To highlight evolving concepts, unmet needs, and research opportunities in endocrine-related secondary osteoporosis (ERSOP), emphasizing the importance of timely recognition.
Key Findings:
Mild autonomous cortisol secretion (MACS) increases fracture risk even at near-normal cortisol levels.
Primary aldosteronism (PA) promotes skeletal fragility through mineralocorticoid receptor activation, oxidative stress, and secondary hyperparathyroidism.
Male hypogonadism is a significant contributor to bone loss, necessitating combined hormonal and anti-osteoporotic therapy for fracture prevention.
Differentiating between PTH-dependent and PTH-independent hypercalciuria is essential for effective management.
FGF23-mediated phosphate-wasting disorders can impair mineralization and may respond to targeted therapies.
Interpretation:
ERSOP should be considered in atypical osteoporosis cases, particularly in men, younger adults, and those with normal BMD but fragility fractures, highlighting the need for structured endocrine assessments to improve clinical outcomes.
Limitations:
ERSOP remains underdiagnosed, especially in men and younger patients, impacting patient outcomes.
Current guidelines on screening for MACS among osteoporotic patients are lacking.
Conclusion:
Optimal care for ERSOP requires correction of the primary endocrine disorder and integration with bone-specific therapies, emphasizing the need for structured endocrine assessments.
These 10 states make it more practical for physicians to participate in hospital ownership by aligning statutory structure, corporate practice of medicine rules, and population trends.
