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Alcoholic liver disease: Causes and cure

Published on Jul 28, 2013

By EMN

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Naga Hospital Authority Kohima holds Continuous Medical Examination

Our Correspondent Kohima, July 28

Naga Hospital Authority Kohima (NHAK) in collaboration with Abbott conducted Continuous Medical Education (CME) on the topic ‘Alcoholic Liver Disease (ALD)’ at Hotel Japfu, Kohima last night. In his presentation, Dr Avoto Richa said ALD is the most prevalent cause of advanced liver disease while also stating that it has a known aetiology but a complex and incompletely known pathogenesis. He said sustained excessive alcohol intake favours progression of other liver diseases, such as virus-related chronic hepatitis, also increasing the risk of hepatocellular carcinoma, because of these understanding ALD epidemiology, etiopathogenesis and treatment options become imperative. He said sustained excessive alcohol consumption is a brain-centred addictive behavioural disorder that crosses all boundaries of gender, race, age, economic strata and in many patients, might lead to ALD. Around 60-100% of heavy drinkers may suffer from fatty liver, among which 20-30% may progress to steatohepatitis of which around 10-15% of patients may suffer from cirrhosis. Dr Richa said ALD comprises an overlapping spectrum of pathological processes -- Steatosis (alcoholic fatty liver), Alcoholic hepatitis and cirrhosis. Steatosis can occur in about 60-100% of chronic and binge drinkers and it may be completely reversible. It is usually asymptomatic. Patients may have an enlarged, firm, mildly tender liver. Liver enzymes may be mildly elevated. Alcoholic hepatitis is often characterised by hepatocyte injury, spotty necrosis, polymorphonuclear infiltrate and fibrosis. It can be mild, moderate or severe Mild: Often asymptomatic, with elevation of liver enzymes to two to three times the upper limit of normal. Moderate: Presents with typical symptoms of hepatitis (fatigue, anorexia, weight loss, vomiting, jaundice, right upper quadrant pain). Severe: Presents with fever, jaundice, ascites, hyperdynamic circulation and encephalopathy. Those with marked encephalopathy have a mortality rate of up to 50 per cent. Indicators of a poor prognosis include: low serum albumin, elevated international normalized ratio (INR), elevated serum bilirubin and signs of encephalopathy. Cirrhosis: Involves permanent destruction of the liver architecture and, thus, function; liver enzymes may be raised. Tests of liver function are abnormal (i.e., low albumin, raised INR). Patients may have hepatomegaly or a small, shrunken right lobe and hypertrophied left lobe (palpable in epigastrium). Stigmata of chronic liver disease may be present (gynecomastia, testicular atrophy, spider nevi, palmar erythema, splenomegaly, ascites). Complications include encephalopathy, ascites, bleeding varices, portal hypertension and subacute bacterial peritonitis. Dr Richa said even though advanced ALD was previously considered to develop only in individuals who consume excessive amounts of alcohol (less than 120 gram of daily intake), it is now known that much smaller quantities of alcohol can induce the disease. “The minimum daily alcohol intake in 15-20 years to induce cirrhosis is estimated to be 40 gram (3-4 drinks) for men and 20 gram (2-3 drinks) for women,” he said, adding only 15-30 percent of heavy drinkers develop advanced ALD such as alcoholic hepatitis and liver cirrhosis. On diagnosis and evaluation, he said patients with ALD are often identified through routine screening tests. Modest elevations in laboratory parameters such as alanine aminotransferase (ALT), aspartate aminotransferase (AST) and GGT are observed. On drug therapy for ADL, he said the foremost is abstinence from alcohol but other therapies are Corticosteroids, Pentoxifylline and Enteral nutritional support. Dr Richa elaborated that Corticosteroid therapy can be used to treat severe alcoholic hepatitis as this class of drugs has broad anti-inflammatory properties. Corticosteroids, prednisolone and methylprednisolone have been shown to provide survival benefit and have, therefore, been recommended as treatment for this condition. He also said there are many reasons which limit the use of steroids in ALD patients. Patients with active bacterial infections should not be given steroids, he said adding that Corticosteroids are also known to increase viral replication; therefore, these drugs should not be prescribed to patients with active viral infections including hepatitis C infection. Pentoxifylline, Dr Richa said, can be offered as alternative treatment to patients with contraindications to corticosteroid therapy. Pentoxifylline has a better safety profile compared with corticosteroids and does not ca cause the same immunosuppressive side-effects.