human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: UNLABELLED Vitamin E has been shown to protect against liver damage induced by oxidative stress in animal experiments . Based on our previous findings of diminished vitamin E levels in patients suffering from viral hepatitis , we treated 23 hepatitis C patients refractory to alpha-interferon therapy  with high doses of vitamin E ( 2 x 400 IU RRR-alpha-tocopherol/day ) for 12 weeks . STUDY DESIGN pro-spective r and omized double-blind crossover design . Clinical parameters including alanine aminotransferase ( ALT ) and aspartate aminotransferase ( AST ) were determined for monitoring the disease state , in parallel  vitamin E plasma levels and plasma lipids were determined . The plasma levels of the alpha-tocopherol  were increased about 2-fold in all 23 patients . In 11 of 23 patients the clinical parameters indicative of liver damage were improved during the phase of vitamin E treatment ( 48 % responders ) . ALT levels in responders were lowered by 46 % and AST levels were lowered by 35 % after 12 weeks of vitamin E treatment . Cessation of vitamin E treatment was followed by a rapid relapse of ALT and AST elevation , whereas retreatment led to a reproducible ALT decrease by 45 % and AST decrease of 37 % after a 6 months followup . Since vitamin E is non-toxic even at elevated doses ingested over extended periods , we suggest the treatment of patients refractory to alpha-interferon therapy  suffering from hepatitis C with vitamin E as a supportive therapy BACKGROUND / AIMS The effect of vitamin E administration on clinical and laboratory parameters of liver function and on markers of fibrogenesis was assessed in patients with mild to moderate alcoholic hepatitis in a double blind placebo controlled r and omized trial . METHODS Twenty-five patients received 1000  I.U.  of vitamin E per day , while 26 patients received placebo for 3 months . The patients were followed for 1 year after entry into the trial . RESULTS Vitamin E did not result in significant greater decreases in serum aminotransferases and serum bilirubin or in greater increases in serum albumin as compared with placebo .  Prothrombin time did not change , while serum creatinine remained in the normal range . Monocyte nuclear nuclear factor-kappa B binding activity decreased in patients who remained abstinent , regardless of whether they received vitamin E. As regards markers of hepatic fibrogenesis , vitamin E treatment decreased serum hyaluronic acid ( P<0.05 ) while serum aminoterminal peptide of type III procollagen did not change in either group . Four patients in the treatment group and five in the placebo group died during the 1-year study . CONCLUSIONS Vitamin E treatment improves serum hyaluronic acid but has no beneficial effects on tests of liver function in patients with mild to moderate alcoholic hepatitis BACKGROUND / AIMS Despite a proposed role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis , antioxidant approaches have not been investigated sufficiently in the therapy of nonalcoholic steatohepatitis . Our aim was to determine whether vitamin E plus C therapy is effective in normalization of liver enzymes compared to ursodeoxycholic acid treatment in patients with fatty liver disease . METHODS This was an open-labeled , prospect i ve , r and omized study enrolling patients with histologically proven fatty liver disease who had chronically elevated alanine aminotransferase , despite a three-month reducing diet . Patients consuming alcohol ( more than 20 g/day ) were excluded . The patients were r and omly prescribed either oral vitamin E ( 600 IU/day ) plus vitamin C ( 500 mg/day ) or ursodeoxycholic acid ( 10 mg/kg/day ) . Patients were r and omized as two groups to receive vitamin E plus vitamin C combination ( 28 patients , 10 F ) or ursodeoxycholic acid treatment ( 29 patients , 13 F ) . RESULTS There was no significant change in body mass index before and after the treatment in both groups . At the end of six months of therapy , serum aspartate aminotransferase and aminotransferase levels significantly decreased in both treatment options . Vitamin E and C combination was more efficacious on serum aminotransferase levels than ursodeoxycholic acid , but the difference was not significant . Alanine aminotransferase decreased to normal levels in 