Evidence map›Paper›PMID 32409880›Full record

ReviewCalcified tissue international2021

Congenital Conditions of Hypophosphatemia Expressed in Adults.

Gemma Marcucci, Maria Luisa Brandi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Calcified tissue international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Osteomalacia Is Not a Single Disease.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Article
  7. Burden of disease and clinical targets in adult patients with X-linked hypophosphatemia. A comprehensive review.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Phosphate Metabolism.Calcified tissue international · 2021
    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

2 authors at 1 institution in 1 country.

Gemma MarcucciBone Metabolic Diseases Unit, Department of Biomedical, Experimental and Clinical Sciences, University of Florence, AOU Careggi, Florence, Italy.
Maria Luisa BrandiBone Metabolic Diseases Unit, Department of Biomedical, Experimental and Clinical Sciences, University of Florence, AOU Careggi, Florence, Italy. marialuisa.brandi@unifi.it.
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main congenital conditions of hypophosphatemia expressed in adulthood include several forms of hereditary hypophosphatemic rickets and a congenital disorder of vitamin D metabolism characterized by osteomalacia and hypophosphatemia in adult patients. Hypophosphatemia in adults is defined as serum phosphate concentration < 0.80 mmol/L. The principal regulators of phosphate homeostasis, as is well known, are parathyroid hormone (PTH), activated vitamin D, and Fibroblast Growth Factor 23 (FGF23). Differential diagnosis of hypophosphatemia is based on the evaluation of mechanisms leading to this alteration, such as high PTH activity, inadequate phosphate absorption from the gut, or renal phosphate wasting, either due to primary tubular defects or high FGF23 levels. The most common inherited form associated to hypophosphatemia is X-linked hypophosphatemic rickets (XLH), caused by PHEX gene mutations with enhanced secretion of the FGF23. Until now, the management of hypophosphatemia in adulthood has been poorly investigated. It is widely debated whether adult patients benefit from the conventional treatments normally used for pediatric patients. The new treatment for XLH with burosumab, a recombinant human IgG1 monoclonal antibody that binds to FGF23, blocking its activity, may change the pharmacological management of adult subjects with hypophosphatemia associated to FGF23-dependent mechanisms.

Indexed as

Familial Hypophosphatemic RicketsHypophosphatemiaOsteomalaciaAdultAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedFibroblast Growth Factor-23Fibroblast Growth FactorsHumansPHEX Phosphate Regulating Neutral EndopeptidasePhosphatesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedburosumabFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsPHEX Phosphate Regulating Neutral EndopeptidasePHEX protein, humanPhosphates1,25-dihydroxyvitamin DHereditaryHypophosphatemiaRickets

Identifiers

PMID32409880
OpenAlexW3025536851

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.