Research Article | Open Access
Pathological Fractures Following Parathyroidectomy: Incidence, Risk Factors, and Clinical Outcomes
Dr. K. Sri Harsha, M.S, Dr. G. Harish, M.S
Pages: 419-425
Abstract
Introduction: Primary hyperparathyroidism (PHPT) is a common endocrine disorder characterized by excessive secretion of parathyroid hormone (PTH) leading to hypercalcemia and subsequent bone resorption. Parathyroidectomy is the definitive treatment for PHPT aimed at restoring normal calcium homeostasis. However, some patients may still experience skeletal manifestations post-parathyroidectomy, including pathological fractures. Understanding the incidence, risk factors, and outcomes of pathological fractures post-parathyroidectomy is crucial for optimizing patient care.
Materials and Methods: This retrospective cohort study analyzed electronic medical records of patients with primary hyperparathyroidism who underwent parathyroidectomy. Data included demographics, biochemical markers, preoperative assessments, surgical details, and postoperative outcomes. Statistical analysis included descriptive statistics and logistic regression.
Results: A total of 30 patients were included, with a mean age of 58 years. Biochemical abnormalities and preoperative skeletal fragility were common. Majority underwent focused parathyroidectomy, with 10% experiencing intraoperative complications. Pathological fractures occurred in 16.7% of patients, primarily involving the femoral neck, vertebral, and radial sites. Conservative treatment was preferred, with 80% achieving fracture healing and 70% functional recovery. Age and preoperative bone mineral density were significant risk factors for fractures.
Conclusion: Further research is needed to refine risk stratification and management strategies for reducing the burden of pathological fractures in patients with primary hyperparathyroidism undergoing parathyroidectomy.
Keywords
hyperparathyroidism (PHPT) is a common endocrine disorder characterized by excessive secretion of parathyroid hormone (PTH) leading to hypercalcemia and subsequent bone resorption.