17 of 27 ( 63 % ) and in 16 of 29 patients ( 55 % ) , respectively , in the two groups . Gamma-glutamyl transpeptidase decreased in patients receiving ursodeoxycholic acid , but no change was obtained in the vitamin-treated patients . CONCLUSIONS Vitamin E plus C combination treatment is a safe , inexpensive and effective treatment option in patients with fatty liver disease , with results comparable to those obtained with ursodeoxycholic acid . Since more effective new therapeutic options are lacking , patients with fatty liver disease should be encouraged to take vitamin E and C supplements , which are safe and affordable Abstract Objective To examine the extent and nature of outcome reporting bias in a broad cohort of published r and omised trials . Design Retrospective review of publications and follow up survey of authors . Cohort All journal articles of r and omised trials indexed in PubMed whose primary publication appeared in December 2000 . Main outcome measures Prevalence of incompletely reported outcomes per trial ; reasons for not reporting outcomes ; association between completeness of reporting and statistical significance . Results 519 trials with 553 publications and 10 557 outcomes were identified . Survey responders ( response rate 69 % ) provided information on unreported outcomes but were often unreliable — for 32 % of those who denied the existence of such outcomes there was evidence to the contrary in their publications . On average , over 20 % of the outcomes measured in a parallel group trial were incompletely reported . Within a trial , such outcomes had a higher odds of being statistically non-significant compared with fully reported outcomes ( odds ratio 2.0 ( 95 % confidence interval 1.6 to 2.7 ) for efficacy outcomes ; 1.9 ( 1.1 to 3.5 ) for harm outcomes ) . The most commonly reported reasons for omitting efficacy outcomes included space constraints , lack of clinical importance , and lack of statistical significance . Conclusions Incomplete reporting of outcomes within published articles of r and omised trials is common and is associated with statistical non- significance . The medical literature therefore represents a selective and biased subset of study outcomes , and trial protocol s should be made publicly available BACKGROUND AND AIM Oxidative DNA damage occurs as an early event in hepatitis C virus ( HCV ) infection and is an indication of the potential for carcinogenesis . The aim of this study was to test a novel antioxidant/immunomodulator in patients with HCV-related cirrhosis . METHODS The study group consisted of 50 patients with HCV-related cirrhosis with transaminase values less than twofold increased ( alanine aminotransferase [ ALT ] < 80 IU/L ) . Patients underwent a st and ardized food-vitamin composition assessment and were assessed for dietary intake , nutritional status and iron level . Patients were r and omly allocated into two groups and then given either alpha-tocopherol 900 IU/day or 9 g/day of a fermented papaya preparation ( FPP , Immun-Age , Osato Research Institute , Gifu , Japan ) at bedtime for 6 months . Ten healthy subjects served as controls . Patients were checked monthly for : routine tests , redox status ( reduced glutathione , glutathione peroxidase , oxidized glutathione , malondialdehyde ) , plasma alpha-tocopherol , 8-hydroxy-deoxy-guanidine ( 8-OHdG ) level in circulating leukocyte DNA and serum levels of cytokines . RESULTS Patients with cirrhosis showed a significant imbalance of redox status ( low antioxidants/high oxidative stress markers ) ( P < 0.005 vs controls ) . Neither treatment regimen affected transaminases as a whole . However , vitamin E supplementation almost normalized ALT only in the limited vitamin-E-deficient subgroup . A significant improvement of redox status was obtained by both regimens . However , only FPP significantly decreased 8-OHdG and the improvement of cytokine balance with FPP was significantly better than with vitamin E treatment ( P < 0.05 ) . CONCLUSIONS Although the present data seem to suggest a potential supportive role of antioxidants/immunomodulators as FPP in HCV patients , more studies are needed to substantiate their effect on the natural history of the disease Alcoholics admitted for detoxification were entered into a double blind placebo controlled trial of oral supplementation