Endocrine Abstracts

Background: An acute fragility fracture is considered a ’bone attack,’ necessitating prompt treatment of osteoporosis. Standard clinical practice involves assessing the patient’s clinical status, comorbidities, and secondary causes of osteoporosis, influencing the choice between osteoanabolic or antiresorptive therapy. Normocalcemic hyperparathyroidism is common among fragility fracture patients. While it is commonly associated with vitamin D deficiency and chronic kidney disease, this study aims to investigate other variables that may also influence parathyroid hormone (PTH) levels.

Methods: Within the Fracture Liaison Service, we retrospectively studied 249 consecutive patients aged 50 and above with no prior anti-osteoporotic therapy, hospitalized for acute fragility fractures (hip, vertebra, distal forearm, humerus, pelvis). Participants were categorized into two groups based on normal or high PTH levels, excluding those with typical primary hyperparathyroidism. We analyzed the prevalence of secondary causes of osteoporosis (vitamin D deficiency, chronic kidney disease, premature menopause, hyperthyroidism, malabsorption, monoclonal gammopathy, use of corticosteroids, aromatase inhibitors, and chemotherapy), as well as the presence of diabetes and malignancies. We also collected data on serum creatinine, albumin, calcium, phosphorus, 25-hydroxy vitamin D, leukocytes, and CRP, and calcium in urine samples.

Results: Among all participants, 91 (36.5%) had high PTH, and 158 (63.5%) had normal PTH levels. Patients with high PTH were older, less likely to receive vitamin D supplementation before the fracture, and showed a higher prevalence of aggregated secondary causes of osteoporosis and diabetes (p≤0.01). Secondary causes of osteoporosis, excluding hyperparathyroidism and chronic kidney disease, were more common in the normal PTH group (P<0.01). No difference in malignant disease presence was observed between groups. The high PTH group had significantly higher creatinine but lower albumin, albumin-corrected calcium, phosphorus, urine calcium, and 25-hydroxy vitamin D (P<0.05). CRP at admission was also significantly higher in this group (P=0.028), while leukocyte count showed no difference. In the multiple regression model, PTH levels were independently predicted by higher creatinine, lower 25-hydroxy vitamin D, albumin-corrected serum calcium, urine calcium, and phosphorus. Diabetes, female gender, and advanced age entered as independent predictors of PTH too (R2=0.37).

Conclusion: Hyperparathyroidism often prevents or postpones timely osteoanabolic therapy after fragility fractures. It is essential to recognize bone metabolism markers beyond the conventional ones that impact elevated PTH levels and to intervene accordingly. The modest proportion of variance explained by standard laboratory and clinical parameters in our model suggests the presence of other unknown variables influencing PTH levels, emphasizing the need for further investigation.