Evidence map›Paper›PMID 33716975›Full record

ReviewFrontiers in endocrinology2021

Familial Hyperparathyroidism.

Jenny E Blau, William F Simonds

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. [Primary hyperparathyroidism in children].Problemy endokrinologii · 2023
    Observational
  10. A Knock-In Mouse Model of theJournal of the Endocrine Society · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Metabolic Bone Diseases and New Drug Developments.Biomolecules & therapeutics · 2022
    Review
  17. Review
  18. Parathyroid Tumors: Molecular Signatures.International journal of molecular sciences · 2021
    Review
  19. Targeted Next-Generation Sequencing ofIndian journal of endocrinology and metabolism
    Article
  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

2 authors at 2 institutions in 1 country.

Jenny E BlauEarly Clinical Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, United States.
William F SimondsMetabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States.
AstraZeneca (United States) · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Hyperparathyroidism-- Etiology, Diagnosis And TreatmentZIADK043006 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JHA, SMITA · 2011 to 2025
$8.9M
Clinical Investigation of FIHP, Parathyroid Cancer & the HPT-JT SyndromeZIADK043012 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONDS, WILLIAM F · 2009 to 2025
$4.3M
Intramural NIH HHS ZIA DK043012
6 · The paper itself

Abstract

Regulation of the serum calcium level in humans is achieved by the endocrine action of parathyroid glands working in concert with vitamin D and a set of critical target cells and tissues including osteoblasts, osteoclasts, the renal tubules, and the small intestine. The parathyroid glands, small highly vascularized endocrine organs located behind the thyroid gland, secrete parathyroid hormone (PTH) into the systemic circulation as is needed to keep the serum free calcium concentration within a tight physiologic range. Primary hyperparathyroidism (HPT), a disorder of mineral metabolism usually associated with abnormally elevated serum calcium, results from the uncontrolled release of PTH from one or several abnormal parathyroid glands. Although in the vast majority of cases HPT is a sporadic disease, it can also present as a manifestation of a familial syndrome. Many benign and malignant sporadic parathyroid neoplasms are caused by loss-of-function mutations in tumor suppressor genes that were initially identified by the study of genomic DNA from patients who developed HPT as a manifestation of an inherited syndrome. Somatic and inherited mutations in certain proto-oncogenes can also result in the development of parathyroid tumors. The clinical and genetic investigation of familial HPT in kindreds found to lack germline variants in the already known HPT-predisposition genes represents a promising future direction for the discovery of novel genes relevant to parathyroid tumor development.

Indexed as

Genetic Predisposition to DiseaseCalciumHumansHyperparathyroidismMutationParathyroid GlandsParathyroid HormoneCalciumParathyroid HormoneCASRCDC73GCM2jaw tumor syndromeMEN1multiple endocrine neoplasiaoncogenetumor suppressor

Identifiers

PMID33716975
PMCPMC7947864
OpenAlexW4205755407

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.