Evidence map›Paper›PMID 32653991›Full record

ReviewHepatology international2020

Ileal bile acid transporter inhibition as an anticholestatic therapeutic target in biliary atresia and other cholestatic disorders.

Saul J Karpen, Deirdre Kelly, Cara Mack, Philip Stein

Abstract readReview
PubMed Publisher
In one paragraph

Review in Hepatology international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

45 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Primary sclerosing cholangitis.Nature reviews. Disease primers · 2025
    Review
  13. Observational
  14. Review
  15. Article
  16. Article
  17. Diseases of bile duct in children.World journal of gastroenterology · 2024
    Review
  18. Article
  19. Article
  20. Article
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

4 authors at 3 institutions in 2 countries.

Saul J KarpenDivision of Pediatric Gastroenterology, Hepatology and Nutrition, Emory University School of Medicine and Children's Healthcare of Atlanta, 1760 Haygood Dr., HSRB E204, Atlanta, GA, 30322, USA. skarpen@emory.edu.ORCID http://orcid.org/0000-0002-3379-7592
Deirdre KellyLiver Unit, Birmingham Women's and Children's NHS Foundation Trust, Steelhouse Lane, Birmingham, B4 6NH, UK.
Cara MackSection of Pediatric Gastroenterology, Hepatology and Nutrition and the Digestive Health Institute, University of Colorado School of Medicine and Children's Hospital Colorado, 13123 E 16th Ave B290, Aurora, CO, 80045, USA.
Philip SteinMedical Affairs, Albireo Pharma, Inc, 10 Post Office Square, Suite 1000, Boston, MA, 02109, USA.
Birmingham Women’s and Children’s NHS Foundation Trust · GBChildren's Hospital Colorado · USEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Biliary atresia is a rare cholestatic liver disease that presents in infants and rapidly advances to death in the absence of intervention. As a result of blockage or destruction of the biliary tract, bile acids accumulate and drive inflammation, fibrosis, and disease progression. The standard of care, Kasai portoenterostomy (KPE), is typically performed shortly after diagnosis (currently at ~ 2 months of age) and aims to restore bile flow and relieve cholestasis. Nevertheless, most patients continue to experience liver injury from accumulation of bile acids after KPE, since there are no known effective therapeutics that may enhance survival after KPE. Improving cholestasis via interruption of the enterohepatic circulation of bile acids may directly attenuate hepatic bile acid retention and reduce the risk of early organ failure. Directly addressing intrahepatic accretion of bile acids to avoid inherent bile acid toxicities provides an attractive and plausible therapeutic target for biliary atresia. This review explores the novel therapeutic concept of inhibiting the sole ileal bile acid transporter (IBAT), also known as ASBT (apical sodium-bile acid transporter, encoded by SLC10A2), as a means to reduce hepatic bile acid concentration after KPE. By reducing return of bile acids to the cholestatic liver, IBAT inhibitors may potentially lessen or delay liver damage associated with the hepatotoxicity and cholangiopathy of bile acid accumulation. The clinical programs of 2 IBAT inhibitors in development for the treatment of pediatric cholestatic liver diseases, maralixibat and odevixibat, are highlighted.

Indexed as

Biliary AtresiaOrganic Anion Transporters, Sodium-DependentPortoenterostomy, HepaticSymportersBenzodiazepinesButyratesDisease ProgressionGastrointestinal AgentsHumansInfantPrognosisProtective AgentsBenzodiazepinesButyratesGastrointestinal AgentsodevixibatOrganic Anion Transporters, Sodium-DependentProtective Agentssodium-bile acid cotransporterSymportersApical sodium-bile acid transporterBile acidsBiliary atresiaCholestasisCholestatic liver diseaseEnterohepatic circulationIleal bile acid transporterKasai portoenterostomyMaralixibatOdevixibatPediatrics

Identifiers

PMID32653991
OpenAlexW3041959992

What OpenQuestion holds

Textmetadata
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.