Evidence map›Paper›PMID 12651881›Full record

ReviewGut2003

Cholestasis.

R Oude Elferink

Open access · bronzeAbstract readReview
In one paragraph

Review in Gut, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Immunology of hepatic diseases during pregnancy.Seminars in immunopathology · 2016
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The bile salt export pump: molecular properties, function and regulation.Pflugers Archiv : European journal of physiology · 2004
    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

1 author at 1 institution in 1 country.

R Oude ElferinkLaboratory Experimental Hepatology, Academic Medical Centre, Amsterdam, The Netherlands. r.p.oude-elferink@amc.uva.nl
Academic Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In contrast with urine formation, bile flow is not dependent on hydrostatic forces, but driven by osmotic pressure of solutes secreted across the apical membrane of hepatocytes and bile duct epithelial cells. This secretory process is mediated by a set of primary active transporters that use ATP hydrolysis to pump solutes against the concentration gradient. The most important solutes in bile are bile salts, lipids, electrolytes, and organic anions. The direct consequence of the osmotic mechanism of bile formation is that impaired function of these pumps leads to impaired bile flow-that is, cholestasis. The function of these pumps is highlighted by a number of inherited cholestatic diseases, which are caused by mutations in these genes. Identification of the molecular defect in these diseases was not only important for diagnostic reasons but also emphasised that impaired transporter function has pathological consequences. Indeed, it is now becoming clear that impaired or downregulated transporter function is also involved in the pathogenesis of acquired cholestatic syndromes.

Indexed as

BileBile Acids and SaltsCholestasisCholestasis, IntrahepaticFemaleHumansMembrane Transport ProteinsMutationPregnancyPregnancy ComplicationsBile Acids and SaltsMembrane Transport Proteins

Identifiers

PMID12651881
PMCPMC1867745
OpenAlexW4241806855

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.