Evidence map›Paper›PMID 20564380›Full record

ArticleHepatology (Baltimore, Md.)2010

Bile acid changes after high-dose ursodeoxycholic acid treatment in primary sclerosing cholangitis: Relation to disease progression.

Emmanouil Sinakos, Hanns-Ulrich Marschall, Kris V Kowdley, Alex Befeler, Jill Keach, Keith Lindor

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 3 pooled it
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 3 syntheses or guidelines pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
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  11. Pathogenesis, Non-Invasive Assessments and Treatment of Hepatic Fibrosis in Autoimmune Liver Diseases.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  12. Gly-βMCA modulates bile acid metabolism to reduce hepatobiliary injury inAmerican journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Synergistic effect ofFrontiers in pharmacology · 2023
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Emmanouil SinakosDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA.
Hanns-Ulrich Marschall
Kris V Kowdley
Alex Befeler
Jill Keach
Keith Lindor
Mayo Clinic in Arizona · USBenaroya Research InstituteKarolinska Institutet · SESaint Louis University · US

Funding

Multicentered Randomized Trial of High-dose Urso in PSCR01DK056924 · NIDDK · MAYO CLINIC ROCHESTER · PI TALWALKAR, JAYANT A · 2001 to 2011
$6.5M
NIDDK NIH HHS DK56924NIDDK NIH HHS R01 DK056924
6 · The paper itself

Abstract

unlabelledHigh-dose (28-30 mg/kg/day) ursodeoxycholic acid (UDCA) treatment improves serum liver tests in patients with primary sclerosing cholangitis (PSC) but does not improve survival and is associated with increased rates of serious adverse events. The mechanism for the latter undesired effect remains unclear. High-dose UDCA could result in the production of hepatotoxic bile acids, such as lithocholic acid (LCA), because of limited small bowel absorption of UDCA and conversion of UDCA by bacteria in the colon. We determined the serum bile acid composition in 56 patients with PSC previously enrolled in a randomized, double-blind controlled trial of high-dose UDCA versus placebo. Samples for analysis were obtained at the baseline and at the end of treatment. The mean changes in the UDCA level (16.86 versus 0.05 micromol/L) and total bile acid level (17.21 versus -0.55 micromol/L) were significantly higher in the UDCA group (n = 29) versus the placebo group (n = 27) when pretreatment levels were compared (P < 0.0001). LCA was also markedly increased (0.22 versus 0.01 micromol/L) in the UDCA group compared to the placebo group (P = 0.001). No significant changes were detected for cholic acid, deoxycholic acid, or chenodeoxycholic acid. Patients (n = 9) in the UDCA group who reached clinical endpoints of disease progression (the development of cirrhosis, varices, liver transplantation, or death) tended to have greater increases in their posttreatment total bile acid levels (34.99 versus 9.21 micromol/L, P < 0.08) in comparison with those who did not.

conclusionHigh-dose UDCA treatment in PSC patients results in marked UDCA enrichment and significant expansion of the total serum bile acid pool, including LCA.

Indexed as

AdolescentAdultAgedBile Acids and SaltsCholagogues and CholereticsCholangitis, SclerosingDisease ProgressionDose-Response Relationship, DrugDouble-Blind MethodFemaleHumansLithocholic AcidMaleMiddle AgedRandomized Controlled Trials as TopicTreatment OutcomeBile Acids and SaltsCholagogues and CholereticsLithocholic AcidUrsodeoxycholic Acid

Identifiers

PMID20564380
PMCPMC2928060
OpenAlexW1982014243

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.