original study
Liv.52 DS Syrup in the Management of Alcoholic Hepatitis: An Open Label Study S Ganesh*, D Palaniyamma**, Suprabha Hegdeâ€
Abstract The course of alcoholic liver disease is prolonged and variable and hence evaluation of beneficial effects of therapy is essential. The aim of the present study was to evaluate clinical efficacy and safety of Liv.52 DS syrup in patients suffering from alcoholic hepatitis (AH). An open clinical study was carried out in 50 patients with AH; all patients were given orally Liv.52 DS syrup (2 tsp) t.i.d. for two months. Patients were evaluated at monthly intervals. The parameters used were: Jaundice, anorexia, nausea/vomiting, fever, pruritus and liver function tests. Routine hematology was done before and after treatment to assess the safety profile. Treatment with Liv.52 DS syrup significantly improved clinical signs and symptoms as well as biochemical parameters. There were no drop outs in the trial period, indicating excellent patient compliance. There were no adverse drug reactions. No difference in hematological parameters was observed after treatment, which clearly indicates safety of the drug. The overall impression by the investigator showed marked improvement in 50%, moderate improvement in 28%, slight improvement in 10% and no change in 12% cases. Overall impression by the patients showed marked improvement in 56%, moderate improvement in 22%, slight improvement in 6% and no change in 16%. So, it can be concluded that Liv.52 DS syrup is safe and effective in patients suffering from AH. Key words: Alcoholic hepatitis, Liv.52 DS syrup
A
lcoholic liver disease (ALD) encompasses a spectrum of injury, ranging from simple steatosis to frank cirrhosis. It is common for patients with ALD to share risk factors for simultaneous injury from other liver insults (e.g., coexisting nonalcoholic fatty liver disease, or chronic viral hepatitis).1 The term alcoholic hepatitis (AH) was first used by Beckett et al in 1961.2 Despite this longstanding observational relationship between alcohol consumption and liver disease, significant work has been required to determine quantity of alcohol to be consumed to cause liver disease, and which cohort of patients are at highest risk of developing significant liver injury.2,3 AH is a common and life-threatening cause of liver failure, especially when severe. It is usually subacute and has been developing for weeks to months before it becomes clinically apparent. Patients with AH usually have a history of drinking heavily for many years.4
*Consultant Gastroenterologist and Hepatologist, Chennai **Medical Advisor †Research Associate R&D Center, The Himalaya Drug Company, Makali, Bangalore Address for correspondence Dr D Palaniyamma Medical Advisor, R&D Center, The Himalaya Drug Company Makali, Bangalore - 562 123 E-mail: dr.palani@himalayahealthcare.com
Indian Journal of Clinical Practice, Vol. 21, No. 12, May 2011
Possible factors that affect development of liver injury include the dose, duration and type of alcohol consumption, drinking patterns, ethnicity and associated risk factors including obesity, iron overload, concomitant infection with viral hepatitis, and genetic factors. Geographic variability exists in the patterns of alcohol intake globally.5 The majority drink small or moderate amounts and do so without evidence of clinical disease.6-8 A subgroup, however, drinks excessively, develop physical tolerance and withdrawal, and are diagnosed with alcohol dependence.9 A second subset, alcohol abusers and problem drinkers, includes those who engage in harmful use of alcohol, defined by the development of negative social and health consequences of drinking (e.g., unemployment, loss of family, organ damage, accidental injury or death).10 ALD takes a prolonged and varied course; hence, evaluation of beneficial effects of therapy has been difficult. Multiple stages of the disease may be present simultaneously in a given individual.11,12 These are often grouped into three histological stages of ALD: Fatty liver or simple steatosis, AH and chronic hepatitis with hepatic fibrosis or cirrhosis. These latter stages may also be associated with several histologic changes (which have varying degrees of specificity for ALD), including the presence of Mallory’s hyaline, megamitochondria or perivenular and perisinusoidal fibrosis.11 Fatty 645