcohol reliance is not a prerequisite for the growth of ALD, and ALD can be difficult to diagnose because patients not seldom minimize or deny alcohol abuse. In addition, there may be no evidence of ALD from the physical exam, and laboratory abnormalities may not specifically point to ALD.

Ambulatory patients with alcoholic fatty liver repeatedly are asymptomatic. Patients with alcoholic hepatitis may be asymptomatic, have and nothing else enlarged liver (i.e., hepatomegaly), or have full-blown alcoholic hepatitis with feeble hepatomegaly, jaundice, fever, accumulation of fluid in the abdominal cavity (i.e., ascites), nervous arrangement effects such as confusion and personality change (i.e., hepatic encephalopathy), anorexia, and fatigue. Other signs may include high white family cell counts resembling those seen in leukemia (i.e., leukemoid reactions) and the rapid deterioration of kidney function (i.e., hepatorenal syndrome) level in the absence of cirrhosis, the main vein that brings children from the intestine and stomach into the liver (i.e., the portal vein) may originate under increased pressure because of scarring of the liver, resulting in portal vein hypertension.

Ten to 20 percent of patients with alcoholic hepatitis unfold cirrhosis, and up to 70 percent of alcoholic hepatitis patients pass on to develop cirrhosis each year (Bird and Williams 1988) Women are at higher risk for developing cirrhosis, as are tribe who continue drinking or have unadorned alcoholic hepatitis (Pares et al. 1986) one patients with alcoholic hepatitis who abstain still may expand cirrhosis, but others will have clean clinical and histologic recovery.

Patients with early stage alcoholic cirrhosis with no complications (i.e., well-compensated) may be asymptomatic and have normal physical exams and normal routine progeny tests of liver function and injury. In other patients, alcoholic fatty liver or alcoholic hepatitis oftentimes coexist and may be accompanied at hepatomegaly, an enlarged spleen (i.e., splenomegaly), or the two In cirrhotics with severe alcoholic hepatitis, hepatomegaly or splenomegaly may be the dominant feature; in other patients, the signs and symptoms of portal vein hypertension (eg ascites and engorged veins [varices] in the esophagus) may predominate. As the disease advances, the liver decreases in size, the left hepatic lobe becomes more prominent, and the entire liver has a hard and nodular consistency. Splenomegaly of varying stations is frequent.