Background: Fatty liver, hepatitis, cirrhosis and hepatic encephalopathy are clinically distinct progressively deteriorating conditions in alcoholic liver disease (ALD). Factors responsible for the progression of ALD are poorly understood. Therefore we compared various biochemical parameters in these conditions to correlate them with disease progression. Methods: Thirty patients of alcoholic liver disease reporting to our hospital were recruited in the study. Analysis included hematological parameters, liver function tests, ammonia, amino acids and measurement of oxidative stress by measuring malanodialdehyde. Based on ultrasonography, patients were classified as fatty liver, alcoholic hepatitis and cirrhosis. Results: Hematological parameters showed significant change in the levels with the progression of the disease. Levels of aspartate transaminase, alanine amino transferase, alkaline phosphatase, biluribin were elevated in all the ALD conditions but were more pronounced in hepatitis and cirrhosis than fatty liver. Oxidative stress was increased with progression of disease. Also significant differences in the levels of ammonia and amino acids were obtained. Conclusions: Alcohol induced oxidative stress is the primary cause of the liver injury. The progressive deterioration of various parameters indicates the extent of liver injury. Therefore, antioxidant therapy may be best course that may halt or slow down the progression of ALD. These observations together, provide a rationale for the possible clinical application of antioxidants in the therapy for ALD. Thus, prevention and therapy opposing the development of steatosis and its progression to more severe injury can be attempted by a multifactorial approach.
Keywords: Alcoholic liver disease, biochemical parameters, liver function tests, oxidative stress, Biochemical Indices, Hematological parameters, aspartate transaminase, alanine amino transferase, alkaline phosphatase, biluribin, hepatitis, fatty liver, Alcohol induced oxidative, liver injury, antioxidant therapy, morbidity, mortality, striking metabolic imbalance, lipids, proteins, inactivating enzymes, cirrhosis, hepatic encephalopathy, Transasia, Fasting venous blood, hepatocytes, ethanol consumption, Anaemia, hypoproteinaemia, non-cirrhotic
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