Nonautonomy of parathyroid hormone and urinary cyclic AMP in primary hyperparathyroidism.
This study demonstrates that appreciable changes in serum parathyroid hormone and urinary cyclic AMP occur during experimentally induced hyper- and hypocalcemia in almost all patients with primary hyperparathyroidism regardless of histology. A single patient with tertiary hyperparathyroidism also demonstrated a significant elevation of serum parathyroid hormone and urinary cyclic AMP in response to EDTA induced reduction in ionized calcium. Thus, total autonomy of hormone secretion was not present in the great majority of the patients with a parathyroid adenoma, parathyroid hyperplasia, or the single patient with tertiary hyperparathyroidism. Therefore, preoperative evaluation of the rsponse of urinary cyclic AMP and serum parapthyroid hormone to EDTA or calcium infusion will not distinguish parathyroid adenomas from hyperplasia on the basis of total autonomy of hormone secretion. If a difference in secretory control is present between parathyroid adenomas and parathyroid hyperplasia, it is more subtle than total autonomy for adenomas and nonautonomy for hyperplasia.
D000236:Adenoma / Q000503:physiopathology*; D002118:Calcium / Q000097:blood; D000242:Cyclic AMP / Q000652:urine*; D004492:Edetic Acid; D006801:Humans; D006961:Hyperparathyroidism / Q000503:physiopathology*; D010280:Parathyroid Glands / Q000378:metabolism / Q000503:physiopathology*; D010281:Parathyroid Hormone / Q000378:metabolism*; D010282:Parathyroid Neoplasms / Q000503:physiopathology*
D010281:Parathyroid Hormone; D004492:Edetic Acid; D000242:Cyclic AMP; D002118:Calcium