Evidence map›Paper›PMID 29049872›Full record

ReviewBritish journal of clinical pharmacology2018

Optimal dosing and delivery of parathyroid hormone and its analogues for osteoporosis and hypoparathyroidism - translating the pharmacology.

Donovan Tay, Serge Cremers, John P Bilezikian

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of clinical pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Advances in Parathyroid Hormone-based medicines.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Metabolic Bone Diseases and New Drug Developments.Biomolecules & therapeutics · 2022
    Review
  18. Article
  19. Article
  20. 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

3 authors at 3 institutions in 2 countries.

Donovan TayDepartment of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.ORCID 0000-0002-2192-2245
Serge CremersDepartment of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
John P BilezikianDepartment of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Columbia University · USColumbia University Irving Medical Center · USSingapore General Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In primary hyperparathyroidism (PHPT), bone loss results from the resorptive effects of excess parathyroid hormone (PTH). Under physiological conditions, PTH has actions that are more targeted to homeostasis and to bone accrual. The predominant action of PTH, either catabolic, anabolic or homeostatic, can be understood in molecular and pharmacokinetic terms. When administered intermittently, PTH increases bone mass, but when present continuously and in excess (e.g. PHPT), bone loss ensues. This dual effect of PTH depends not only on the dosing regimen, continuous or intermittent, but also on how the PTH molecule interacts with various states of its receptor (PTH/PTHrP receptor) influencing downstream signalling pathways differentially. Altering the amino-terminal end of PTH or PTHrP could emphasize the state of the receptor that is linked to an osteoanabolic outcome. This concept led to the development of a PTHrP analogue that interacts preferentially with the transiently linked state of the receptor, emphasizing an osteoanabolic effect. However, designing PTH or PTHrP analogues with prolonged state of binding to the receptor would be expected to be linked to a homeostatic action associated with the tonic secretory state of the parathyroid glands that is advantageous in treating hypoparathyroidism. Ideally, further development of a drug delivery system that mimics the physiological tonic, circadian, and pulsatile profile of PTH would be optimal. This review discusses basic, translational and clinical studies that may well lead to newer approaches to the treatment of osteoporosis as well as to different PTH molecules that could become more advantageous in treating hypoparathyroidism.

Indexed as

Drug Delivery SystemsTranslational Research, BiomedicalBone and BonesBone DensityDose-Response Relationship, DrugHomeostasisHumansHypoparathyroidismOsteoporosisParathyroid HormoneProtein BindingReceptor, Parathyroid Hormone, Type 1Parathyroid HormoneReceptor, Parathyroid Hormone, Type 1abaloparatideclinical pharmacologyhypoparathyroidismosteoporosisparathyroid hormoneprimary hyperparathyroidismPTHPTHrP

Identifiers

PMID29049872
PMCPMC5777439
OpenAlexW2801829254

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.