Abstract
Primary hyperparathyroidism continues to increase in prevalence. It is characterized by inappropriate parathyroid hormone production from one or more parathyroid glands leading to hypercalcemia. The diagnosis is biochemical and clinical presentation is heterogenous. This may include neurocognitive, constitutional, musculoskeletal, and/or genitourinary signs and symptoms. The majority of patients with primary hyperparathyroidism have a solitary adenoma, although multigland disease is present in up to 20% of patients. Preoperative imaging should include cervical ultrasonography, which may identify concurrent thyroid pathology. It may also include other imaging modalities such as sestamibi and/or four-dimensional computed tomography for improved sensitivity and specificity. Although imaging may help limit the extent of surgery, nonlocalizing imaging should not preclude surgery. Surgery is the only curative option for primary hyperparathyroidism, and surgeons should be familiar with the various intraoperative adjuncts that may aid in successful parathyroidectomy. These include intraoperative parathyroid hormone monitoring, bilateral internal jugular vein sampling, gamma probe mediated localization, and gland confirmation techniques. However, none of these replaces a thorough understanding of parathyroid anatomy and embryology. Parathyroidectomy may be performed via a minimally invasive approach or bilateral exploration. The choice of operative approach is dependent on preoperative imaging, the availability of intraoperative parathyroid hormone monitoring, and surgeon experience and preference. Although the risks of parathyroidectomy are low, temporary hypoparathyroidism is quite common and routine postoperative calcium supplementation should be considered. Surgical cure after parathyroidectomy is defined as calcium homeostasis for at least 6 months postoperatively and is achieved in more than 95% of cases.