E2171. Hyperparathyroidism in Musculoskeletal Radiology: A Review of the Radiographic Manifestations of Hyperparathyroidism
  1. Robert Taylor Bragg; LSU Health Sciences Center
  2. Caroline Galliano; LSU Health Sciences Center
  3. Mark Froom; LSU Health Sciences Center
Hyperparathyroidism is the pathologic state of elevated parathyroid hormone levels and can present due to primary, secondary or tertiary causes. The mechanism behind bone manifestations of the disease involves the dysregulation of serum calcium and phosphate involved in bone turnover. Parathyroid hormone (PTH) binds to receptors on osteoclasts in bone, stimulating bone resorption. In the setting of chronic kidney disease, phosphate retention and decreased serum calcium due to kidney dysfunction causes the release of more PTH. This results in secondary hyperparathyroidism, the predominant cause of increased bone turnover in renal osteodystrophy. Progression of disease without treatment and irreversible disruption of the parathyroid–bone–kidney feedback loop leads to severe hypercalcemia, hyperphosphatemia, and hyperparathyroidism, known as tertiary hyperparathyroidism. The hormonal and metabolic dysregulations described above manifest radiographically as skeletal disease and allows the radiologist to communicate with the referring physician about the presence, progression, or complications of this disease state.

Educational Goals / Teaching Points
The objective of this educational exhibit is to review the radiologic characteristics and findings associated with hyperparathyroidism through radiography, computed tomography (CT), and magnetic resonance imaging (MRI). The underlying pathophysiology will also be reviewed to correlate the clinical presentation of the disease with radiographic findings.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
This educational exhibit will be a visual guide on reviewing the radiographic musculoskeletal manifestations of hyperparathyroidism and the characteristic findings on radiography and cross sectional imaging. A differential diagnosis will be discussed to include any mimics of these findings. Additionally, pathophysiology, associated eponyms, disease complications, and clinical correlations will be reviewed.

It is imperative that the radiologist understands the radiographic findings of hyperparathyroidism to properly differentiate causes of skeletal pathology in metabolic bone disease and to reliably guide clinical management of this disease.