Normocalcemic Hyperparathyroidism in Vietnamese Immigrants Living in Southern California

Lương, Khanh vinh quốc; Nguyễn, Lan

doi:10.1097/00000441-200006000-00007

Cited by 5 publications

(1 citation statement)

References 19 publications

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“…However, a significant fraction of the patients with primary hyperparathyroidism (PHPT) can maintain a normal serum calcium concentration despite the primary increase in PTH secretion [17,19]. They were categorized to the normocalcemic PHPT (NCPHPT) in the earlier studies mainly based on the normal total serum calcium concentration [11,12,14,21,24,26,27,30], but various proportions of thus defined NCPHPT patients were later found to have persistent or intermittent elevation of ionized serum calcium [8,[17][18][19][20]31]. However, still other patients exhibiting symptomatic PHPT maintained normocalcemia in terms of both ionizing and total serum calcium concentrations [19,20].…”

Section: Introductionmentioning

confidence: 99%

Normocalcemic primary hyperparathyroidism in patients with recurrent kidney stones: pathological analysis of parathyroid glands

et al. 2006

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The lack of overt elevation of serum calcium concentration in some patients suffering from primary hyperparathyroidism is an intriguing clinical phenomenon. Previous studies have substantiated abnormal parathyroid tissue in these patients, but the extent and mode of derangements remained largely undefined. The parathyroid tissues from patients of normocalcemic primary hyperparathyroidism (NCPHPT) and those having normal parathyroid glands, hypercalcemic primary hyperplasia, secondary hyperplasia, and adenoma were compared by undertaking quantitative immunohistochemistry analysis on tissue microarray. The statistic results suggested that the parathyroid tissue of NCPHPT approximates more to normal gland than to its counterpart in other groups of parathyroid proliferative diseases in terms of the lack of significant alterations of calcium-sensing receptor (CaSR), chromogranin A (CGA), parathyroid hormone (PTH), and proliferation index (Ki67). On the other hand, the depressed vitamin D receptor (VitDR) and elevated cyclin D1 (CyD1) of NCPHPT indicated the inherent functional abnormalities in parathyroid cells. Our results imply that inherent functional disengagement may exist between CaSR and CyD1 or between CaSR and VitDR or both in parathyroid cells of symptomatic NCPHPT. Lack of enhanced release of CGA and PTH and discordance between proliferative activity and CyD1 expression in parathyroid cells may further hinder the development of hypercalcemia.

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