Ursodeoxycholic acid for treatment of primary sclerosing cholangitis: a placebo-controlled trial. Weight reduction and ursodeoxycholic acid in subjects with nonalcoholic fatty liver disease. A double-blind, placebo-controlled trial. [Dietetic therapy of obesity. Preliminary considerations on the combined therapy with ursodeoxycholic acid in the prevention of cholesterol lithiasis]. Cholesterol-lowering effect of ursodeoxycholic acid in patients with primary biliary cirrhosis. A Double-Blind Placebo-controlled Trial of Ursodeoxycholic Acid in the Prevention of Gallstones during Weight Loss after Vertical Banded Gastroplasty Chenodeoxycholic acid and ursodeoxycholic acid effects in endogenous hypertriglyceridemias. A controlled double-blind trial. Ursodeoxycholic acid as adjunctive therapy for problematic type 1 autoimmune hepatitis: a randomized placebo-controlled treatment trial. Impact of combined therapy with alpha-lipoic and ursodeoxycolic acid on nonalcoholic fatty liver disease: double-blind, randomized clinical trial of efficacy and safety 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. Uric Acid Reduction Rectifies Prehypertension in Obese Adolescents A double-blind, randomized, placebo-controlled trial of n-3 versus n-6 fatty acid-based lipid infusion in atopic dermatitis. High-dose ursodeoxycholic acid therapy for nonalcoholic steatohepatitis: a double-blind, randomized, placebo-controlled trial. Pentoxifylline decreases oxidized lipid products in nonalcoholic steatohepatitis: new evidence on the potential therapeutic mechanism. Effect of Uric Acid–Lowering Agents on Endothelial Function: A Randomized, Double-Blind, Placebo-Controlled Trial α-Lipoic acid treatment of aged type 2 diabetes mellitus complicated with acute cerebral infarction. Effect of Lipid-Lowering Treatment on Progression of Atherosclerotic Lesions—a Duplex Ultrasonographic Investigation
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 OBJECTIVE Nonalcoholic fatty liver disease is an increasingly recognized condition that may progress to end-stage liver disease . We investigated the effects of weight reduction and ursodeoxycholic acid administration in patients with this disease . RESEARCH METHODS AND PROCEDURES A double-blind , placebo-controlled trial . Twenty-seven women with a body mass index of > 30 kg/m2 and willing to participate in the diet plan for six weeks were studied were assigned to one of two treatment groups ( ursodeoxycholic acid , n = 14 : placebo n = 13 ) . Both groups received a normal diet ( 1,200 kcal/d ) plus 1200 mg/d of ursodeoxycholic acid or placebo .  Hepatic steatosis , was assessed by abdominal ultrasound . Fasting glucose , cholesterol , triglycerides , and aminotransferases levels were determined before and after treatment . RESULTS Body mass index decreases significantly from 34.2 + /- 4.2 kg/m2 and 33.3 + /- 1.6 kg/m2 to 31.8 + /- 4.5 kg/m2 and 30.6 + /- 2.6 kg/m2 in the ursodeoxycholic acid and placebo groups , p < 0.001 . The hepatic steatosis index decreased from 2.3 + /- 0.7 to 1.0 + /- 0.6 and 2.2 + /- 0.7 to 1.1 + /- 0.7 in the ursodeoxycholic acid and placebo groups , p<0.003 . Serum AST decreased significantly from 41.2 + /- 5.6 to 34.5 + /- 3.4 in the ursodeoxycholic acid group , p < 0.001 , and from 43.6 + /- 4.2 to 35.3 + /- 2.9 in the placebo group , p < 0.001 . Serum ALT decreased from 62.9 + /- 6.5 to 44.0 + /- 3.5 in the ursodeoxycholic acid group , p < 0.001 , and from 63.5 + /- 4.5 to 44.0 + /- 3.5 in the placebo group . We did not find any differences in all variables studied between groups . CONCLUSIONS The present study shows beneficial effect of weight reduction , producing improvements in biochemical and imaging markers of liver disease The use of ursodeoxycholic acid ( UDCA ) was found useful in reducing the incidence of cholelithiasis ( p < 0.05 ) without provoking any other alteration in hepatic function . This preliminary experience underlines the appropriateness of carrying out further studies on the utility of preventive treatment for the formation of cholesterol calculi with biliary acids , and in particular