Endocrine-related osteoporosis: the state of the art
Abstract
Background: Endocrine-related secondary osteoporosis (ERSOP) comprises disorders in which bone fragility results from hormonal abnormalities other than age-related or menopausal hypogonadism. Its prevalence is underestimated, and timely recognition is essential because many forms improve or reverse when the underlying endocrine disturbance is corrected.
Objective: This Review highlights the evolving concepts, unmet needs, and research opportunities in ERSOP, with focus on hypercortisolism, primary aldosteronism, male hypogonadism, hypercalciuria, and FGF23-dependent phosphate-wasting disorders.
Recent findings: Mild autonomous cortisol secretion (MACS) is increasingly recognized as a contributor to fracture risk even at near-normal cortisol levels.Primary aldosteronism promotes skeletal fragility via mineralocorticoid receptor activation, oxidative stress, hypercalciuria, and secondary hyperparathyroidism.Male hypogonadism is a major driver of bone loss, and optimal fracture prevention may require combined hormonal and anti-osteoporotic therapy.Differentiating PTH-dependent from PTH-independent hypercalciuria is crucial for management.FGF23-mediated phosphate-wasting disorders impair mineralization and may respond to targeted therapy, including burosumab.
Conclusion: ERSOP should be considered in patients with atypical osteoporosis phenotypes, including men, younger adults, and individuals with normal BMD but fragility fractures. Optimal care requires structured endocrine…
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