with an antioxidant cocktail ( vitamin E , beta carotene , vitamin C and selenium ) in order to determine the effect of this supplementation on the rate of resolution of a serum marker of free radical activity and abnormal serum biochemistry . The molar proportion of linoleic acid that was diene conjugated ( a marker of free radical activity ) , was increased in the alcoholics 2.9 % + /- 1.2 ( mean + /- S.D. ) compared to normal controls 1.3 % + /- 0.6 ( P < 0.0001 ) but fell at a similar rate during the first week of hospitalisation in supplemented and placebo-treated patients with a mean fall of 53.7 % ( + /- 16.4 S.D. ) in the placebo group and 56.0 % ( + /- 23.7 ) ( P = 0.32 , NS ) in the antioxidant supplemented group . Similarly , there was no difference in the rate of fall between serum aspartate transaminase ( AST ) concentration in the two groups : the placebo group falling by a mean of 68.9 % ( + /- 35.2 ) and the antioxidant supplemented group falling by 70.1 % ( + /- 10.0 ) ( P = 0.41 , NS ) over the first 7 days of hospitalization . Alcoholics had low serum concentrations of vitamin E compared with controls ( 15.6 mg/l + /- 6.2 S.D. ) which rose more in the supplemented group over the period of a week ( 7.7 mg/l + /- 4.4 to 21.6 mg/l + /- 5.1 ) ( a mean rise of 180.5 % ) compared with the placebo group ( 8.6 mg/l + /- 6.8 to 9.6 mg/l + /- 5.7)--a mean rise of 11.6 % ( P = 0.006 ) . ( ABSTRACT TRUNCATED AT 250 WORDS Thirty abstinent male alcoholics with sexual dysfunction  were r and omized to treatment with 3 mg RE ( 10,000 IU ) vitamin A or placebo daily for 4 mo . Age , drinking history , period of abstinence before enrollment , and base-line laboratory indices were comparable in both groups at entry . Of the 15 subjects given placebo  , 13 had a partial or full recovery of sexual functioning . By contrast , of those given vitamin A , 10 had a partial response . There were no complete responders . Six subjects ( 1 placebo , 5 vitamin A ) who developed liver abnormalities during treatment underwent liver biopsies ; five had fibrosis or cirrhosis . A significant decrease in luteinizing hormone was noted in the group given vitamin A compared with the placebo-treated group . Thus vitamin A therapy did not improve  sexual functioning in male alcoholics and may have been associated with toxicity Patients with chronic hepatitis C virus ( HCV ) infection often develop liver cirrhosis and hepatocellular carcinoma ( HCC ) . The purpose of this study was to test the chemopreventive effect of alpha-tocopherol on hepatocarcinogenesis in patients with liver cirrhosis and a history of HCV infection . Eighty-three patients with liver cirrhosis and with positive history of HCV infection were divided at r and om into two groups . Forty-four patients were treated with alpha-tocopherol ( Vit E group ) while the other 39 were followed as controls . The clinical background ( gender , age , and laboratory data ) was similar in the two groups . Serum levels of alpha-tocopherol , albumin , alanine aminotransferase ( ALT ) , and total cholesterol and platelet count were measured serially over a period of five years . The mean serum concentration of alpha-tocopherol was low in both groups at entry and was significantly higher in the Vit E group than in the control group one month after treatment . Platelet count , serum albumin , ALT , and total cholesterol were not different between the two groups during the five-year period . Cumulative tumor-free survival and cumulative survival rate tended to be higher in the Vit E group than in controls , albeit statistically insignificant . The serum level of alpha-tocopherol was low in patients with liver cirrhosis and positive for HCV . Although the administration of alpha-tocopherol normalized the level one month later , it could neither improve liver function , suppress hepatocarcinogenesis , nor improve cumulative survival . Patients treated with alpha-tocopherol tended to live longer without development of HCC but the difference was not statistically significant Background Clinical evidence continues to exp and and is increasingly difficult to overview . We aim ed at conceptualizing a visual assessment tool , i.e. , a matrix for overviewing studies and their data in order to assess the clinical evidence at a glance . Methods A four-step 
    Output:
    
