Evidence map›Paper›PMID 30207609›Full record

ReviewBritish journal of clinical pharmacology2019

Pharmacological management of X-linked hypophosphataemia.

Erik A Imel, Kenneth E White

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of clinical pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Observational
  2. Article
  3. Article
  4. Observational
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  6. Article
  7. Observational
  8. Article
  9. Review
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  11. Article
  12. The Osteocyte: New Insights.Annual review of physiology · 2020
    Review
  13. Review
  14. Drugs for the treatment of metabolic bone diseases.British journal of clinical pharmacology · 2019
    Article
  15. Pharmacological management of X-linked hypophosphataemia.British journal of clinical pharmacology · 2019
    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.

Erik A ImelDepartment of Medicine, Division of Endocrinology and Metabolism, Indiana University School of Medicine, Indianapolis, IN, USA.
Kenneth E WhiteDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Indiana University – Purdue University Indianapolis · US

Funding

Resource CoreP30AR072581 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI Sharon M Moe · 2017 to 2026
$8.3M
NIAMS NIH HHS P30 AR072581
6 · The paper itself

Abstract

The most common heritable disorder of renal phosphate wasting, X-linked hypophosphataemia (XLH), was discovered to be caused by inactivating mutations in the phosphate regulating gene with homology to endopeptidases on the X-chromosome (PHEX) gene in 1995. Although the exact molecular mechanisms by which PHEX mutations cause disturbed phosphate handling in XLH remain unknown, focus for novel therapies has more recently been based upon the finding that the bone-produced phosphaturic hormone fibroblast growth factor-23 is elevated in XLH patient plasma. Previous treatment strategies for XLH were based upon phosphate repletion plus active vitamin D analogues, which are difficult to manage, fail to address the primary pathogenesis of the disease, and can have deleterious side effects. A novel therapy for XLH directly targeting fibroblast growth factor-23 via a humanized monoclonal antibody (burosumab-twza/CRYSVITA, henceforth referred to just as burosumab) has emerged as an effective, and recently approved, pharmacological treatment for both children and adults. This review will provide an overview of the clinical manifestations of XLH, the molecular pathophysiology, and summarize its current treatment.

Indexed as

Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedBiomarkersFamilial Hypophosphatemic RicketsFibroblast Growth Factor-23Fibroblast Growth FactorsGenetic Predisposition to DiseaseHumansMutationPhenotypePHEX Phosphate Regulating Neutral EndopeptidaseTreatment OutcomeUp-RegulationAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedBiomarkersburosumabFibroblast Growth Factor-23Fibroblast Growth FactorsPHEX Phosphate Regulating Neutral EndopeptidasePHEX protein, humanburosumab-twzafibroblast growth factor 23PHEXX-linked hypophosphataemia

Identifiers

PMID30207609
PMCPMC6533442
OpenAlexW2889946405

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.