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Therapy of Nonalcoholic Steatohepatitis (NASH) – Antioxidants and Cytoprotective Agents

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Therapy of Nonalcoholic Steatohepatitis (NASH) – Antioxidants and Cytoprotective Agents Tropical Gastroenterology 2011;Suppl:S33–37 Therapy of nonalcoholic steatohepatitis (NASH) – antioxidants and cytoprotective agents Ajay Duseja ABSTRACT Department of Hepatology Pathogenesis of nonalcoholic fatty liver disease (NAFLD) and its progressive form Postgraduate Institute of Medical nonalcoholic steatohepatitis (NASH) is not completely understood. Because of the role of Education & Research (PGIMER) oxidative stress in the pathogenesis, antioxidants and cytoprotective agents have been used Chandigarh – 160012, India. in the treatment of patients with NAFLD/NASH. Various antioxidants and cytoprotective Correspondence: agents used in these patients include Vitamin E, Vitamin C, Betaine, N- acetyl cysteine, silybin, Dr. Ajay Duseja lecithin, beta carotene, metadoxine, selenium and ursodeoxycholic acid (UDCA). Most of the Email: [email protected] data is available with vitamin E and UDCA, either in isolation or in combination with various agents. The available data on the use of various agents are either experimental or have small number of patients and randomized controlled trials with histological efficacy are sparse. More data is required before any conclusions are drawn regarding the use of anti oxidants and cytoprotective agents in patients NAFLD/NASH. KEYWORDS: Nonalcoholic fatty liver disease, NAFLD, oxidative stress, vitamin E, ursodeoxycholic acid, UDCA Introduction Nonalcoholic fatty liver disease (NAFLD) is a recently coined and human studies.6,7 In the absence of alcohol intake, patients entity and includes patients with simple steatosis and who either have metabolic syndrome or any of its components nonalcoholic steatohepatitis (NASH). Under the broad umbrella with insulin resistance, develop hepatic steatosis due to of NAFLD, NASH is an intermediate stage of liver damage and increased lipolysis and increased delivery of fatty acids from has the maximum propensity of progressing into cirrhosis and adipose tissue to liver.8 The increased load of fatty acids in hepatocellular carcinoma (HCC).1 Ludwig et al introduced the the hepatocytes increases the mitochondrial β-oxidation and term NASH in 1980 to describe histological changes increase in cytochrome P450 4A and cytochrome P4502E1 indistinguishable from alcoholic hepatitis in patients with no levels, leading to increase in reactive oxygen species. The or insignificant alcohol intake of less than 20g/day.2 Even though increased mitochondrial oxidative stress leads to the second the clinicopathological profile may be different from that hit from steatosis to steatohepatitis and fibrosis by three main reported from the west, NAFLD/NASH is common in India and mechanisms, namely lipid peroxidation, cytokine induction, is responsible for significant liver disease.3-5 and Fas ligand induction. Lipid peroxidation, apoptosis and recruitment of various cytokines lead on to hepatic Oxidative stress in the pathogenesis of NAFLD/ inflammation and or fibrosis in addition to steatosis and NASH progression from a stage of simple steatosis to NASH, setting the stage for future complications like cirrhosis and HCC. 9, 10 Pathogenesis of the NAFLD/NASH is not completely Data from India has also confirmed the role of oxidative understood. Oxidative stress has been shown to play an stress in the pathogenesis NAFLD/NASH. In one of the important role in the pathogenesis of NAFLD/NASH in animal studies from New Delhi, oxidative stress and antioxidant status © Tropical Gastroenterology 2011 S34 Tropical Gastroenterology 2011;Suppl:S33–37 was studied in 29 prospectively enrolled patients with NAFLD/ analysis on the use of various drugs reported extreme NASH, 25 diseased controls with chronic viral hepatitis, and heterogeneity of trials of antioxidants and cytoprotective 23 healthy controls.11 Apart from standard biochemical agents, which prevents any firm conclusions on the effect of parameters, lipid peroxidation products were measured as antioxidants in patients with NAFLD/NASH.13 thiobarbituric acid reactive substances (TBARS). As measures Various antioxidants and cytoprotective agents used in the of antioxidant capacity, superoxide dismutase, vitamin C levels treatment of NAFLD/NASH include vitamin E, vitamin C, and ferric reducing ability of plasma were measured. Products betaine, N- acetyl cysteine, silybon, lecithin, beta carotene, of lipid peroxidation were significantly increased among metadoxine, selenium and ursodeoxycholic acid (UDCA). patients with NAFLD/NASH in comparison to chronic viral hepatitis or healthy controls.11 In an attempt to explore the Vitamin E alone interrelationship of oxidative stress and insulin resistance in NAFLD/NASH