:::::::::: ALCOHOLIC LIVER DISEASE(ALD):::::::::::::
Alcoholic liver disease consists of three major lesions:-
(1) fatty liver,
(2) alcoholic hepatitis, and
(2) alcoholic hepatitis, and
(3) cirrhosis.
-Possible factors that affect the development of liver injury include the dose, duration, and type of
alcohol consumption; drinking patterns; sex; ethnicity; and associated risk factors including obesity, iron overload, concomitant infection with viral hepatitis, and genetic factors.
-Women have been found to be twice as sensitive to alcohol-mediated hepatotoxicity and may develop more severe alcoholic liver disease at lower doses and with shorter duration of
alcohol consumption than men.
-The presence and extent of protein calorie malnutrition play an important role in determining the outcome of patients with ALD.
-High fat intake, Obesity and excess body weight have been associated with an increased risk of ALD.
- In addition to environmental factors, genetic factors predispose to both alcoholism and ALD.
- The combination of hepatitis C virus and alcohol predisposes to more advanced liver injury than alcohol alone,with disease at a younger age, more severe histological features, and adecreased survival.
-Fatty liver is the initial and most common histologic response to hepatotoxic stimuli, Continuing alcohol ingestion results in fat accumulation throughout the entire hepatic lobule.
-The hallmark of alcoholic hepatitis is hepatocyte injury characterized by ballooning degeneration, spotty necrosis, polymorphonuclear infiltrate, and fibrosis in the perivenular and perisinusoidal
space of Disse.
Alcoholic hepatitis is thought to be a precursor to the development of cirrhosis. However, like fatty liver, it is potentially reversible with cessation of drinking. Cirrhosis is present in up to 50% of patients with biopsy-proven alcoholic hepatitis and its regression is uncertain, even with cessation of drinking.
CLINICAL FEATURES:-
-Physical examination in acute alcoholic hepatitis can reveal fever, malnutrition, jaundice, fatigue, anorexia, malaise, hepatic encephalopathy (confusion,stupor,coma) , asterixis tremor, parotid gland enlargement, hepatomegaly, right upper quadrant pain, ascites, spider nevi, and leukocytosis,
- physical findings are more commonly observed in ALD (parotid enlargement, Dupuytren’s contracture)
- Can present with portal hypertension esophageal varices and ascites as disease progresses; hepatorenal syndrome, hepato- pulmonary syndrome is a frequent cause of death in severe acute alcoholic liver disease.
Lab:-
In alcoholic hepatitis and in contrast to other causes of fatty liver, the AST and ALT are usually elevated two- to sevenfold. They are rarely >400 IU, and the AST/ ALT ratio >1.
In alcoholic hepatitis and in contrast to other causes of fatty liver, the AST and ALT are usually elevated two- to sevenfold. They are rarely >400 IU, and the AST/ ALT ratio >1.
Hyperbilirubinemia is common and is accompanied by modest increases in the alkaline phosphatase,γ-glutamyl transpeptidase (GGTP) level.
Hypoalbuminemia and coagulopathy are common in advanced liver injury.
Ultrasonography is useful in detecting fatty infiltration of the liver and determining liver size.
Mallory bodies are a classic finding on biopsy but are not specific for alcoholic liver disease.
Screening for Alcohol Abuse:- CAGE Questionnaire
TREATMENT:-
Therapy of ALD is based on the stage of the disease.
Complications of cirrhosis, including evidence of hepatic failure (encephalopathy) as well as portal hypertension (ascites, variceal bleeding), are treated as in patients with non- ALD, with additional attention given to other organ dysfunction associated specifically with alcohol. Complete abstinence from alcohol is the cornerstone in the treatment of alcoholic liver disease. Continued alcohol ingestion results in an increased risk of portal hypertensive bleeding especially in patients who have previously bled.
Therapy of ALD is based on the stage of the disease.
Complications of cirrhosis, including evidence of hepatic failure (encephalopathy) as well as portal hypertension (ascites, variceal bleeding), are treated as in patients with non- ALD, with additional attention given to other organ dysfunction associated specifically with alcohol. Complete abstinence from alcohol is the cornerstone in the treatment of alcoholic liver disease. Continued alcohol ingestion results in an increased risk of portal hypertensive bleeding especially in patients who have previously bled.
-Naltrexone or acamprosate may be considered in combination with counseling to decrease the likelihood of relapse in patients with alcohol abuse/ dependence in those who achieve abstinence.
- Nutrition Therapy, The presence of significant protein calorie malnutrition is a common finding in alcoholics, as are deficiencies in a number of vitamins and trace minerals, including vitamin A, vitamin D, thiamine,folate, pyridoxine, and zinc.
-Because of data suggesting that the pathogenic mechanisms in alcoholic hepatitis involve cytokine release and the perpetuation of injury by immunologic processes,Glucocorticoids(Prednisolone 32 mg p.o. daily for 4 weeks, then taper for 4 weeks) have been extensively evaluated in the treatment of alcoholic hepatitis. Or TNF inhibitor (Pentoxifylline 400 mg p.o. TID for 4 weeks)
Last option of treatment is the Liver transplantation.
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