Cholesterol-lowering effect of ursodeoxycholic acid in patients with primary biliary cirrhosis. Chenodeoxycholic acid and ursodeoxycholic acid effects in endogenous hypertriglyceridemias. A controlled double-blind trial. Effect of ursodeoxycholic acid on serum lipids of patients with primary biliary cirrhosis. High-dose ursodeoxycholic acid in primary sclerosing cholangitis: a 5-year multicenter, randomized, controlled study. Ursodeoxycholic acid in the treatment of cholestasis of pregnancy: a randomized, double-blind study controlled with placebo. Effects of additional administration of colchicine in ursodeoxycholic acid-treated patients with primary biliary cirrhosis: a prospective randomized study. Ursodeoxycholic acid for symptomatic primary biliary cirrhosis. Preliminary analysis of a double-blind multicenter trial. Italian Multicenter Group for the Study of UDCA in PBC. A randomized double-blind study of the short-time treatment of obese patients with nonalcoholic fatty liver disease with ursodeoxycholic acid. Efficacy and safety of ursodeoxycholic acid versus cholestyramine in intrahepatic cholestasis of pregnancy. Ursodeoxycholic acid for treatment of primary sclerosing cholangitis: a placebo-controlled trial. Failure of ursodeoxycholic acid to prevent acute cellular rejection after liver transplantation. Ursodeoxycholic acid treatment lowers the serum level of antibodies against pyruvate dehydrogenase and influences their inhibitory capacity for the enzyme complex in patients with primary biliary cirrhosis Ursodeoxycholic acid as adjunctive therapy for problematic type 1 autoimmune hepatitis: a randomized placebo-controlled treatment trial. The effect of diet on bile acid kinetics and biliary lipid secretion in gallstone patients treated with ursodeoxycholic acid. DISSOLUTION OF CHOLESTEROL GALLSTONES BY URSODEOXYCHOLIC ACID Comparative efficacy and side effects of ursodeoxycholic and chenodeoxycholic acids in dissolving gallstones. A double-blind controlled study.
We have previously shown in a 2-yr controlled trial that hypercholesterolemia , frequent in primary biliary cirrhosis , is lowered by ursodeoxycholic acid ( 13 to 15 mg daily ) . To further investigate this effect , we analyzed the influence of long-term ursodeoxycholic acid administration on serum lipids , lipoproteins and bile acids . The study involved a subgroup of 33 noncirrhotic patients ( 17 received ursodeoxycholic acid and 16 received a placebo ) analyzed at inclusion and after 2 yr . The total serum cholesterol concentration was markedly reduced in the  ursodeoxycholic acid-treated  patients in comparison with the controls ( mean + /- S.E.M. = 7.49 + /- 0.42 mmol/L and 7.07 + /- 0.23 mmol/L at entry and 4.44 + /- 0.40 mmol/L and 6.89 + /- 0.27 mmol/L at 2 yr in the ursodeoxycholic acid and placebo groups , respectively ; p < 0.02 ) . Quantitatively , this decrease was mainly caused by a fall in low-density-lipoprotein cholesterol , but very low density-lipoprotein cholesterol levels also fell significantly . High-density-lipoprotein cholesterol levels remained stable in both groups , but the high-density-lipoprotein2/high-density-lipoprotein3 cholesterol ratio fell significantly during ursodeoxycholic acid treatment . No significant change occurred in total triglyceride or total phospholipid levels . In the treated group , the proportion of ursodeoxycholic acid  increased ( up to 60 % of total circulating bile acids ) , whereas that of cholic and chenodeoxycholic acids  fell significantly . In conclusion , the cholesterol-lowering effect of ursodeoxycholic acid could be related to an improvement of cholestasis , modifications in cholesterol metabolism or both . Changes in endogenous bile acid composition induced by ursodeoxycholic acid might be the common denominator of these two mechanisms A double-blind controlled trial was carried out to compare the effects of chenodeoxycholic acid ( CDCA ) , ursodeoxycholic acid ( UDCA ) , and placebo on cholesterol and triglyceride levels in patients with endogenous hypertriglyceridemias . The dose of both bile acids was four 150-mg capsules day . Total serum cholesterol levels did not show appreciable changes with any of the treatments . HDL cholesterol was significantly increased after CDCA but not after UDCA or placebo . CDCA feeding was associated with a significant decrease in serum triglyceride levels , whereas the other treatments failed to show an effect . It is concluded that UDCA does not affect serum lipid levels , whereas CDCA lowers serum triglycerides and may be useful in the treatment of endogenous hypertriglyceridemia OBJECTIVE To study the effects of ursodeoxycholic acid ( UDCA ) on lipid levels in patients with primary biliary cirrhosis ( PBC ) . DESIGN A r and omized , placebo-controlled prospect i ve trial of UDCA was conducted in 177 well-characterized patients with PBC . MATERIAL AND METHODS The two treatment groups ( placebo and UDCA ) were matched at entry with respect to age , sex , histologic stage of PBC , biochemical values , and serum lipid levels . Serum cholesterol , high-density lipoprotein cholesterol , and triglyceride levels were measured at entry , 1 year , and 2 years . RESULTS The decrease in total cholesterol level at 1 and 2 years in the UDCA-treated group was significant in comparison with that in the placebo group . Serum high-density lipoprotein cholesterol and triglyceride levels , however , were unchanged . No severe side effects from UDCA were noted . The changes in serum cholesterol levels at 2 years were directly and strongly correlated with changes in serum bilirubin concentrations ( r = 0.70 ; P < 0.001 ) and inversely correlated with initial serum cholesterol levels ( r = -0.86 ; P < 0.00001 ) . CONCLUSION The cholesterol-lowering effect of UDCA could be related to amelioration of the underlying liver disease or to a direct effect of the drug on the metabolism of cholesterol in patients with hypercholesterolemia BACKGROUND & AIMS There is no medical treatment of proven benefit for primary sclerosing cholangitis . This study aim ed at study ing the effect of a higher dose of ursodeoxycholic acid than previously used on survival , symptoms , biochemistry , and quality of life in this disease . METHODS A r and omized placebo-controlled study was performed in tertiary and secondary gastroenterology units . A total of 219 patients were r and omized to 17 to 23 mg/kg body weight per day of ursodeoxycholic acid ( n = 110 ) or placebo ( n = 109 ) for 5 years . Follow-up data are available from 97 patients r and omized to ursodeoxycholic acid  and for 101 r and omized to placebo .  Quality of life was assessed by using the Medical Outcomes Study 36-item Short-Form Health Survey . RESULTS The combined end point " death or liver transplantation " occurred in 7 of 97 ( 7.2 % ) patients in the ursodeoxycholic acid group vs 11 of 101 ( 10.9 % ) patients in the placebo group ( P = .368 ; 95 % confidence interval , -12.2 % to 4.7 % ) . The occurrence of liver transplantation as a single end point showed a similar positive trend for ursodeoxycholic acid treatment ( 5/97 [ 5.2 % ] vs 8/101 [ 7.9 % ] ; 95 % confidence interval , -10.4 % to 4.6 % ) . Three ursodeoxycholic acid and 4 placebo patients died from cholangiocarcinoma , and 1 placebo patient died from liver failure . Alkaline phosphatase and alanine aminotransferase tended to decrease during the first 6 months . There were no differences between the 2 groups in symptoms or quality of life . Analyses of serum ursodeoxycholic acid concentration gave no evidence that noncompliance may have influenced the results . CONCLUSIONS This study found no statistically significant beneficial effect of a higher dose of ursodeoxycholic acid than previously used on survival or prevention of cholangiocarcinoma in primary sclerosing cholangitis BACKGROUND / AIMS Intense pruritus and the risk of stillbirths and premature deliveries justify the search for an effective pharmacologic treatment of intrahepatic cholestasis of pregnancy . This study was design ed to test the efficacy of ursodeoxycholic acid in maternal pruritus , the biochemical abnormalities and the outcome of pregnancy , in patients with intrahepatic cholestasis of pregnancy of early onset . METHODS Pregnant patients hospitalized in a secondary case-referral center with intense pruritus and abnormal serum levels of bile salts and aminotransferases , detected before week 33 of pregnancy , were r and omly assigned to receive ursodeoxycholic acid , 1 g per day orally , or an identical placebo , until delivery , in a double-blind study . A 3-week trial period was chosen to compare drug and placebo effects . The follow-up was extended for 3 months after delivery . RESULTS Twenty-four patients entered the trial ; eight had deliveries before 2 weeks of treatment and one dropped out . The study was then