Evidence map›Paper›PMID 36213261›Full record

ArticleFrontiers in endocrinology2022

A novel

Qingyao Zuo, Weili Yang, Baoyue Liu, Dong Yan, Zhixin Wang, Hong Wang, Wei Deng, Xi Cao, Jinkui Yang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 31% 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, 5 citations in OpenAlex.

  1. Emerging concepts on the FGF23 regulation and activity.Molecular and cellular biochemistry · 2025
    Review
  2. Article
  3. Structural and molecular imaging-based characterization of soft tissue and vascular calcification in hyperphosphatemic familial tumoral calcinosis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
    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

9 authors at 4 institutions in 1 country.

Qingyao ZuoDepartment of Endocrinology, Beijing Jishuitan Hospital, Beijing, China.
Weili YangBeijing Diabetes Institute, Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Baoyue LiuDepartment of Pathology, Beijing Jishuitan Hospital, Beijing, China.
Dong YanDepartment of Radiology, Beijing Jishuitan Hospital, Beijing, China.
Zhixin WangDepartment of Endocrinology, Beijing Jishuitan Hospital, Beijing, China.
Hong WangDepartment of Endocrinology, Beijing Jishuitan Hospital, Beijing, China.
Wei DengDepartment of Endocrinology, Beijing Jishuitan Hospital, Beijing, China.
Xi CaoBeijing Diabetes Institute, Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Jinkui YangBeijing Diabetes Institute, Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Beijing Jishuitan Hospital · CNCapital Medical University · CNPeking University · CNBeijing Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hyperphosphatemic familial tumoral calcinosis (HFTC) is a rare disease characterized by hyperphosphatemia and ectopic calcification, predominantly at periarticular locations. This study was performed to characterize the clinical profile of tumoral calcinosis and to identify gene mutations associated with HFTC and elucidated its pathogenic role. Methods: The three subjects (two male and one female) were aged 30, 25 and 15 years, respectively. The clinical features, histopathological findings, and outcomes of three subjects with HFTC were retrospectively reviewed. The three subjects were analyzed for Results: All subjects had hyperphosphatemia and elevated calcium-phosphorus product. Calcinosis positions included the left shoulder, left index finger, and right hip. Bone and joint damage were present in two cases and multiple foci influenced body growth in one case. The histopathological features were firm, rubbery masses comprising multiple nodules of calcified material bordered by the proliferation of mononuclear or multinuclear macrophages, osteoclastic-like giant cells, fibroblasts, and chronic inflammatory cells. The novel mutation c.484A>G (p.N162D) in exon 3 of Conclusion: We identified a novel

Indexed as

CalcinosisHyperostosis, Cortical, CongenitalHyperphosphatemiaCalciumFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsGlycosylationHumansMaleMutant ProteinsMutationPhosphorusRetrospective StudiesWheat Germ AgglutininsCalciumFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsMutant ProteinsPhosphorusWheat Germ Agglutininsfibroblast growth factor 23glycosylationhyperphosphatemiamutationtumoral calcinosis

Identifiers

PMID36213261
PMCPMC9540505
OpenAlexW4296823088

What OpenQuestion holds

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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.