Evidence map›Paper›PMID 38038882›Full record

ReviewHormones (Athens, Greece)2024

Genetics of hereditary forms of primary hyperparathyroidism.

Katherine A English, Kate E Lines, Rajesh V Thakker

Open access · hybridAbstract readReview
In one paragraph

Review in Hormones (Athens, Greece), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  7. Genotype-Phenotype Correlations in the Hyperparathyroidism-Jaw Tumor Syndrome.The Journal of clinical endocrinology and metabolism · 2025
    Review
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  12. Article
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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 1 institution in 1 country.

Katherine A EnglishOCDEM, Radcliffe Department of Medicine, Churchill Hospital, University of Oxford, Oxford, OX3 7LJ, UK.ORCID http://orcid.org/0000-0003-1439-1834
Kate E LinesOCDEM, Radcliffe Department of Medicine, Churchill Hospital, University of Oxford, Oxford, OX3 7LJ, UK.ORCID http://orcid.org/0000-0002-0764-8681
Rajesh V ThakkerOCDEM, Radcliffe Department of Medicine, Churchill Hospital, University of Oxford, Oxford, OX3 7LJ, UK. rajesh.thakker@ndm.ox.ac.uk.ORCID http://orcid.org/0000-0002-1438-3220
Churchill Hospital · GB

Funding

Cancer Research UK C2195/A28699
6 · The paper itself

Abstract

Primary hyperparathyroidism (PHPT), a relatively common disorder characterized by hypercalcemia with raised or inappropriately normal serum parathyroid hormone (PTH) concentrations, may occur as part of a hereditary syndromic disorder or as a non-syndromic disease. The associated syndromic disorders include multiple endocrine neoplasia types 1-5 (MEN1-5) and hyperparathyroidism with jaw tumor (HPT-JT) syndromes, and the non-syndromic forms include familial hypocalciuric hypercalcemia types 1-3 (FHH1-3), familial isolated hyperparathyroidism (FIHP), and neonatal severe hyperparathyroidism (NS-HPT). Such hereditary forms may occur in > 10% of patients with PHPT, and their recognition is important for implementation of gene-specific screening protocols and investigations for other associated tumors. Syndromic PHPT tends to be multifocal and multiglandular with most patients requiring parathyroidectomy with the aim of limiting end-organ damage associated with hypercalcemia, particularly osteoporosis, nephrolithiasis, and renal failure. Some patients with non-syndromic PHPT may have mutations of the MEN1 gene or the calcium-sensing receptor (CASR), whose loss of function mutations usually cause FHH1, a disorder associated with mild hypercalcemia and may follow a benign clinical course. Measurement of the urinary calcium-to-creatinine ratio clearance (UCCR) may help to distinguish patients with FHH from those with PHPT, as the majority of FHH patients have low urinary calcium excretion (UCCR < 0.01). Once genetic testing confirms a hereditary cause of PHPT, further genetic testing can be offered to the patients' relatives and subsequent screening can be carried out in these affected family members, which prevents inappropriate testing in normal individuals.

Indexed as

AdenomaFibromaHypercalcemiaHyperparathyroidismHyperparathyroidism, PrimaryJaw NeoplasmsCalciumHumansInfant, NewbornCalciumCalcium-sensing receptorMultiple endocrine neoplasiaParathyroidPHPT

Identifiers

PMID38038882
PMCPMC10847196
OpenAlexW4389244307

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Registered trials

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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.