completed in 15 patients : eight received ursodeoxycholic acid and seven placebo . No adverse effects were detected in the mothers or in their babies . After 3 weeks of treatment , patients receiving ursodeoxycholic acid ( mean daily dose 16 mg/kg body weight ) had a significant improvement in pruritus ( p<0.02 ) , in serum bilirubin ( 0.36+/-0.19 mg/dl ( mean+/-SD ) versus 0.95+/-0.48 in patients receiving placebo , p<0.01 ) , in aspartate aminotransferase ( 52+/-42 IU/l vs 98+/-44 , p<0.05 ) and in alanine aminotransferase ( 54+/-50 IU/l vs 229+/-154 , p<0.01 ) ; serum total bile salts also tended to be lower in patients receiving ursodeoxycholic acid ( 26.3+/-33.7 micromol/l vs 55.0+/-44.8 , p N.S. ) . Deliveries occurred at or near term in all mothers who received ursodeoxycholic acid ( mean week of pregnancy : 38 ) , while they occurred before week 36 of pregnancy in five patients who received placebo , including one stillbirth . All babies born alive had birth weights adequate for gestational age and they were thriving normally 3 months after delivery . CONCLUSIONS Ursodeoxycholic acid is effective and safe in patients with intrahepatic cholestasis of pregnancy of early onset , attenuating pruritus and correcting some biochemical abnormalities in the mothers . Relevant aspects of fetal outcome were also improved in patients receiving ursodeoxycholic acid compared to placebo BACKGROUND / AIMS Although ursodeoxycholic acid is effective for the treatment of primary biliary cirrhosis , some patients do not respond to this treatment . The objective of the present study was to investigate the effects of additional administration of colchicine in  ursodeoxycholic acid-treated patients with primary biliary cirrhosis . METHODS Twenty-two patients with primary biliary cirrhosis treated with ursodeoxycholic acid ( 600 mg/day ) for 30 months were r and omly assigned to two groups : group 1 , colchicine ( 1 mg/day ) and ursodeoxycholic acid ( n = 10 ) ; group 2 , ursodeoxycholic acid alone ( n = 12 ) . RESULTS In group 1 , there were significant decreases in mean serum levels of alkaline phosphatase , total bilirubin , gamma-glutamyltranspeptidase , alanine aminotransferase , aspartate aminotransferase , and IgM , and these changes were more remarkable in those who responded poorly to ursodeoxycholic acid . In contrast , there were no significant changes in those values in group 2 . CONCLUSIONS Additional administration of colchicine to ursodeoxycholic acid may be beneficial for patients with primary biliary cirrhosis , especially those who respond poorly to ursodeoxycholic acid .  It is necessary , however , to further confirm the efficacy of colchicine by examining histological changes and following the patients for longer periods The administration of ursodeoxycholic acid , a hydrophilic bile acid not hepatotoxic to humans , has been suggested for treatment of primary biliary cirrhosis to improve cholestasis and reduce hepatocellular damage . Efficacy of treatment has been studied mainly in patients with asymptomatic or early-stage disease . In January 1988 , to establish the efficacy and safety of ursodeoxycholic acid in a population with more severe disease , we started a multicenter , double-blind , placebo-controlled trial in patients with symptomatic disease , that is , with pruritus or serum bilirubin exceeding 2 mg/dl . Forty-four patients were assigned to ursodeoxycholic acid , 500 mg daily ( corresponding to about 8.7 mg/kg body weight in these patients ) , and 44 to a placebo . As planned at the beginning of the study , a preliminary analysis was performed when all patients had been followed for at least 6 months ( 33 patients up to 12 months ) . Pruritus , self-evaluated by the patients , and cholestyramine consumption , as recorded in a diary , decreased significantly ( p < 0.01 ) in both groups . In patients who initially had abnormal levels , serum bilirubin decreased significantly ( p < 0.05 ) in the ursodeoxycholic acid group compared to placebo . After 6 months the following were also significantly better in the ursodeoxycholic acid than in the placebo group : a composite weighted biochemical index taking into account the changes in serum bilirubin , alkaline phosphatase , gamma-GT and AST ( p < 0.001 ) ; serum prealbumin ( p < 0.05 ) ; IgG ( p < 0.01 ) and IgM ( p < 0.01 ) levels . ( ABSTRACT TRUNCATED AT 250 WORDS In order to determine the effect of ursodeoxycholic