Dissimilar PTH, gastrin, and ionized calcium response to oral peptones in normocalcemic primary hyperparathyroidism, hypercalcemic primary hyperparathyroidism and normal subjects
Maurizio Bevilacqua1, Marco Invernizzi2, Stefano Carda2 & Carlo Cisari2,3
It has been hypothesized that primary hyperparathyroidism (PH) has a biphasic disease course. During the first phase hypercalcemia is not yet present. Subsequently, the second phase starts with the development of hypercalcemia. In an attempt to identify differences in the calcium regulating hormonal handling in the clinical setting, we evaluated the hormonal responses of gastrin, PTH, phosphate and ionized calcium to oral peptones (a mixture containing L-amino acids with known CaSR-activation properties) in patients with normocalcemic PH (PH-N) and hypercalcemic PH (PH-H) compared to a control group of healthy subjects.
Fifteen PH-H patients, fifteen PH-N patients and 30 healthy controls were enrolled. Both controls and patients had normal renal function and normal 25(OH) vitamin D serum levels. The inclusion criteria for PH-N patients were: presence of high serum levels of intact PTH, serum ionized calcium levels in the high normality range and absence of potential causes of secondary hyperparathyroidism. All subjects performed a peptone-meal test (10 g Liebig meat extract diluted in 250 ml of 0.9% saline) and subsequent blood samples collected every 15 min for 2 h. Ionized calcium, phosphate, gastrin and PTH levels were evaluated.
PTH increased significantly at 60 and 90 min after oral peptone load in PH-H patients and ionized calcium significantly decreased in PH-H patients since 60 min from oral peptone load. Controls and PH-N didnt show significant modifications in PTH and ionized calcium serum levels. The increase in gastrin levels in PH-H patients was about one-half the one observed in PH-N and controls.
These data suggest that in PH-N patients the CaSR-dependent pathway is still preserved and produces responses similar to those of healthy subjects. However, in the later phase of the disease a disregulation occurs, leading to altered response to peptones meal.