Hyperparathyroidism persisted in a 36-yr-old woman after surgical exploration of the neck and removal of 2-½ normal parathyroid glands. Arteriography, selective venous sampling and radioimmunoassay allowed identification of the source of excess parathyroid hormone (PTH) as a mediastinal lesion at the level of the tracheal bifurcation. The artery feeding the lesion was deliberately compromised by embolic occlusion with a mixture of autologous clot and gelfoam. This procedure led to transient hypoparathyroidism. Serial monitoring of plasma parathyroid hormone levels, renal phosphate clearance, and urinary cyclic-adenosine monophosphate excretion indicated that parathyroid ischemia had not resulted in release of large amounts of biologically or immunologically active parathyroid hormone. Within five days after the procedure the concentration of parathyroid hormone in plasma increased indicating the presence of residual parathyroid tissue in the neck or mediastinum. Mild hyperparathyroidism reappeared within several months with less marked elevations of PTH and calcium levels suggesting that the tumor had not infarcted completely.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical