OBJECTIVE: The objective of the present study was to elucidate the parathyroid responsiveness by measurements of blood ionized calcium and serum intact parathyroid hormone (PTH) concentrations, before and during trisodium citrate induced hypocalcaemia. PATIENTS AND CONTROLS: Sixteen patients with primary hyperparathyroidism and 32 healthy volunteers. DESIGN: Blood ionized calcium concentration was lowered by about 0.20 mmol/l and maintained at this level for 2 hours by blood ionized calcium controlled trisodium citrate infusion. MEASUREMENTS: Serum PTH(1-84) was measured by an immunoradiometric assay. RESULTS: In patients and controls, baseline measurements of blood ionized calcium were 1.39 +/- 0.07 vs 1.24 +/- 0.04 mmol/l (mean +/- SD) (P < 0.001) and of serum PTH (1-84) 9.7 +/- 5.4 vs 3.2 +/- 1.1 pmol/l (P < 0.001). During a trisodium citrate clamp, serum PTH(1-84) rose to a maximal concentration after 5-10 minutes in both groups, the patients to 2-10 times baseline, whereas controls rose to 4-7 times baseline values. In both groups the peak of serum PTH(1-84) declined to a steady state concentration around 2-4 times baseline. CONCLUSIONS: In conclusion, adenoma cells seem to react in almost the same way as normal parathyroid cells. They respond to initiation of hypocalcaemia by the release of preformed PTH(1-84), and continue to secrete increased amounts of PTH(1-84) during the maintenance of relative hypocalcaemia. The increased baseline concentrations of blood ionized calcium and serum PTH(1-84) and the serum PTH(1-84) response during blood ionized calcium lowering all suggest a shift upwards in the calcium set point.
OBJECTIVE: The objective of the present study was to elucidate the parathyroid responsiveness by measurements of blood ionizedcalcium and serum intact parathyroid hormone (PTH) concentrations, before and during trisodium citrate induced hypocalcaemia. PATIENTS AND CONTROLS: Sixteen patients with primary hyperparathyroidism and 32 healthy volunteers. DESIGN: Blood ionizedcalcium concentration was lowered by about 0.20 mmol/l and maintained at this level for 2 hours by blood ionizedcalcium controlled trisodium citrate infusion. MEASUREMENTS: Serum PTH(1-84) was measured by an immunoradiometric assay. RESULTS: In patients and controls, baseline measurements of blood ionizedcalcium were 1.39 +/- 0.07 vs 1.24 +/- 0.04 mmol/l (mean +/- SD) (P < 0.001) and of serum PTH (1-84) 9.7 +/- 5.4 vs 3.2 +/- 1.1 pmol/l (P < 0.001). During a trisodium citrate clamp, serum PTH(1-84) rose to a maximal concentration after 5-10 minutes in both groups, the patients to 2-10 times baseline, whereas controls rose to 4-7 times baseline values. In both groups the peak of serum PTH(1-84) declined to a steady state concentration around 2-4 times baseline. CONCLUSIONS: In conclusion, adenoma cells seem to react in almost the same way as normal parathyroid cells. They respond to initiation of hypocalcaemia by the release of preformed PTH(1-84), and continue to secrete increased amounts of PTH(1-84) during the maintenance of relative hypocalcaemia. The increased baseline concentrations of blood ionizedcalcium and serum PTH(1-84) and the serum PTH(1-84) response during blood ionizedcalcium lowering all suggest a shift upwards in the calcium set point.