agent
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: UNLABELLED Vitamin E has been shown to protect against liver damage induced by oxidative stress in animal experiments . Based on our previous findings of diminished vitamin E levels in patients suffering from viral hepatitis , we treated 23 hepatitis C patients refractory to alpha-interferon therapy  with high doses of vitamin E ( 2 x 400 IU RRR-alpha-tocopherol/day ) for 12 weeks . STUDY DESIGN pro-spective r and omized double-blind crossover design . Clinical parameters including alanine aminotransferase ( ALT ) and aspartate aminotransferase ( AST ) were determined for monitoring the disease state , in parallel  vitamin E plasma levels and plasma lipids were determined . The plasma levels of the alpha-tocopherol  were increased about 2-fold in all 23 patients . In 11 of 23 patients the clinical parameters indicative of liver damage were improved during the phase of vitamin E treatment ( 48 % responders ) . ALT levels in responders were lowered by 46 % and AST levels were lowered by 35 % after 12 weeks of vitamin E treatment . Cessation of vitamin E treatment was followed by a rapid relapse of ALT and AST elevation , whereas retreatment led to a reproducible ALT decrease by 45 % and AST decrease of 37 % after a 6 months followup . Since vitamin E is non-toxic even at elevated doses ingested over extended periods , we suggest the treatment of patients refractory to alpha-interferon therapy  suffering from hepatitis C with vitamin E as a supportive therapy BACKGROUND / AIMS The effect of vitamin E administration on clinical and laboratory parameters of liver function and on markers of fibrogenesis was assessed in patients with mild to moderate alcoholic hepatitis in a double blind placebo controlled r and omized trial . METHODS Twenty-five patients received 1000  I.U.  of vitamin E per day , while 26 patients received placebo for 3 months . The patients were followed for 1 year after entry into the trial . RESULTS Vitamin E did not result in significant greater decreases in serum aminotransferases and serum bilirubin or in greater increases in serum albumin as compared with placebo .  Prothrombin time did not change , while serum creatinine remained in the normal range . Monocyte nuclear nuclear factor-kappa B binding activity decreased in patients who remained abstinent , regardless of whether they received vitamin E. As regards markers of hepatic fibrogenesis , vitamin E treatment decreased serum hyaluronic acid ( P<0.05 ) while serum aminoterminal peptide of type III procollagen did not change in either group . Four patients in the treatment group and five in the placebo group died during the 1-year study . CONCLUSIONS Vitamin E treatment improves serum hyaluronic acid but has no beneficial effects on tests of liver function in patients with mild to moderate alcoholic hepatitis BACKGROUND / AIMS Despite a proposed role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis , antioxidant approaches have not been investigated sufficiently in the therapy of nonalcoholic steatohepatitis . Our aim was to determine whether vitamin E plus C therapy is effective in normalization of liver enzymes compared to ursodeoxycholic acid treatment in patients with fatty liver disease . METHODS This was an open-labeled , prospect i ve , r and omized study enrolling patients with histologically proven fatty liver disease who had chronically elevated alanine aminotransferase , despite a three-month reducing diet . Patients consuming alcohol ( more than 20 g/day ) were excluded . The patients were r and omly prescribed either oral vitamin E ( 600 IU/day ) plus vitamin C ( 500 mg/day ) or ursodeoxycholic acid ( 10 mg/kg/day ) . Patients were r and omized as two groups to receive vitamin E plus vitamin C combination ( 28 patients , 10 F ) or ursodeoxycholic acid treatment ( 29 patients , 13 F ) . RESULTS There was no significant change in body mass index before and after the treatment in both groups . At the end of six months of therapy , serum aspartate aminotransferase and aminotransferase levels significantly decreased in both treatment options . Vitamin E and C combination was more efficacious on serum aminotransferase levels than ursodeoxycholic acid , but the difference was not significant . Alanine aminotransferase decreased to normal levels in 