UDCA , in obese subjects who are receiving dietary treatment . The protective action of ursodeoxycholic acid in the prevention of biliary lithiasis during the course of low-calorie diets was evaluated in 40 obese subjects ( 31 females , 9 males ) treated for 4 months with fibre-rich ( approximately 40 g/day ) low-calorie diets  of 900 - 1200 Kcal , of whom 20 received 450 - 750 mg of UDCA/day and 20 were treated with placebo 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 One hundred and seven patients whose gallbladder was normal at the time of vertical b and ed gastroplasty ( VBG ) were considered for entry into a r and omized placebo-controlled double-blind study to determine the effectiveness of ursodeoxycholic acid ( UDCA ) in preventing cholelithiasis during the period of weight loss . Twenty-one patients ( 20 % ) developed gallstones in the six-week period post-VBG and prior to r and omization and were therefore excluded . Eighty-six patients were r and omized at 6 weeks to active medication or placebo . Of these , 61 patients ( 71 % ) completed the study . Twenty-five patients ( 29 % ) failed to completed the study because of incompliance , intolerance to the medication or pregnancy ; 17 of these were in the active treatment group and eight were in the placebo group . None of the 27 patients treated with UDCA developed gallstones , whereas eight of 34 ( 24 % ) patients taking placebo developed gallstones . This difference was statistically significant ( p = 0.0061 ) . These results suggest that UDCA is fully effective in preventing gallstone formation following VBG in patients who follow the prescribed regimen 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 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 Background and purpose Nonalcoholic fatty liver disease ( NAFLD ) is one of the causes of a fatty liver , occurring when fat is deposited ( steatosis ) in the liver not due to excessive alcohol use . It is related to insulin resistance and the metabolic syndrome . The purpose of the present study was to evaluate the impact of combination therapy with alpha-lipoic acid ( ALA ) and ursodeoxycholic acid ( UDCA ) on NAFLD . Methods Alpha-lipoic acid 400 mg/day plus UDCA 300 mg/day ( ALAUDCA ) was investigated in patients over a period of 12 months using a r and omized , placebo (PLA)-controlled study with four parallel groups . Serum concentration of gamma-glutamyl transpeptidase ( GGT ) , alanine aminotransferase ( ALT ) , aspartate aminotransferase ( AST ) , albumin and platelets ( PLT ) were measured at the beginning and at the end of the treatment . Moreover , the AST/ALT ratio and the NAFLD fibrosis score were examined . Results A total of 120 patients were r and omly assigned to the four groups . ALA and UDCA were safe and well tolerated in the oral daily administration only . AST , ALT , GGT ( p < 0.001 ) showed a significant difference between ALAUDCA and other three groups . Besides , NAFLD fibrosis score underlined a significant reduction ( p < 0.04 ) in the ALAUDCA group , while AST/ALT ratio presented a moderate decline ( p > 0.05 ) . Conclusion ALAUDCA therapy reduced AST , ALT , GGT values and improved NAFLD fibrosis score and AST/ALT ratio , especially in patients who were on a hypocaloric diet . These findings will be useful in patient selection in future clinical trials with ALAUDCA in long-term studies 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 Epidemiologic studies , animal models , and preliminary clinical trials in children implicate uric acid in the development of essential hypertension . Controversy remains as to whether the observations indicate a general mechanism or a surrogate phenomenon . We sought to determine whether uric acid is a causative mediator of increased blood pressure ( BP ) and impaired vascular compliance . We report a r and omized , double-blinded , placebo-controlled trial comparing 2 mechanisms of urate reduction with placebo in prehypertensive , obese , adolescents , aged 11 to 17 years . Subjects were r and omized to the xanthine oxidase inhibitor , allopurinol , uricosuric , probenecid , or placebo . Subjects treated with urate-lowering therapy experienced a highly significant reduction in BP . In clinic systolic BP fell 10.2 mm Hg and diastolic BP fell 9.0 mm Hg in treated patients compared with a rise of 1.7 mm Hg and 1.6 mm Hg systolic and diastolic BP , respectively in patients on placebo . Urate-lowering therapy also result ed in significant reduction in systemic vascular resistance . These data indicate that , at least in adolescents with prehypertension , uric acid causes increased BP that can be mitigated by urate lowering therapy BACKGROUND In the involved epidermis of patients with atopic dermatitis , changes in the metabolism of eicosanoids with increased quantities of the arachidonic acid (AA)-derived lipoxygenase products have been observed . Free eicosapentaenoic acid ( EPA ) , a fish oil-derived alternative ( n-3 ) fatty acid , may compete with AA , result ing in an anti-inflammatory effect . METHODS In a 10-day double-blind , r and omized , placebo-controlled trial , 22 patients hospitalized for moderate-to-severe atopic dermatitis were r and omly assigned to receive daily infusions of either a n-3 fatty acid-based lipid emulsion ( fish oil , 10 % ; 200 mL/d ) or a conventional n-6-lipid emulsion ( soybean oil , 10 % ; 200 mL/d ) . Topical treatment was restricted to emollients . The severity of disease was evaluated daily with scoring of erythema , infiltration , and desquamation and by subjective patient scoring of clinical manifestations . In addition , plasma-free and total-bound fatty acids and the composition of membrane fatty acids in blood cells ( thrombocytes , granulocytes , and erythrocytes ) , lipid mediators from isolated neutrophils and platelets , and lymphocyte-activation parameters were determined . RESULTS Twenty patients completed the trial . Marked improvement from baseline was seen in both groups . On days 6 , 7 , 8 , and 10 , disease severity score-defined as the sum of all scores-was more pronounced ( p < .05 ) in the n-3 group compared with the n-6 group . Free arachidonic acid in plasma did not change substantially in both groups , whereas plasma-free EPA , total-bound EPA , and the membrane EPA/AA ratio markedly increased in response to n-3-lipid infusion . In parallel , EPA-derived lipid mediators appeared , whereas lymphocyte functions were unaffected . In the post-treatment period ( 2/4 weeks ) , relapse was observed in some patients after n-3 psoralene-ultraviolet A ( PUVA ) infusion , whereas there was a marked long-term improvement in the n-6 group . CONCLUSIONS IV n-3-fatty acid administration is effective in acutely improving the severity of atopic dermatitis , paralleled by changes in plasma and membrane fatty acid composition and lipid mediator synthesis . The long-term beneficial effects of IV n-6 fatty acids should be evaluated further UNLABELLED In uncontrolled clinical studies , ursodeoxycholic acid ( UDCA ) had a beneficial effect on  nonalcoholic steatohepatitis ( NASH ) .  However , a large controlled trial using UDCA ( 13 - 15 mg/kg/day ) was unable to confirm these results . Accordingly , a r and omized , placebo-controlled study was initiated with a high dose of UDCA ( 23 - 28 mg/kg/day ) . The allocation of patients and the evaluation of liver histology were performed according to a modified Brunt score and the nonalcoholic fatty liver disease activity score ( NAS ) . With the modified Brunt score , 185 patients with histologically proven NASH were r and omized [ intention to treat ( ITT ) ] , and 147 were treated per protocol ( PP ) . With the NAS , 137 patients were confirmed to have NASH , 48 had borderline NASH , and 1 did not have NASH . The treatment time was 18 months . At entry , the treatment groups were comparable . A second biopsy sample was obtained from 139 of 185 patients ( NAS : 107/137 ) . The primary criterion for evaluation was a change in the liver histology ; the secondary criteria were single histological variables and liver biochemistry . Significant differences in the overall histology could not be detected between the two treatment