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1 60% with inflammatory bowel disease, 46% on ursodeoxycholic acid).
2 ation of cholestasis, with weight-dosed oral ursodeoxycholic acid.
3 be attributable to liver transplantation or ursodeoxycholic acid.
4 maining 17% of bile acids were identified as ursodeoxycholic acid.
5 mplete response to first-line treatment with ursodeoxycholic acid.
6 re commonly in the 21 patients randomized to ursodeoxycholic acid.
7 ely to treatment with mitochondrially active ursodeoxycholic acid.
8 mic reticulum stress, which was countered by ursodeoxycholic acid.
9 recommended in favor of prophylactic use of ursodeoxycholic acid.
10 gitis may have never received treatment with ursodeoxycholic acid.
11 eceptor bile acid receptor agonists, and nor-ursodeoxycholic acid.
12 transformed 20 years ago with the advent of ursodeoxycholic acid.
13 intolerant to or inadequately responsive to ursodeoxycholic acid.
14 limit of normal (ULN) despite treatment with ursodeoxycholic acid.
15 r in patients with an inadequate response to ursodeoxycholic acid.
16 adequate response to first-line therapy with ursodeoxycholic acid.
17 c acid > cholic acid > hyodeoxycholic acid > ursodeoxycholic acid.
18 apidly triggered by a diet supplemented with ursodeoxycholic acid.
19 ry cirrhosis who had inadequate responses to ursodeoxycholic acid.
20 All patients were treated with ursodeoxycholic acid.
22 e, or incomplete response were randomized to ursodeoxycholic acid (13-15 mg/kg daily) or placebo for
23 lic acid (3alpha-OH, 7alpha-OH, 12alpha-OH), ursodeoxycholic acid (3alpha-OH, 7beta-OH), and lithocho
24 binations of gentamicin and chaperone drugs (ursodeoxycholic acid, 4-phenylbutyrate [4-PB]) were inve
25 colonic mucosal tissue in vitro In contrast, ursodeoxycholic acid (50-200 microM) inhibited both basa
27 4-Phenyl butyric acid and taurine-conjugated ursodeoxycholic acid alleviated ER stress in cells and w
28 mittance and following treatment with either ursodeoxycholic acid alone (10 mg/kg thrice daily, n = 1
29 lus ursodeoxycholic acid was not superior to ursodeoxycholic acid alone for the prevention or occlusi
30 hemical response occurred under therapy with ursodeoxycholic acid, alone or in combination with immun
32 acid, radioactivity was detected in both the ursodeoxycholic acid and chenodeoxycholic acid fractions
34 alysis in 168 patients with PSC treated with ursodeoxycholic acid and followed up from November 2004
37 activity calculation, and the routine use of ursodeoxycholic acid and low-dose steroids (modified pro
38 were similar before and after treatment with ursodeoxycholic acid and no different than after placebo
39 e drugs that antagonize BS toxicity, such as ursodeoxycholic acid and nor-ursodeoxycholic acid, may b
43 on in serum alkaline phosphatase levels with ursodeoxycholic acid and the need to add second-line age
44 ients do not, however, respond adequately to ursodeoxycholic acid and therefore still remain at risk
45 might be reduced by early enteral feedings, ursodeoxycholic acid, and cholecystokinin-octapeptide.
46 its were corrected by oral administration of ursodeoxycholic acid, and the addition of an oral proton
47 compound ursolic acid and the licensed drug ursodeoxycholic acid are chemically closely related to u
48 results indicate that substantial amounts of ursodeoxycholic acid are formed in patients treated with
51 acid as a naturally occurring compound, and ursodeoxycholic acid as an already licensed drug as prom
52 r, phenylbutyric acid and taurine-conjugated ursodeoxycholic acid attenuated HNE-induced leukocyte ro
54 mong patients with an inadequate response to ursodeoxycholic acid but may improve symptoms of pruritu
55 d by restoring biliary secretion with 24-nor-ursodeoxycholic acid but were significantly reduced by o
60 , sitosterol, cholic acid, deoxycholic acid, ursodeoxycholic acid, cholestyramine, bile fistula, lova
62 ith an incomplete response or intolerance to ursodeoxycholic acid, clinical trials have indicated tha
63 modifying BA synthesis or dietary intake of ursodeoxycholic acid could improve tumor immunotherapy i
68 holic acid, the specific activity of biliary ursodeoxycholic acid exceeded the specific activity of c
69 nts with primary biliary cholangitis in whom ursodeoxycholic acid failed, based on a surrogate endpoi
74 henodeoxycholic, deoxycholic, lithocholic or ursodeoxycholic acids, free and as their glycine or taur
75 e occurred in 74 (23%) of 322 infants in the ursodeoxycholic acid group and 85 (27%) of 318 infants i
76 serious adverse events were reported in the ursodeoxycholic acid group and six serious adverse event
77 is included 304 women and 322 infants in the ursodeoxycholic acid group, and 300 women and 318 infant
78 important, because effective treatment with ursodeoxycholic acid has been shown to halt disease prog
79 s a second-line therapy for patients failing ursodeoxycholic acid has improved outcomes for patients
81 ining factor in the pathogenesis of PBC with ursodeoxycholic acid helping to restore this protective
82 biliary cholangitis who are unresponsive to ursodeoxycholic acid; however, approximately 50% of pati
83 was confirmed for both ursocholanic acid and ursodeoxycholic acid in a Parkin-deficient neuronal mode
87 periority of 24-norursodeoxycholic acid over ursodeoxycholic acid in reducing histological disease pr
90 o not respond sufficiently, or patients with ursodeoxycholic acid intolerance, conditionally licensed
92 experiments provide the first evidence that ursodeoxycholic acid is effective for preventing adenoma
98 of multiple cholesterol stone formation, and ursodeoxycholic acid may partially halt the formation of
99 xicity, such as ursodeoxycholic acid and nor-ursodeoxycholic acid, may be effective at all disease st
104 ng the effects of deoxycholic acid (DCA) and ursodeoxycholic acid on the expression and release of Hb
105 Participants were randomly assigned 1:1 to ursodeoxycholic acid or placebo, given as two oral table
107 recommended for patients who cannot tolerate ursodeoxycholic acid or who have an inadequate response
108 id (deoxycholic acid, chenodeoxycholic acid, ursodeoxycholic acid, or glycochenodeoxycholic acid) in
109 he concentrations of the secondary bile acid ursodeoxycholic acid (p = 0.033) and the plant sterol si
110 s with inadequate response or intolerance to ursodeoxycholic acid, peroxisome proliferator-activated
117 = 0.02). A sensitivity analysis that defined ursodeoxycholic acid response as normalization of alkali
118 C, which is unrelated to disease severity or ursodeoxycholic acid response, is significant and comple
120 el insights into the mechanisms of action of ursodeoxycholic acid should advance our understanding of
121 ears following biopsy, including response to ursodeoxycholic acid, show identical changes to patients
123 ies, showed identical treatment responses to ursodeoxycholic acid, similar rates and types of nonhepa
125 ewed interest in developing therapies beyond ursodeoxycholic acid that are aimed at both slowing dise
127 bile acid--binding resins and the choleretic ursodeoxycholic acid, the medical management of cholesta
129 dults with PBC and an inadequate response to ursodeoxycholic acid therapy (i.e., alkaline phosphatase
130 The precise role of weight reduction and ursodeoxycholic acid therapy in the favorable alteration
133 esponse to or unacceptable side effects with ursodeoxycholic acid to receive once-daily elafibranor,
134 ative reductions in ALP were similar between ursodeoxycholic acid-treated and untreated patients.