17 of 27 ( 63 % ) and in 16 of 29 patients ( 55 % ) , respectively , in the two groups . Gamma-glutamyl transpeptidase decreased in patients receiving ursodeoxycholic acid , but no change was obtained in the vitamin-treated patients . CONCLUSIONS Vitamin E plus C combination treatment is a safe , inexpensive and effective treatment option in patients with fatty liver disease , with results comparable to those obtained with ursodeoxycholic acid . Since more effective new therapeutic options are lacking , patients with fatty liver disease should be encouraged to take vitamin E and C supplements , which are safe and affordable Abstract Objective To examine the extent and nature of outcome reporting bias in a broad cohort of published r and omised trials . Design Retrospective review of publications and follow up survey of authors . Cohort All journal articles of r and omised trials indexed in PubMed whose primary publication appeared in December 2000 . Main outcome measures Prevalence of incompletely reported outcomes per trial ; reasons for not reporting outcomes ; association between completeness of reporting and statistical significance . Results 519 trials with 553 publications and 10 557 outcomes were identified . Survey responders ( response rate 69 % ) provided information on unreported outcomes but were often unreliable — for 32 % of those who denied the existence of such outcomes there was evidence to the contrary in their publications . On average , over 20 % of the outcomes measured in a parallel group trial were incompletely reported . Within a trial , such outcomes had a higher odds of being statistically non-significant compared with fully reported outcomes ( odds ratio 2.0 ( 95 % confidence interval 1.6 to 2.7 ) for efficacy outcomes ; 1.9 ( 1.1 to 3.5 ) for harm outcomes ) . The most commonly reported reasons for omitting efficacy outcomes included space constraints , lack of clinical importance , and lack of statistical significance . Conclusions Incomplete reporting of outcomes within published articles of r and omised trials is common and is associated with statistical non- significance . The medical literature therefore represents a selective and biased subset of study outcomes , and trial protocol s should be made publicly available BACKGROUND AND AIM Oxidative DNA damage occurs as an early event in hepatitis C virus ( HCV ) infection and is an indication of the potential for carcinogenesis . The aim of this study was to test a novel antioxidant/immunomodulator in patients with HCV-related cirrhosis . METHODS The study group consisted of 50 patients with HCV-related cirrhosis with transaminase values less than twofold increased ( alanine aminotransferase [ ALT ] < 80 IU/L ) . Patients underwent a st and ardized food-vitamin composition assessment and were assessed for dietary intake , nutritional status and iron level . Patients were r and omly allocated into two groups and then given either alpha-tocopherol 900 IU/day or 9 g/day of a fermented papaya preparation ( FPP , Immun-Age , Osato Research Institute , Gifu , Japan ) at bedtime for 6 months . Ten healthy subjects served as controls . Patients were checked monthly for : routine tests , redox status ( reduced glutathione , glutathione peroxidase , oxidized glutathione , malondialdehyde ) , plasma alpha-tocopherol , 8-hydroxy-deoxy-guanidine ( 8-OHdG ) level in circulating leukocyte DNA and serum levels of cytokines . RESULTS Patients with cirrhosis showed a significant imbalance of redox status ( low antioxidants/high oxidative stress markers ) ( P < 0.005 vs controls ) . Neither treatment regimen affected transaminases as a whole . However , vitamin E supplementation almost normalized ALT only in the limited vitamin-E-deficient subgroup . A significant improvement of redox status was obtained by both regimens . However , only FPP significantly decreased 8-OHdG and the improvement of cytokine balance with FPP was significantly better than with vitamin E treatment ( P < 0.05 ) . CONCLUSIONS Although the present data seem to suggest a potential supportive role of antioxidants/immunomodulators as FPP in HCV patients , more studies are needed to substantiate their effect on the natural history of the disease Alcoholics admitted for detoxification were entered into a double blind placebo controlled trial of oral supplementation