| Abstrakt: |
Basal parathyroid hormone (PTH) levels measured by a chemiluminescent immunoassay for intact PTH showed good discrimination between normal, n=82 (1.2–9.4 pmol/l), and hyperparathyroid subjects, n=55 (9–200 pmol/l). In malignant hypercalcemia, all PTH levels were within the normal range or suppressed (0.8–5.2 pmol/l). Dynamic studies of PTH release in response to intramuscular salmon calcitonin (100 u) showed no significant rise out of the normal range in controls, but adenoma patients demonstrated a mean rise at 120, 180, and 240 minutes of 22%, 22%, and 35%, respectively, and hyperplasia patients a mean rise of 44%, 63%, and 46%, respectively. The mean absolute rise in PTH concentration was 10.6±7.2 pmol/g parathyroid adenoma and 26.6±19.2 pmol/g hyperplastic parathyroid tissue; this difference being significant (p <0.01). In vitro studies were performed in which dispersed cells prepared from both parathyroid adenomas and hyperplastic tissue were exposed to low (0.5 mM) and high (2.5 mM) extracellular calcium. Intact PTH secretion was measured under these conditions and compared with the results obtained by a mid-region (44–68) specific immunoassay for PTH. There was parallel secretion of intact and mid-region hormone under all conditions, the secretion rate of hyperplastic cells being greater than that of adenomas. Suppressibility of PTH release by high extracellular calcium was significantly greater in hyperplasia than in adenomas. These differences in the behavior of adenomatous and hyperplastic tissues both in vivo, in response to calcitonin, and in vitro, in response to changes in extracellular calcium concentration, suggest that the underlying pathogenesis of hyperparathyroidism may be heterogenous at the cellular level. |
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