acid on nonalcoholic fatty liver disease , 30 patients with body mass indices higher than 25 , serum levels of alanine aminotransferase ( ALT ) , aspartate aminotransferase ( AST ) or gamma-glutamyltransferase ( gamma-GT ) at least more than 1.5 times the upper limit of normality , and hepatic steatosis demonstrated by ultrasonography were r and omized into two groups of 15 patients to receive placebo or 10 mg kg-1 day-1 ursodeoxycholic acid for three months . Abdominal computed tomography was performed to quantify hepatic fat content , which was significantly correlated with histological grading of steatosis ( r s = -0.83 , P < 0.01 ) . Patient body mass index remained stable for both groups throughout the study , but a significant reduction in mean ( + /- SEM ) serum levels of ALT , AST and gamma-GT was observed only in the treated group ( ALT = 81.2 + /- 9.7 , 44.8 + /- 7.7 , 48.1 + /- 7.7 and 52.2 + /- 6.3 IU/l at the beginning and after the first , second and third months , respectively , N = 14 , P < 0.05 ) . For the placebo group ALT values were 66.4 + /- 9.8 , 54.5 + /- 7 , 60 + /- 7.6 and 43.7 5 IU/l , respectively . No alterations in hepatic lipid content were observed in these patients by computed tomography examination ( 50.2 + /- 4.2 Hounsfield units ( HU ) at the beginning versus 51.1 + /- 4.1 HU at the third month ) . These results show that ursodeoxycholic acid is able to reduce serum levels of hepatic enzymes in patients with nonalcoholic fatty liver disease , but this effect is not related to modifications in liver fat content BACKGROUND & AIMS Treatment of intrahepatic cholestasis of pregnancy with ursodeoxycholic acid appears promising , but data are limited so far . The aim of this r and omized study was to evaluate the efficacy and safety of ursodeoxycholic acid in comparison with cholestyramine . METHODS Eighty-four symptomatic patients with intrahepatic cholestasis of pregnancy were r and omized to receive either ursodeoxycholic acid , 8 - 10 mg/kg body weight daily ( n = 42 ) , or cholestyramine , 8 g daily ( n = 42 ) , for 14 days . The primary end point was a reduction of pruritus by more than 50 % after 14 days of treatment as evaluated by a pruritus score . Secondary end points were outcome of pregnancy , reduction of serum aminotransferase activities and serum bile acid levels , and drug safety . Intention-to-treat analysis was applied . RESULTS Pruritus was more effectively reduced by ursodeoxycholic acid than cholestyramine ( 66.6 % vs 19.0 % , respectively ; P < .005 ) . Babies were delivered significantly closer to term by patients treated with ursodeoxycholic acid than those treated with cholestyramine ( 38.7 + /- 1.7 vs 37.4 + /- 1.5 weeks , respectively , P < .05 ) . Serum alanine and aspartate aminotransferase activities were markedly reduced by 78.5 % and 73.8 % , respectively , after ursodeoxycholic acid , but by only 21.4 % , each , after cholestyramine therapy ( P < .01 vs ursodeoxycholic acid ) . Endogenous serum bile acid levels decreased by 59.5 % and 19.0 % , respectively ( P < .02 ) . Ursodeoxycholic acid , but not cholestyramine was free of adverse effects . CONCLUSIONS Ursodeoxycholic acid is safe and more effective than cholestyramine in intrahepatic cholestasis of pregnancy The efficacy and safety of ursodeoxycholic acid for the treatment of primary sclerosing cholangitis were evaluated in a prospect i ve , r and omized , double-blind , placebo-controlled trial . Fourteen patients with primary sclerosing cholangitis documented by cholestatic serum enzyme pattern , liver histological appearance and endoscopic retro grade cholangiography were included in the trial . Six patients received ursodeoxycholic acid ( 13 to 15 mg/kg body wt/day ) , and eight patients received placebo . Two patients had to be withdrawn from the study , one because of UDCA-related diarrhea and the other because of worsening of the disease during placebo treatment . Patients in the ursodeoxycholic acid group improved significantly during 1 yr of treatment with respect to serum levels of bilirubin ( median = -50 % ) , alkaline phosphatase ( median = -67 % ) , gamma-glutamyltransferase ( median = -53 % ) , AST ( median = -54 % ) and ALT ( median = -36 % ) compared with the placebo group , but not with respect to serum levels of hydrophobic bile acids . During ursodeoxycholic acid treatment , histopathological features also improved significantly , as evaluated by multiparametric score . Expression of human leukocyte antigen class I molecules appeared to be markedly reduced on liver cells after ursodeoxycholic acid treatment . We conclude that ursodeoxycholic acid is beneficial in reducing disease activity in patients with primary sclerosing cholangitis BACKGROUND / AIMS Acute rejection is still a major problem after liver transplantation .  