Evidence map›Paper›PMID 32761341›Full record

ArticleHormones & cancer2020

Outcome of Clinical Genetic Testing in Patients with Features Suggestive for Hereditary Predisposition to PTH-Mediated Hypercalcemia.

Shafaq Khairi, Jenae Osborne, Michelle F Jacobs, Gregory T Clines, Barbra S Miller, David T Hughes, Tobias Else

Open access · bronzeAbstract read
In one paragraph

Article in Hormones & cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. American Association of Clinical Endocrinology Consensus Statement on Management of Multiple Endocrine Neoplasia Type 1.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2025
    Guideline
  2. Article
  3. Familial states of primary hyperparathyroidism: an update.Journal of endocrinological investigation · 2024
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. 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

7 authors at 1 institution in 1 country.

Shafaq KhairiDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, University of Michigan, 1150 West Medical Center Drive, Ann Arbor, MI, 48109, USA.
Jenae OsborneDepartment of Internal Medicine, Division of Genetic Medicine, University of Michigan, Ann Arbor, MI, USA.
Michelle F JacobsDepartment of Internal Medicine, Division of Genetic Medicine, University of Michigan, Ann Arbor, MI, USA.
Gregory T ClinesDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, University of Michigan, 1150 West Medical Center Drive, Ann Arbor, MI, 48109, USA.
Barbra S MillerDepartment of Surgery, Division of Endocrine Surgery, University of Michigan, Ann Arbor, MI, USA.
David T HughesDepartment of Surgery, Division of Endocrine Surgery, University of Michigan, Ann Arbor, MI, USA.
Tobias ElseDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, University of Michigan, 1150 West Medical Center Drive, Ann Arbor, MI, 48109, USA. telse@umich.edu.ORCID 0000-0002-2262-0011
University of Michigan · US

Funding

TRAINING PROGRAM IN ENDOCRINOLOGY AND METABOLISM.T32DK007245 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RICHARD J. AUCHUS · 1986 to 2026
$7.2M
NIDDK NIH HHS T32 DK007245NIDDK NIH HHS T32DK007245
6 · The paper itself

Abstract

Primary hyperparathyroidism (pHPT) is associated with familial syndromes such as multiple endocrine neoplasia type 1 (MEN1), 2A (MEN2A), MEN-like syndromes (CDKN1B), and CDC73-related disorder (hyperparathyroidism - jaw tumor syndrome (HPJT)). Familial hypocalciuric hypercalcemia (FHH) caused by CASR variants is an important differential diagnosis for pHPT. In order to evaluate the contribution of hereditary causes to pHPT in patients encountered in a specialized clinic, we conducted a retrospective study on patients with pHPT that underwent germline genetic testing. We evaluated 46 patients referred to a Cancer Genetics Clinic. Reasons for referral were young age (age < 40) for 29 patients (63%), multi-gland disease for 23 patients (50%), and a positive family history of pHPT for 11 patients (24%). All 46 patients underwent genetic evaluation. A total of 11 rare variants were found (CASR (4), CDC73 (2), MEN1 (2) CDKN1B (1), and RET (2)). One MEN1 variant was classified as pathogenic, and all others were variants of uncertain significance (VUS). All patients with CASR variants had clinical features of FHH and were counselled against parathyroidectomy. Both patients with CDC73 variants were counselled about recurrence of pHPT and parathyroid cancer. Neither of the RET variants were MEN2-associated. The CDKN1B variant was regarded as a true VUS and no action was taken. In this study, genetic testing impacted clinical care in 7 (15%) patients. We suggest that all patients < 40 years of age, with multi-gland disease, single gland disease refractory to treatment, and a positive family history for pHPT or associated tumors should be considered for genetic evaluation.

Indexed as

AdultGenetic Predisposition to DiseaseGenetic TestingHumansHypercalcemiaHyperparathyroidism, PrimaryTreatment OutcomeFamilial hypocalciuric hypercalcemiaGenetic predisposition syndromesGermline variantsPrimary hyperparathyroidism

Identifiers

PMID32761341
PMCPMC7945006
OpenAlexW3047071777

What OpenQuestion holds

Textmetadata
LicenceTDM
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.