Skeletal abnormalities in Hypoparathyroidism and in Primary Hyperparathyroidism.


Journal

Reviews in endocrine & metabolic disorders
ISSN: 1573-2606
Titre abrégé: Rev Endocr Metab Disord
Pays: Germany
ID NLM: 100940588

Informations de publication

Date de publication:
12 2021
Historique:
accepted: 11 11 2020
pubmed: 18 11 2020
medline: 15 3 2022
entrez: 17 11 2020
Statut: ppublish

Résumé

Both hypoparathyroidism (HypoPT), as well as its pathological counterpart, primary hyperparathyroidism (PHPT), can lead to skeletal abnormalities. Chronic deficiency of PTH in patients with HypoPT is associated with a profound reduction in bone remodeling, with consequent increases in bone density, and abnormalities in microarchitecture and bone strength. It is still not clear whether there is an increase in fracture risk in HypoPT. While standard therapy with calcium supplements and active vitamin D does not restore bone homeostasis, treatment of HypoPT with PTH appears to correct some of those abnormalities. In PHPT, the continuous exposure to high levels of PTH causes an increase in bone remodeling, in which bone resorption prevails. In the symptomatic form of PHPT, patients can present with fragility fractures, and/or the classical radiological features of osteitis fibrosa cystica. However, even in mild PHPT, catabolic skeletal actions of PTH are evident through reduced BMD, deterioration of bone microarchitecture and increased risk of fragility fractures. Successful parathyroidectomy improves skeletal abnormalities. Medical treatment, such as bisphosphonates and denosumab, can also increase bone density in patients with PHPT who do not undergo surgery. This article reviews skeletal involvement in HypoPT and in PHPT, as assessed by bone remodeling, DXA, trabecular bone score, and quantitative computed tomography, as well as data on bone strength and fracture risk. The effects of PTH replacement on the skeleton in subjects with HypoPT, and the outcome of parathyroidectomy in patients with PHPT, are also reviewed here.

Identifiants

pubmed: 33200346
doi: 10.1007/s11154-020-09614-0
pii: 10.1007/s11154-020-09614-0
doi:

Substances chimiques

Parathyroid Hormone 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

789-802

Subventions

Organisme : NIH HHS
ID : NIH DK32333
Pays : United States

Informations de copyright

© 2020. Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Barbara C Silva (BC)

Department of Medicine, Centro Universitario de Belo Horizonte - UNI BH, Belo Horizonte, Brazil.
Endocrinology Unit, Felicio Rocho Hospital, Belo Horizonte, Brazil.
Endocrinology Unit, Santa Casa Hospital, Belo Horizonte, Brazil.

John P Bilezikian (JP)

Metabolic Bone Diseases Unit, Division of Endocrinology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, 630 W. 168th Street, PH 8E: 105G, New York, NY, 10032, USA. jpb2@columbia.edu.

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