Ursodeoxycholic acid has beneficial effects in cholestasis by reducing the expression of major histocompatibility complex antigens . METHODS We have performed a double-blind r and omised study comparing ursodeoxycholic acid with placebo for the prevention of acute cellular rejection after liver transplantation . Twenty-six patients received ursodeoxycholic acid 600 mg per day and 24 patients received placebo  for 2 months . RESULTS Neither rejection incidence nor rejection severity was significantly different in the two groups ( p > 0.90 ) . CONCLUSIONS We conclude that adjuvant ursodeoxycholic acid administration does not prevent rejection after liver transplantation A two-year r and omized , double-blind , placebo-controlled clinical trial used paired serum sample s from 122 patients with primary biliary cirrhosis to compare the effect of ursodeoxycholic acid and colchicine on their immune parameters . IgG antibodies to pyruvate dehydrogenase , the major autoantigen in primary biliary cirrhosis , were determined by enzyme-linked immunosorbent assay and immunoblot ; enzyme inhibition assay against pyruvate dehydrogenase was used to test the changes of the functional reactivity of the serum autoantibodies . Treatment with ursodeoxycholic acid decreased both the level of IgG antibodies to pyruvate dehydrogenase ( P<0.01 ) and the inhibitory titer of the sera for pyruvate dehydrogenase ( P<0.01 ) . Treatment with colchicine or placebo showed no statistically significant changes in either the antibody levels or the inhibitory titers .  Ursodeoxycholic acid thus alters the immune parameters of patients with primary biliary cirrhosis . The mechanism of these changes needs further investigation To evaluate the efficacy of ursodeoxycholic acid as adjunctive therapy in type 1 autoimmune hepatitis , 37 patients who had experienced treatment failure , repeated relapse , or incomplete response were r and omized to ursodeoxycholic acid ( 13 - 15 mg/kg daily ) or placebo for 6 months in addition to their usual corticosteroid schedule . Serum aspartate transaminase ( 70 % vs. 31 % , P = .04 ) and alkaline phosphatase ( 47 % vs. 7 % , P = .02 ) levels improved more commonly in the 21 patients r and omized to ursodeoxycholic acid .  Mean serum levels , however , were similar before and after the treatment period . The frequency of dose reduction or corticosteroid withdrawal was comparable in both groups ( 29 % versus 31 % , P > .9 ) , and clinical improvement ( 48 % vs. 44 % , P > .9 ) or its absence ( 52 % vs. 56 % , P > .9 ) occurred as commonly in patients receiving ursodeoxycholic acid or placebo . The modified histological activity score ( 3.5 + /- 0.8 vs. 3 . 5 + /- 0.9 ) and the modified fibrosis score ( 2.4 + /- 0.4 vs. 2.4 + /- 0.4 ) were similar before and after treatment with ursodeoxycholic acid and no different than after placebo therapy . We conclude that ursodeoxycholic acid can improve certain laboratory tests in problematic patients with type 1 autoimmune hepatitis when administered adjunctively for 6 months . Short-term therapy , however , does not facilitate reduction in the dose of corticosteroids or its withdrawal , affect clinical outcome , or reduce histological activity Effects of specific dietary alterations in patients with radiolucent gallstones treated with ursodeoxycholic acid ( UDCA , 750 mg at bedtime ) were investigated . Patients were allocated r and omly to one of four diets : st and ard ( 500 mg cholesterol/day ) , low-cholesterol ( 250 mg/day ) , added-bran ( 30 g/day ) , or substituted medium-chain triglycerides ( MCT ) oil ( 20 % of fat ) . Dietary intake and good compliance were verified by computerized analysis of dietary diaries . Bile-acid kinetics ( 26 patients ) or secretion of biliary lipids ( 23 other patients ) were determined at enrollment and at 6 and 9 mo , respectively , during treatment . Although MCT further decreased the UDCA-induced decrease in the synthesis of chenodeoxycholic acid , it did not lessen desaturation of bile . Otherwise , compared to the st and