137 18:0/18:1), PS(14:1/14:0), dihydroxyacetone, ursodeoxycholic acid, tryptophan, L-valine, cycloserine,
138 assigned to ceftriaxone also received 300 mg ursodeoxycholic acid twice daily and those assigned to p
140 d, double-blind, placebo-controlled trial of ursodeoxycholic acid (UDCA) (10-12 mg/kg/d) taken as a s
144 uate the safety and estimate the efficacy of ursodeoxycholic acid (UDCA) and clofibrate in the treatm
148 ated the potential of therapeutic bile acids ursodeoxycholic acid (UDCA) and obeticholic acid (OCA, 6
149 patients with AMA-negative PBC treated with ursodeoxycholic acid (UDCA) and/or liver transplantation
150 igation (BDL) in mice and how treatment with ursodeoxycholic acid (UDCA) and/or S-adenosylmethionine
151 olic acid (DCA), lithocholic acid (LCA), and ursodeoxycholic acid (UDCA) are implicated in the pathog
152 tients with PBC do not adequately respond to Ursodeoxycholic acid (UDCA) as a first-line treatment, p
153 iary cholangitis (PBC) patients treated with ursodeoxycholic acid (UDCA) at month 12 and at last chec
155 acid (DCA), chenodeoxycholic acid (CDCA) or ursodeoxycholic acid (UDCA) caused sustained MAPK activa
158 s are inconclusive regarding the efficacy of ursodeoxycholic acid (UDCA) for treating primary scleros
165 d-line treatment for PBC in combination with ursodeoxycholic acid (UDCA) in adults with an inadequate
167 more, we investigated the mechanism by which ursodeoxycholic acid (UDCA) inhibits LXR-induced lipogen
175 nt of primary biliary cholangitis (PBC) with ursodeoxycholic acid (UDCA) is not always sufficient to
185 This study sought to assess the effects of ursodeoxycholic acid (UDCA) on endothelial function and
186 d a meta-analysis to evaluate the effects of ursodeoxycholic acid (UDCA) on pruritus, liver test resu
194 rmine the influence of IBD and the effect of ursodeoxycholic acid (UDCA) therapy on the course of the
195 aimed at investigating the effect of adding Ursodeoxycholic acid (UDCA) to CBD stenting alone in ord
197 ed that feeding the cytoprotective bile acid ursodeoxycholic acid (UDCA) to rats resulted in signific
198 ound z-guggulsterone and the off-patent drug ursodeoxycholic acid (UDCA) to reduce FXR signalling and
208 e of them were treated in the follow up with ursodeoxycholic acid (UDCA), eight received during a tri
209 hypertransaminasemia (ADAH), its response to ursodeoxycholic acid (UDCA), elucidate its pathophysiolo
210 efficacy criteria determined the response to ursodeoxycholic acid (UDCA), fibrates (n=93), and OCA (n
211 se and the first line available treatment is ursodeoxycholic acid (UDCA), however, direct and indirec
212 diagnosis reports, response to therapy with ursodeoxycholic acid (UDCA), laboratory results, and sym
214 frequently progresses despite treatment with ursodeoxycholic acid (UDCA), the only approved therapy.
215 eutic option available for these patients is ursodeoxycholic acid (UDCA), which slows the progression
217 alkaline phosphatase levels in this largely ursodeoxycholic acid (UDCA)-responding, early-disease st
218 Normal alkaline phosphatase (ALP) levels in ursodeoxycholic acid (UDCA)-treated patients with primar
228 Administration of the secondary bile acid ursodeoxycholic acid (UDCA; ursodiol) inhibits the life
229 ecifically, our approach involves the use of ursodeoxycholic acid (Urso) due to its ability to decrea
230 Sulindac was tested in combination with ursodeoxycholic acid (ursodiol), a naturally occurring 7
231 deoxycholate, an ionic salt of berberine and ursodeoxycholic acid), versus placebo that was conducted
233 f 1 kg), and the finding that ofloxacin plus ursodeoxycholic acid was not superior to ursodeoxycholic
236 ith inadequate response to or intolerance to ursodeoxycholic acid were randomised to receive placebo,
237 NF-kappaB, an effect that was attenuated by ursodeoxycholic acid, whereas an NF-kappaB inhibitor, BM
238 , the foundational treatment of PBC has been ursodeoxycholic acid, which delays disease progression i
240 Moreover, the hepatoprotective bile acid ursodeoxycholic acid, which reverses hydrophobic bile ac
241 ed drug in primary sclerosing cholangitis is ursodeoxycholic acid, which, despite a range of potentia
242 gitis and intolerance/inadequate response to ursodeoxycholic acid who initiated OCA therapy were comp
244 properties of hydrophilic bile acids such as ursodeoxycholic acid, with the distinct ability to speci