groups with the modified Brunt score ( P = 0.881 ) or NAS ( P = 0.355 ) . Only lobular inflammation improved significantly ( P for the modified Brunt score = 0.011 , P for NAS = 0.005 ) . In subgroup analyses , significant improvements in lobular inflammation were also observed in males , younger patients up to 50 years of age , slightly overweight patients , and patients with hypertension and an increased histology score . The fibrosis score did not change ( P for ITT = 0.133 , P for PP = 0.140 ) . With the exception of gamma-glutamyl transferase , UDCA did not improve laboratory data . CONCLUSION High-dose UDCA failed to improve the overall histology in patients with NASH in comparison with placebo UNLABELLED Pentoxifylline ( PTX ) improved the histological features of nonalcoholic steatohepatitis ( NASH ) in a recent r and omized placebo-controlled trial . However , the underlying mechanism responsible for the beneficial effects of PTX in NASH remains unidentified . A key role of lipid oxidation in the pathogenesis and progression of NASH has been established . PTX is known to decrease free-radical-mediated oxidative stress and inhibit lipid oxidation . The primary aim of this study was to evaluate the effects of PTX on levels of lipid oxidation products in patients with NASH . Levels of multiple structurally specific oxidized fatty acids including hydroxy-octadecadienoic acids ( HODEs ) , oxo-octadecadienoic acids ( oxoODEs ) , and hydroxy-eicosatetraenoic acids ( HETEs ) were quantified by mass spectrometry in plasma obtained at baseline and at study completion in patients who completed 1 year of therapy with PTX or placebo  in a r and omized controlled trial . Therapy with PTX result ed in significant decreases in 9-HODE and 13-oxoODE , oxidized lipid products of linoleic acid ( LA ) linked to histological severity in nonalcoholic fatty liver disease . Similarly , PTX therapy was associated with significant decreases in 8-HETE , 9-HETE , and 11-HETE compared to placebo . Statistically significant correlations were demonstrated between the decrease in HODEs and oxoODEs and improved histological scores of fibrosis and between the decrease in HETEs and improved lobular inflammation . CONCLUSION Therapy with PTX compared to placebo was associated with a significant reduction of oxidized fatty acids . This novel evidence supports that the beneficial effects of PTX in patients with NASH are likely partly mediated through decreasing lipid oxidation , largely free-radical-mediated lipid oxidation . Additionally , this is the first report on the link between decreased oxidized lipid products and improved histological disease in the setting of a therapeutic trial in NASH Higher levels of serum uric acid are independently associated with endothelial dysfunction , a mechanism for incident hypertension . Overweight/obese individuals are more prone to endothelial dysfunction than their lean counterparts . However , the effect of lowering serum uric acid on endothelial dysfunction in these individuals has not been examined thoroughly . In this r and omized , double-blind , placebo-controlled trial of nonhypertensive , overweight , or obese individuals with higher serum uric acid ( body mass index ≥25 kg/m2 and serum uric acid ≥5.0 mg/dL ) , we assigned subjects to probenecid ( 500–1000 mg/d ) , allopurinol ( 300–600 mg/d ) , or matching placebo . The primary outcome was endothelium-dependent vasodilation measured by brachial artery ultrasound at baseline and 8 weeks . By the end of the trial , 47 , 49 , and 53 participants had been allocated to receive probenecid , allopurinol , and placebo , respectively . Mean serum uric acid levels significantly decreased in the probenecid ( from 6.1 to 3.5 mg/dL ) and allopurinol groups ( from 6.1 to 2.9 mg/dL ) but not in the placebo group ( 6.1 to 5.6 mg/dL ) . None of the interventions produced any significant change in endothelium-dependent vasodilation  ( probenecid , 7.4±5.1 % at baseline and 8.3±5.1 % at 8 weeks ; allopurinol , 7.6±6.0 % at baseline and 6.2±4.8 % at 8 weeks ; and placebo , 6.5±3.8 % at baseline and 