Evidence map›Paper›PMID 39519190›Full record

ReviewInternational journal of molecular sciences2024

Bone Disease in Primary Hyperparathyroidism-Changes Occurring in Bone Metabolism and New Potential Treatment Strategies.

Mirella Iwanowska, Magdalena Kochman, Alicja Szatko, Wojciech Zgliczyński, Piotr Glinicki

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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. Bone metabolism in primary hyperparathyroidism.Wiener klinische Wochenschrift · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Identification of Surrogate Biomarkers for Mucopolysaccharidosis Type IVA.International journal of molecular sciences · 2025
    Article
  7. Review
  8. Review
  9. Review
  10. 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

5 authors.

Mirella IwanowskaDepartment of Endocrinology, Centre of Postgraduate Medical Education, 01-813 Warsaw, Poland.
Magdalena KochmanDepartment of Endocrinology, Centre of Postgraduate Medical Education, 01-813 Warsaw, Poland.
Alicja SzatkoDepartment of Endocrinology, Centre of Postgraduate Medical Education, 01-813 Warsaw, Poland.
Wojciech ZgliczyńskiDepartment of Endocrinology, Centre of Postgraduate Medical Education, 01-813 Warsaw, Poland.
Piotr GlinickiDepartment of Endocrinology, Centre of Postgraduate Medical Education, 01-813 Warsaw, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary hyperparathyroidism (PHPT) is a common endocrinopathy, predominantly caused by a single parathyroid adenoma that is responsible for the excessive secretion of parathyroid hormone (PTH)-the hallmark of disease. Excess of this hormone causes remarkable changes in bone metabolism, including an increased level of bone remodeling with a predominance of bone resorption. Those changes lead to deterioration of bone structure and density, especially in cortical bone. The main treatment for PHPT is surgical removal of the adenoma, which normalizes PTH levels and terminates the progression of bone disease and leads to its regeneration. However, because not all the patients are suitable candidates for surgery, alternative therapies are needed. Current non-surgical treatments targeting bone disease secondary to PHPT include bisphosphonates and denosumab. Those antiresorptives prevent further bone loss, but they lack the ability to regenerate already degraded bone. There is ongoing research to find targeted drugs capable of halting resorption alongside stimulating bone formation. This review presents the advancements in understanding the molecular mechanisms responsible for bone disease in PHPT and assesses the efficacy of new potential therapeutic approaches (e.g., allosteric inhibitors of the PTH receptor, V-ATPase, or cathepsin inhibitors) aimed at mitigating bone loss and enhancing bone regeneration in affected patients.

Indexed as

Bone and BonesHyperparathyroidism, PrimaryAnimalsBone Density Conservation AgentsBone DiseasesBone RemodelingBone ResorptionDenosumabDiphosphonatesHumansParathyroid HormoneBone Density Conservation AgentsDenosumabDiphosphonatesParathyroid Hormonebone metabolismosteoporosisparathyroid hormoneprimary hyperparathyroidismPTH

Identifiers

PMID39519190
PMCPMC11546563

What OpenQuestion holds

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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.