Evidence map›Paper›PMID 21088237›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2011

Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases.

Fayez K Ghishan, Pawel R Kiela

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 5 pooled it
3.2field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 5 syntheses or guidelines pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Bone Health in Paediatric Inflammatory Bowel Disease.Diagnostics (Basel, Switzerland) · 2025
    Review
  13. The NaJournal of extracellular vesicles · 2024
    Article
  14. Review
  15. Article
  16. Review
  17. Irisin and Secondary Osteoporosis in Humans.International journal of molecular sciences · 2022
    Review
  18. Intestinal Inflammation Promotes MDL-1Cellular and molecular gastroenterology and hepatology · 2022
    Article
  19. Article
  20. Bone disease in chronic pancreatitis.World journal of clinical cases · 2020
    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

2 authors at 1 institution in 1 country.

Fayez K GhishanDept. of Pediatrics, Steele Children's Research Center, Univ. of Arizona Health Sciences Center; 1501 N. Campbell Ave., Tucson, AZ 85724, USA.
Pawel R Kiela
Children's Center · US

Funding

DEVELOPMENT OF INTESTINAL TRANSPORT OF CA++ AND PIR37DK033209 · NIDDK · UNIVERSITY OF ARIZONA · PI GHISHAN, FAYEZ KHALAF · 1995 to 2017
$4.7M
NIDDK NIH HHS 3R37DK033209-27S1NIDDK NIH HHS 5R37DK033209NIDDK NIH HHS R37 DK033209
6 · The paper itself

Abstract

Chronic inflammatory disorders such as inflammatory bowel diseases (IBDs) affect bone metabolism and are frequently associated with the presence of osteopenia, osteoporosis, and increased risk of fractures. Although several mechanisms may contribute to skeletal abnormalities in IBD patients, inflammation and inflammatory mediators such as TNF, IL-1β, and IL-6 may be the most critical. It is not clear whether the changes in bone metabolism leading to decreased mineral density are the result of decreased bone formation, increased bone resorption, or both, with varying results reported in experimental models of IBD and in pediatric and adult IBD patients. New data, including our own, challenge the conventional views, and contributes to the unraveling of an increasingly complex network of interactions leading to the inflammation-associated bone loss. Since nutritional interventions (dietary calcium and vitamin D supplementation) are of limited efficacy in IBD patients, understanding the pathophysiology of osteopenia and osteoporosis in Crohn's disease and ulcerative colitis is critical for the correct choice of available treatments or the development of new targeted therapies. In this review, we discuss current concepts explaining the effects of inflammation, inflammatory mediators and their signaling effectors on calcium and phosphate homeostasis, osteoblast and osteoclast function, and the potential limitations of vitamin D used as an immunomodulator and anabolic hormone in IBD.

Indexed as

Calcification, PhysiologicAnimalsBone Diseases, MetabolicCalciumColitis, UlcerativeCrohn DiseaseGastroenterologyHomeostasisHormonesHumansImmunologic FactorsInflammation MediatorsMetabolismOsteoblastsOsteoclastsOsteoporosisCalciumHormonesImmunologic FactorsInflammation MediatorsPhosphatesVitamin D

Identifiers

PMID21088237
PMCPMC3043650
OpenAlexW2134325452

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.