7.1±4.9 % at 8 weeks ) . In this r and omized , double-blind , placebo-controlled trial , uric acid lowering did not affect endothelial function in overweight or obese nonhypertensive individuals . These data do not support the hypothesis that uric acid is causally related to endothelial dysfunction , a potential mechanism for development of hypertension OBJECTIVE This study aims to evaluate the efficacy and safety of α-lipoic acid in the treatment of aged type 2 diabetes mellitus ( T2DM ) complicated with acute cerebral infa rct ion . PATIENTS AND METHODS 90 patients were r and omly divided into two groups , on the basis of conventional treatment . The experiment group was administrated with α-lipoic acid , while only Vitamin C for the control group , for 3 consecutive weeks . Before and after the experiment , superoxide dismutase ( SOD ) , glutathione peroxidase ( GSH-Px ) and malondialdehyde ( MDA ) levels were measured and scored with the NIHSS ( National Institutes of Health Stroke Scale ) , and the changes of blood glucose , insulin function and other indicators were observed . RESULTS After the treatment , the plasma SOD and GSH-Px levels increased , while MDA decreased ( p < 0.05 ) , with statistical significance when compared with the control group ( p < 0.01 ) . NIHSS score , blood glucose , blood lipids and HOMA-IA of the experiment group decreased significantly ( p < 0.01 ) ; and no significant adverse reactions were found in both groups . CONCLUSIONS α-lipoic acid was safe and effective in the treatment of aged T2DM complicated with acute cerebral infa rct ion , significantly reducing the patient 's oxidative stress , blood glucose and lipid levels and being able to improve islet function The Prevenzione Aterosclerosi Studio Torino ( P.A.S.T. ) was a prospect i ve , r and omized trial testing the effect on carotid and femoral atherosclerotic lesions of lipid-lowering therapy , as assessed by duplex scanning ( DS ) technique , in 85 patients ( 12 women , 73 men ) , forty-five to fifty-five years old , with ischemic heart disease ( IHD ) , and r and omly assigned to a hypolipidemic diet or diet + 250 mg acipimox ( a nicotinic acid compound ) two to three times/day . Forty-one patients , without inclusion criteria , were compared with the r and omized groups as a reference population . All three groups were su bmi tted to DS and to hematic monitoring of lipid levels at the beginning and at the end of the study . During three years of treatment , there was a significant reduction ( -6.5 % ) in total plasma cholesterol in the diet+drug group ( P=0.04 ) and a simultaneous elevation of high-density lipoprotein cholesterol , significant in the treatment groups ( respectively , + 15 % P=0.02 in the diet and + 16 % P=0.016 in the diet+drug group ) . Every group showed a trend toward the increasing number of lesions in all explored areas and toward the progression in size of the already existing ones . Whereas in the initial DS the prevalence of lesions was significantly lower in the nonr and omized group in every site , at the end of the study the total number of lesions did not differ among groups , and there was a significant increase of plaques in carotid area in the nonran domized group in comparison with the treatment groups . ( continued on next page ) The final number of stable plaques was greater in the treatment groups as compared with the nonr and omized group ( P=0.01 diet vs nonr and omized , P=0.03 diet+drug vs nonr and omized ) . In conclusion , lipid-lowering treatment , with diet and with diet+drug , was useful in slowing the natural progression of atherosclerosis ; particularly , it reduced the develop ment of new lesions in the carotid and femoral arteries and increased the stability of the already existing ones . In these patients , diet was equivalent to diet+drug in regard to progression of lesions . The most favorable results in the treatment groups seem to correlate with high-density lipoprotein cholesterol , significantly increased in comparison with the nonr and omized group
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 .