Abstinence remains the cornerstone of management of all forms of alcoholic liver disease. The numerous therapies investigated in an attempt to reverse the process of acute alcoholic hepatitis. These include nutritional supplements, corticosteroids, TNF modulation, propylthiouracil and antioxidants. 1.Nutritional Supplementation 2.Phosphatidylcholine 3.Corticosteroids 4.Pentoxifylline 5.Propylthiouracil 6.Insulin and Glucagon 7.Colchicine New Approaches to Therapy S-adenosylmethionine. S-adenosylmethionine is a source of cysteine for the production of GSH. In cirrhosis,SAMe synthase activity is reduced. S-adenosylmethionine supplementation of ethanol-fed rats restores the mitochondrial pool of GSH, suggesting a role for therapy with SAMe. Treatment with SAMe has been shown to lead to increased survival of patients with alcoholic cirrhosis. Polyenylphosphatidylcholine. Animal studies have shown that polyenylphosphatidylcholine (PPC) reverses a number of the adverse effects of ethanol on the liver. Polyenylphosphatidylcholine acts as an antioxidant, down regulates CYP2E1 activity, restores SAMe synthase activity, and reduces stellate cell activation and collagen synthesis. The most active component is dilinoleoylphosphatidylcholine (DLPC), but pure preparations are not readily available. The efficacy of this treatment is unclear. N-acetyl cysteine. Glutathione depletion is responsible for the toxicity of alcohol.Conficting results regarding the benefits have been documented. Cytokines. In view of the central role of TNF-á in alcoholic hepatitis, inhibition of TNF-á might be useful clinically.Monoclonal antibodies are now available for clinical use (Infliximab). But TNF-á inhibition may have adverse effects. Metadoxine Metadoxine is a new therapeutic option for the treatment of alcoholic liver disease. It has a unique chemical structure. Metadoxine not only accelerates the metabolism of alcohol but it also reduces the effects of alcohol intoxication and has hepatoprotective effects. It restores the redox balance and the glutathione levels in the hepatocytes.It is well tolerated and is documented to be of benefit in preventing the progression of ALD.