Dissimilar PTH, gastrin, and calcitonin responses to oral calcium and peptones in hypocalciuric hypercalcemia, primary hyperparathyroidism, and normal subjects: A useful tool for differential diagnosis

We analyzed gastrin, PTH, and calcitonin responses to oral calcium and peptones in hypocalciuric hypercalcemia, mild primary hyperparathyroidism, and normal controls. We observed diverse hormonal responses that may help in the differential diagnosis of these conditions. Introduction: Hypocalciuric hypercalcernia (HH) is consequent to calcium-sensing receptor (CaSR) genetic mutations or anti-CaSR antibodies. CaSR is expressed in parathyroid tissue, thyroid C cells, and gastrin-secreting cells, where it has been suggested that on calcium and/or amino acid allosteric activation, promotes gastrin secretion. Materials and Methods: We evaluated gastrin, PTH, and calcitonin responses to oral calcium (1 g) and peptones (10 g) in 10 patients with HH (mean age, 58.5 +/- 10.3 years; F/M = 9/1), 15 patients with primary hyperparathyroidism (PH; mean age, 60.4 +/- 8.3 years; F/M = 11/4), and 30 healthy controls (mean age, 60.3 +/- 8.1 years). Statistical analyses for differences during oral loading tests were calculated with ANOVA for repeated measurements and comparisons between two groups were performed with Student's t-test. Results: PTH response to peptones was markedly increased in patients with PH compared with flat responses in controls and HH patients (p < 0.05). Gastrin increase after oral calcium was absent in HH and PH subjects (p < 0.05 versus controls), and gastrin responses to peptones were blunted in HH and PH subjects compared with controls (p < 0.05). PTH drop and calcitonin increase after calcium load observed in controls were absent in HH and PH subjects (p < 0.05). Conclusions: The marked difference in PTH response elicited by peptones observed in PH compared with subjects with HH may help in the differential diagnosis of these conditions without genetic studies. Peptones may stimulate CaSR-controlled hormones as an allosteric regulatory pathway. CaSR abnormalities may help to explain the different calcium- and peptones-induced hormonal responses observed in PH and HH compared with normal subjects.