ard diet , no experimental diet significantly altered the UDCA-induced increase of the pools of total bile acids and UDCA or the UDCA-induced decrease in synthesis of bile acids and in biliary secretion or saturation of cholesterol . If these dietary manipulations facilitate dissolution of gallstones by UDCA , they do so by other mechanisms 44 patients with radiolucent gallstones in gallbladders visible on cholecystography were r and omly alloted to three treatment groups : ursodeoxycholic acid ( 600 mg/day ) , ursodeoxycholic acid ( 150 mg/day ) , a placebo . At the end of six months ' treatment , cholecystograms of all the patients were interpreted by radiologists who were not aware of the treatment . Dissolution of gallstones occurred in 8 ( 26 % ) of the 31 patients treated with ursodeoxycholic acid , but not in the placebo group . Ursodeoxycholic acid had no hepatotoxicity , as assessed by st and ard liver-function tests . These results indicate that ursodeoxycholic acid , the 7beta epimer of chenodeoxycholic acid , is effective in the dissolution of cholesterol gallstones In a double-blind controlled study of ursodeoxycholic acid ( 400 and 800 mg/day ) and chenodeoxycholic acid ( 375 and 750 mg/day ) , in comparison with placebo , ursodeoxycholic acid was significantly more effective than chenodeoxycholic acid in dissolving gallstones after 12 mo of treatment . Although there continued to be better dissolution during ursodeoxycholic acid treatment ( dissolution complete in 30 % and partial in another 30 % of the patients ) than during chenodeoxycholic acid treatment ( dissolution complete in 7 % and partial in 40 % ) at 24 mo , this difference between the treatment groups was no longer statistically significant . The incidence of floating stones was significantly higher in the patients who dissolved their stones than in those who did not ( p less than 0.001 ) . The three failures of dissolution of floating stones during bile acid treatment were associated with chenodeoxycholic acid therapy -- two of them with the 750-mg and the third with the 375-mg doses . Gallstone dissolution with ursodeoxycholic acid occurred in spite of a rise in biliary cholesterol saturation , which was consistent with a nonmicellar mechanism of cholelitholysis . Furthermore , more than threefold serum elevations of L-alanine aminotransferase were observed only during chenodeoxycholic acid therapy . They occurred in 2 patients treated with 375 and 750 mg/day , respectively . The enzyme levels normalized after discontinuation of chenodeoxycholic acid and have remained normal for 13 and 8 mo , respectively , after the institution of treatment with 800 mg/day of ursodeoxycholic acid . There was no correlation between the liver tests and biliary levels of lithocholic acid . Of all the symptoms studied , only constipation showed changes that approached statistical significance ( p = 0.0681 ) . There was a significant improvement of constipation in the combined chenodeoxycholic acid groups when they were compared with the combined ursodeoxycholic acid groups . The total bile acid pool exp and ed significantly in both the chenodeoxycholic acid and in the 800-mg ursodeoxycholic acid treatment groups . The marked increases of biliary ursodeoxycholic acid and chenodeoxycholic acid  , respectively , indicated compliance with the treatment in all but 1 bile acid-treated patient . Neither serum triglycerides nor serum cholesterol showed significant changes in any of the treatment groups . The study shows that ursodeoxycholic acid  dissolves gallstones faster and with fewer side effects than chenodeoxycholic acid . The results of the study are also consistent with the view that ursodeoxycholic acid is cholelitholytic at a lower dose than is chenodeoxycholic acid
In the subgroup of patients with primary biliary cirrhosis  , ursodeoxycholic acid  reduced total cholesterol ( WMD : − 29.86 mg/dL , 95 % CI : -47.39 , − 12.33 , p = 0.001 ) and LDL-C ( WMD : -37.27 mg/dL , 95 % CI : -54.16 , − 20.38 , p < 0.001 ) concentrations without affecting TG and HDL-C. Conclusion This meta- analysis suggests that ursodeoxycholic acid therapy might be associated with significant total cholesterol lowering particularly in patients with primary biliary cirrhosis
Objective The aim of this meta- analysis of r and omized placebo-controlled trials was to examine whether ursodeoxycholic acid treatment is an effective lipid-lowering agent .