subjects with and without type 2 diabetes, 200 Studies on usage of vitamin E are available either as pilot studies subjects were recruited from the Chennai Urban Rural or randomized controlled trials comparing results with placebo, Epidemiology Study group and tested for TBARS, protein UDCA or pioglitazone. Combinations of vitamin E with vitamin carbonyl (PCC) and glutathione levels.12 TBARS and PCC levels C, pioglitazone and UDCA have also been studied in patients were significantly elevated and reduced to oxidized glutathione with NAFLD/NASH. (GSH/GSSG) ratio was significantly decreased in diabetic One of the earlier pilot studies showed the efficacy of subjects with NAFLD/NASH compared to all other groups, vitamin E in children with NAFLD/NASH, used in the dosage suggesting that oxidative stress markers are significantly of oral vitamin E between 400 and 1200 IU per day.14 Serum associated with NAFLD/NASH even after adjusting for age, biochemistry values were monitored monthly during treatment gender, BMI and glycemic status.12 We recently evaluated the and treated patients were followed up for 4 to 10 months. Serum role of oxidative stress in 25 patients with NAFLD/NASH and alanine aminotransferase (ALT) decreased from 175 ± 106 IU/L compared results with age and BMI matched 25 chronic viral to 40 ± 26 IU/L (P <0.001), serum aspartate aminotransferase hepatitis patients and 25 healthy volunteers (HV) (AST) decreased from 104 ± 61 IU/L to 33 ± 11 IU/L (P <0.002), (unpublished). Patients with NAFLD/NASH had significantly and alkaline phosphatase decreased from 279 ± 42 IU/L to 202 higher malondialdehyde (MDA) in comparison to patients with ± 66 IU/L (P <0.003) during treatment but returned to abnormal chronic viral hepatitis and healthy volunteers. NAFLD/NASH in those electing to stop treatment and liver remained diffusely patients also had higher conjugated dienes levels in comparison echogenic during therapy.14 Another pilot study evaluated to HVs and reduced glutathione levels, higher glutathione the effects of a step 1 American Heart Association diet plus peroxidase levels and lower catalase activity in comparison to aerobic exercise with or without 800 IU of vitamin E daily on HVs, suggesting higher oxidative stress in patients with cytokine profiles and liver enzyme levels in 16 patients with NAFLD/NASH. biopsy-proven NASH.15 Lifestyle modifications (low-fat diet and exercise) were associated with improvement in liver Role of Antioxidants and cytoprotective agents enzymes, cholesterol, and plasma hyaluronic acid levels in patients with NASH, whereas the vitamin E supplementation Given the important role of oxidative stress in the pathogenesis used in this short-term pilot study provided no apparent added of NAFLD/NASH, various antioxidants and cytoprotective benefit.15 A small-randomized trial compared the efficacy of agents have been used in the treatment of NAFLD/NASH alpha-tocopherol (vitamin E) with ursodeoxycholic acid [3 patients with variable success. Treatment by antioxidants also patients received UDCA (250 mg TID) and six aTP (100 mg shares the similar drawbacks as observed by other modes of TID)] in patients with NAFLD/NASH. Ultrasound showed treatment in patients with NAFLD. Most of the studies have favorable changes in four patients (44%), two in each group. either experimental design or have small number of patients. ALT and AST average diminished by 40% and normalization Studies most often have pilot design rather than being the was obtained in five of six patients in treatment with aTP (83%) randomized controlled trials and the histological efficacy has and in one of the UDCA group (33%) with no statistically not been shown in majority of studies. Rather, a recent meta- significant difference between two groups.16 Therapy of nonalcoholic steatohepatitis S35 Vitamin E + Vitamin C in steatosis (mean grade, 2.2 vs. 1.4; p < 0.02). Compared with baseline, combination therapy produced a significant decrease The efficacy of combination of alpha-tocopherol (vitamin E) in steatosis (mean, 2.3 vs. 1; p < 0.002), cytologic ballooning and vitamin C in reducing histologic inflammation and fibrosis (1.3 vs. 0.2; p < 0.01), Mallory’s hyaline (0.7 vs. 0.2; p < 0.04), was evaluated in a prospective, double-blind, randomized, and pericellular fibrosis (1.2 vs. 0.6; p < 0.03). Although vitamin placebo-controlled trial.17 Forty five patients were randomized E had no significant effects, combination therapy produced a to receive either vitamins E and C (1000 IU and 1000 mg, significant increase in metabolic clearance of glucose and a respectively) or placebo daily for 6 months, based on their decrease in fasting free fatty acid and insulin.20 More data on initial histologic diagnosis of NASH. Additionally, all patients this combination is required to substantiate the results. were given standard weight-loss counseling
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