Evidence map›Paper›PMID 30361844›Full record

ArticleEndocrine pathology2018

A Young Male with Parafibromin-Deficient Parathyroid Carcinoma Due to a Rare Germline HRPT2/CDC73 Mutation.

Alisha Kapur, Narendra Singh, Ozgur Mete, Robert A Hegele, I George Fantus

Abstract readCase Reports
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In one paragraph

Article in Endocrine pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. The Consistency ofInternational journal of endocrinology · 2025
    Review
  3. Article
  4. 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

5 authors at 3 institutions in 1 country.

Alisha KapurDepartment of Medicine and Biochemistry and London Regional Genomics Centre, Robarts Research Institute, Western University, London, ON, N6A 5B7, Canada.
Narendra SinghDivision of Endocrinology and Metabolism, Department of Medicine, University of Toronto and Mount Sinai Hospital, Toronto, ON, M5T 3L9, Canada.
Ozgur MeteDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5G 2C4, Canada.
Robert A HegeleDepartment of Medicine and Biochemistry and London Regional Genomics Centre, Robarts Research Institute, Western University, London, ON, N6A 5B7, Canada.
I George FantusDivision of Endocrinology and Metabolism, Department of Medicine, University of Toronto and Mount Sinai Hospital, Toronto, ON, M5T 3L9, Canada. george.fantus@mcgill.ca.
University of Toronto · CAWestern University · CAMount Sinai Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperparathyroidism, commonly observed in asymptomatic middle-aged women, with mild hypercalcemia, is usually caused by a benign adenoma. Some cases present with more severe manifestation and greater hypercalcemia. Within this spectrum, several familial/genetic associations have been discovered. While the majority are caused by benign disease, adenomas, or hyperplasia, a small proportion (< 1%) are associated with malignant tumors and present with more severe symptoms. Although usually sporadic, recent reports document various gene mutations that strongly predispose to the development of parathyroid carcinoma. An increasing number of cases of hyperparathyroidism, benign or malignant, require and benefit from genetic analysis. We describe a 25-year-old male with hyperparathyroidism presenting with a pathological fracture, brown tumors, hypercalcemia, and markedly elevated parathyroid hormone levels. There was no family history of hyperparathyroidism or jaw tumors. Surgical removal revealed a single large tumor confirmed to be malignant. Immunohistochemical analysis revealed the absence of parafibromin and decreased APC (adenomatosis polyposis coli) expression. Genetic analysis revealed a rare germline nonsense mutation (R76X) in the parafibromin gene, HRPT2/CDC73. Parathyroid carcinoma should be suspected as a cause of hyperparathyroidism when clinical manifestations are severe, particularly in young individuals, < 59 years. Immunohistochemistry may lead to suspicion for a germline mutation as a significant contributor despite absence of a family history. The discovery of a germline mutation in parathyroid carcinoma alters the clinical management of the index case and that of family members. Long-term follow-up studies of such patients are necessary to develop evidence-based clinical guidelines.

Indexed as

AdultGenetic Predisposition to DiseaseGerm-Line MutationHumansHyperparathyroidismMaleParathyroid NeoplasmsTumor Suppressor ProteinsCDC73 protein, humanTumor Suppressor ProteinsHRPT2/CDC73ParafibrominParathyroid carcinoma

Identifiers

PMID30361844
OpenAlexW2898394488

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.