with an antioxidant cocktail ( vitamin E , beta carotene , vitamin C and selenium ) in order to determine the effect of this supplementation on the rate of resolution of a serum marker of free radical activity and abnormal serum biochemistry . The molar proportion of linoleic acid that was diene conjugated ( a marker of free radical activity ) , was increased in the alcoholics 2.9 % + /- 1.2 ( mean + /- S.D. ) compared to normal controls 1.3 % + /- 0.6 ( P < 0.0001 ) but fell at a similar rate during the first week of hospitalisation in supplemented and placebo-treated patients with a mean fall of 53.7 % ( + /- 16.4 S.D. ) in the placebo group and 56.0 % ( + /- 23.7 ) ( P = 0.32 , NS ) in the antioxidant supplemented group . Similarly , there was no difference in the rate of fall between serum aspartate transaminase ( AST ) concentration in the two groups : the placebo group falling by a mean of 68.9 % ( + /- 35.2 ) and the antioxidant supplemented group falling by 70.1 % ( + /- 10.0 ) ( P = 0.41 , NS ) over the first 7 days of hospitalization . Alcoholics had low serum concentrations of vitamin E compared with controls ( 15.6 mg/l + /- 6.2 S.D. ) which rose more in the supplemented group over the period of a week ( 7.7 mg/l + /- 4.4 to 21.6 mg/l + /- 5.1 ) ( a mean rise of 180.5 % ) compared with the placebo group ( 8.6 mg/l + /- 6.8 to 9.6 mg/l + /- 5.7)--a mean rise of 11.6 % ( P = 0.006 ) . ( ABSTRACT TRUNCATED AT 250 WORDS Thirty abstinent male alcoholics with sexual dysfunction  were r and omized to treatment with 3 mg RE ( 10,000 IU ) vitamin A or placebo daily for 4 mo . Age , drinking history , period of abstinence before enrollment , and base-line laboratory indices were comparable in both groups at entry . Of the 15 subjects given placebo  , 13 had a partial or full recovery of sexual functioning . By contrast , of those given vitamin A , 10 had a partial response . There were no complete responders . Six subjects ( 1 placebo , 5 vitamin A ) who developed liver abnormalities during treatment underwent liver biopsies ; five had fibrosis or cirrhosis . A significant decrease in luteinizing hormone was noted in the group given vitamin A compared with the placebo-treated group . Thus vitamin A therapy did not improve  sexual functioning in male alcoholics and may have been associated with toxicity Patients with chronic hepatitis C virus ( HCV ) infection often develop liver cirrhosis and hepatocellular carcinoma ( HCC ) . The purpose of this study was to test the chemopreventive effect of alpha-tocopherol on hepatocarcinogenesis in patients with liver cirrhosis and a history of HCV infection . Eighty-three patients with liver cirrhosis and with positive history of HCV infection were divided at r and om into two groups . Forty-four patients were treated with alpha-tocopherol ( Vit E group ) while the other 39 were followed as controls . The clinical background ( gender , age , and laboratory data ) was similar in the two groups . Serum levels of alpha-tocopherol , albumin , alanine aminotransferase ( ALT ) , and total cholesterol and platelet count were measured serially over a period of five years . The mean serum concentration of alpha-tocopherol was low in both groups at entry and was significantly higher in the Vit E group than in the control group one month after treatment . Platelet count , serum albumin , ALT , and total cholesterol were not different between the two groups during the five-year period . Cumulative tumor-free survival and cumulative survival rate tended to be higher in the Vit E group than in controls , albeit statistically insignificant . The serum level of alpha-tocopherol was low in patients with liver cirrhosis and positive for HCV . Although the administration of alpha-tocopherol normalized the level one month later , it could neither improve liver function , suppress hepatocarcinogenesis , nor improve cumulative survival . Patients treated with alpha-tocopherol tended to live longer without development of HCC but the difference was not statistically significant Background Clinical evidence continues to exp and and is increasingly difficult to overview . We aim ed at conceptualizing a visual assessment tool , i.e. , a matrix for overviewing studies and their data in order to assess the clinical evidence at a glance . Methods A four-step 
    Output:
    