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Maurizio Bevilacqua, Marco Invernizzi, Velella Righini, Stefano Carda and Carlo Cisari

Context

In healthy subjects and in patients with primary hyperparathyroidism (PH), the administration of a low dose of 25(OH)D (25 μg/day) increases the serum levels of both 25(OH)D and 1,25(OH)2D. It is unknown whether this relationship is present in patients affected by familial benign hypocalciuric hypercalcemia (FBH).

Objective

To evaluate the different vitamin D substrate–product relationship after oral vitamin D supplementation in familial benign hypercalcemia, PH, and healthy controls.

Design

We evaluated the main physiological regulators of 1α-hydroxylase and the substrate–product relationship of 25(OH)D and 1,25(OH)2D in 20 patients with PH, 25 with FBH, and 122 healthy sex- and age-matched controls before and after administration of 25(OH)D for 2 weeks.

Results

25(OH)D increased significantly in all subjects, whereas 1,25(OH)2D serum levels increased significantly in PH patients and healthy controls but not in patients with FBH. Therefore, a significant positive substrate–product relationship of 25(OH)D–1,25(OH)2D was found in PH and healthy controls, but not in FBH. Monomeric calcitonin (hCT-M) was significantly lower at baseline and after 25(OH)D supplementation in the FBH group compared with the other two groups.

Conclusions

The lack of 1,25(OH)2D increase in FBH may be due to a direct inhibitory effect on 1α-hydroxylase of hypercalcemia per se, increased metabolic clearance of 1,25(OH)2D, or a decreased stimulus of 1α-hydroxylase related to persistently low levels of hCT.

Free access

Marco Invernizzi, Stefano Carda, Velella Righini, Alessio Baricich, Carlo Cisari and Maurizio Bevilacqua

Background

Normocalcemic primary hyperparathyroidism (PHPT-N) is a condition that may have similar long-term implications to primary hyperparathyroidism (PHPT); however, differential diagnosis and treatment for parathyroid disorders are not clearly defined. We investigated the effect of an oral peptone and an oral calcium load on calcium-regulating hormones in PHPT-N compared with PHPT and healthy controls to provide a new potential diagnostic tool.

Design

Case–control study.

Methods

We evaluated serum gastrin, PTH, ionized calcium, and phosphate responses to oral calcium (1 g) and peptone (10 g) load in 22 PHPT and 20 PHPT-N patients matched for PTH serum values. Moreover, 30 healthy subjects were enrolled as controls. In 12 patients for each group, we also performed the oral peptone test adding aluminum hydroxide (AH) to suppress phosphate absorption.

Results

In PHPT patients, PTH increased significantly 30 min after the oral peptone load, while no significant increase was found in PHPT-N and controls. After oral calcium load, PTH remained stable in PHPT while it decreased dramatically in PHPT-N patients, and ionized calcium increased significantly in each of the three groups. Peptones plus AH induced a blunted PTH increase in the three groups.

Conclusions

Considering the marked difference in PTH response elicited by peptones in PHPT compared with PHPT-N, we suggest that the oral peptone test could be added to the diagnostic evaluation of PHPT patients. In case of absent response to peptones, patients should have their serum calcium levels assessed twice a year in accordance with recent guidelines.