Review examines current endocrine causes of secondary osteoporosis and clinical management approaches.

This comprehensive review addresses endocrine-related secondary osteoporosis, encompassing specific conditions such as hypercortisolism, primary aldosteronism, male hypogonadism, hypercalciuria, and FGF23-dependent phosphate-wasting disorders. The detailed scope focuses on patients with atypical osteoporosis phenotypes, including men, younger adults, and individuals with normal bone mineral density but fragility fractures across diverse clinical settings.

The authors synthesize key pathophysiological mechanisms linking endocrine disorders to bone health. Mild autonomous cortisol secretion is increasingly recognized as a contributor to increased fracture risk. Primary aldosteronism promotes fragility via mineralocorticoid receptor activation, oxidative stress, hypercalciuria, and secondary hyperparathyroidism. Male hypogonadism is identified as a major driver of bone loss, while FGF23-mediated phosphate-wasting disorders impair mineralization. Additionally, the text outlines these mechanisms. These insights inform clinical decision making.

The authors note that prevalence is underestimated within the current literature. Safety data regarding adverse events, serious adverse events, and discontinuations are not reported in available data. Optimal care requires structured endocrine assessment, correction of the primary disorder, and integration with bone-specific therapy where appropriate. ERSOP should be considered in patients with atypical osteoporosis phenotypes. Clinicians must interpret these findings cautiously given the review nature and lack of reported certainty or causality notes. Furthermore, the authors emphasize these points to ensure patient safety.