Bone Disease in Primary Hyperparathyroidism

Primary Hyperparathyroidism (PHPT) is a common endocrine disorder characterized by autonomous secretion of parathyroid hormone (PTH) leading to hypercalcemia.Whereas bone mineral density (BMD) is generally preserved at skeletal sites rich in trabecular bone, such as the lumbar spine (LS), studies, using peripheral quantitative computed tomography (pQC) and high-resolution peripheral quantitative computed tomography (HR-pQC), have revealed disruption of both cortical and trabecular bone microarchitecture, even in the contemporary 'asymptomatic' form of the disease, highlighting the catabolic effect of PHPT on bone.Moreover, epidemiological studies reported increased fracture risk in patients with PHPT, even in those with BMD T-score within normal or osteopenic range, suggesting that there is a discrepancy between BMD and fracture risk in patients with PHPT and that new diagnostic methods are needed for assessing bone fragility in this population.Surgery is the only definitive treatment for PHPT.Non-surgical treatment is recommended in patients who do not meet the criteria for surgical management, in patients who deny surgical treatment or are high-risk surgical patients.The most frequently used agents are bisphosphonates, denosumab, cinacalcet and vitamin D supplementation.

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Publication Details

Journal
Journal of Musculoskeletal and Neuronal Interactions
Published
2025-11-30
DOI
https://doi.org/10.22540/jmni-25-486
Primary Topic
Parathyroid Disorders and Treatments
Type
article
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article

Bone Disease in Primary Hyperparathyroidism

Ioannis Vlamis, Eva N. Kassi, Ismene Dontas, Efstathios Chronopoulos et al.
Journal of Musculoskeletal and Neuronal Interactions
Parathyroid Disorders and Treatments
article

Bone Disease in Primary Hyperparathyroidism

Ioannis Vlamis, Eva N. Kassi, Ismene Dontas, Efstathios Chronopoulos, Efthymia Karlafti, Symeon Tournis, Ιrene Lambrinoudaki
article en

Abstract

Primary Hyperparathyroidism (PHPT) is a common endocrine disorder characterized by autonomous secretion of parathyroid hormone (PTH) leading to hypercalcemia.Whereas bone mineral density (BMD) is generally preserved at skeletal sites rich in trabecular bone, such as the lumbar spine (LS), studies, using peripheral quantitative computed tomography (pQC) and high-resolution peripheral quantitative computed tomography (HR-pQC), have revealed disruption of both cortical and trabecular bone microarchitecture, even in the contemporary 'asymptomatic' form of the disease, highlighting the catabolic effect of PHPT on bone.Moreover, epidemiological studies reported increased fracture risk in patients with PHPT, even in those with BMD T-score within normal or osteopenic range, suggesting that there is a discrepancy between BMD and fracture risk in patients with PHPT and that new diagnostic methods are needed for assessing bone fragility in this population.Surgery is the only definitive treatment for PHPT.Non-surgical treatment is recommended in patients who do not meet the criteria for surgical management, in patients who deny surgical treatment or are high-risk surgical patients.The most frequently used agents are bisphosphonates, denosumab, cinacalcet and vitamin D supplementation.

Journal of Musculoskeletal and Neuronal InteractionsVol. 25(4)
National and Kapodistrian University of Athens (GR), Laiko General Hospital of Athens (GR), Aretaeio Hospital (GR), KAT General Hospital of Attica (GR)
Openalex Percentile: Top 55%
Parathyroid Disorders and Treatments
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