Evidence map›Paper›PMID 34850000›Full record

ArticleThe Journal of clinical endocrinology and metabolism2022

Risk Factors for and Effects of Persistent and Severe Hypophosphatemia Following Ferric Carboxymaltose.

Benedikt Schaefer, Heinz Zoller, Myles Wolf

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Hypophosphatemia attenuates improvements in vitality after intravenous iron treatment in patients with inflammatory bowel disease.Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation · 2024
    Trial
  4. Trial
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

3 authors at 2 institutions in 2 countries.

Benedikt SchaeferChristian Doppler Laboratory of Iron and Phosphate Biology at the Department of Medicine I, Medical University of Innsbruck, Innsbruck, Austria.
Heinz ZollerChristian Doppler Laboratory of Iron and Phosphate Biology at the Department of Medicine I, Medical University of Innsbruck, Innsbruck, Austria.
Myles WolfDivision of Nephrology, Department of Medicine, Duke Clinical Research Institute, Duke University School of Medicine, Durham, NC, USA.ORCID 0000-0002-1127-1442
Innsbruck Medical University · ATDuke University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextHypophosphatemia, osteomalacia, and fractures are complications of certain intravenous iron formulations.

objectiveThis study investigated risk factors for incident, severe, and persistent hypophosphatemia, and associated alterations in bone and mineral biomarkers following intravenous iron treatment.

methodsWe analyzed data from the PHOSPHARE-IDA randomized clinical trials, comprising 245 patients aged 18 years or older with iron deficiency anemia at 30 outpatient clinics in the United States who received intravenous ferric carboxymaltose (FCM) or ferric derisomaltose (FDI). Outcome measures included serum phosphate, intact fibroblast growth factor-23 (iFGF23), 1,25-dihydroxyvitamin D (1,25(OH)2D), ionized calcium, parathyroid hormone (PTH), and alkaline phosphatase.

resultsFCM was the only consistent risk factor for incident hypophosphatemia (< 2.0 mg/dL; odds ratio vs FDI: 38.37; 95% CI: 16.62, 88.56; P < 0.001). Only FCM-treated patients developed severe hypophosphatemia (< 1.0 mg/dL; 11.3%; 13/115) or persistent hypophosphatemia (< 2.0 mg/dL at study end; 40.0%; 46/115). More severe hypophosphatemia associated with significantly greater increases in iFGF23, PTH, and alkaline phosphatase, and more severe decreases in 1,25(OH)2D and ionized calcium (all P < 0.05). Patients with persistent vs resolved hypophosphatemia demonstrated significantly greater changes in iFGF23, PTH, 1,25(OH)2D, and N-terminal procollagen-1 peptide levels (all P < 0.01), but alkaline phosphatase increased similarly in both groups.

conclusionTreatment with FCM was the only consistent risk factor for hypophosphatemia. Patients who developed severe or persistent hypophosphatemia after FCM treatment manifested more severe derangements in bone and mineral metabolism. Changes in bone biomarkers continued beyond resolution of hypophosphatemia, suggesting ongoing effects on bone that may help explain the association of FCM with osteomalacia and fractures.

Indexed as

Anemia, Iron-DeficiencyFamilial Hypophosphatemic RicketsHypophosphatemiaOsteomalaciaAlkaline PhosphataseBiomarkersCalciumDisaccharidesFemaleFerric CompoundsHumansIronMaleMaltoseMineralsParathyroid HormoneAlkaline PhosphataseBiomarkersCalciumDisaccharidesferric carboxymaltoseFerric Compoundsferric derisomaltoseIronMaltoseMineralsParathyroid Hormonealkaline phosphataseclinical trialsFGF23hypophosphatemiaintravenous ironPTH

Identifiers

PMID34850000
PMCPMC8947794
OpenAlexW3217248635

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.