Calcium regulation fo parathyroid and C cell function in familial benign hypercalcemia

M. M. Rajala, G. G. Klee, H. Heath

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The roles of parathyroid hormone (PTH) and calcitonin (CT) in the pathogenesis of familial benign hypercalcemia (FBH, or hypocalciuric hypercalcemia) are uncertain. Thus we performed studies in 26 patients with FBH, 12 patients with primary hyperparathyroidism (HPT), and 20 normal volunteers, to answer these questions: are plasma levels of intact or biologically active PTH frequently elevated in FBH? Is plasma intact PTH nonsuppressible during calcium infusion? Is there blunting of the C cell CT response to calcium infusion as occurs in primary HPT? We used three methods for measurement of PTH: a mid region-specific radioimmunoassay (iPTH, antiserum GP-1M), an extraction-concentration bioassay (bioPTH, stimulation of cAMP generation in osteoblastlike cells), and a two-site immunoradiometric assay (IRMA) for intact PTH. PTH levels were significantly elevated in primary HPT by all three methods, but mean PTH was normal in FBH and 85-92% of values overlapped the normal range. During 5 minute calcium infusions (2 mg Ca2+ per kg) iPTH values fell little, but bioPTH and intact PTH fell sharply in all three groups. Mean calcium-induced decreases of intact and bioPTH were indistinguishable from normal in FBH, but PTH levels generally remained elevated at 5 minutes in primary HPT. In FBH basal and postinfusion CT levels were normal. The data show that, in the majority of patients with FBH, PTH concentrations and bioactivity in blood are within the normal range and are suppressed rapidly to very low levels with further increases of calcium. The data suggest that the abnormality of parathyroid function in FBH differes from that in primary HPT. There was no deficiency of CT or C cell responsiveness in FBH, another difference from primary HPT. Nonetheless, in 8-15% of cases, measurement of PTH could not discriminate FBH from primary HPT.

Original languageEnglish (US)
Pages (from-to)117-124
Number of pages8
JournalJournal of Bone and Mineral Research
Volume6
Issue number2
StatePublished - 1991

Fingerprint

Parathyroid Hormone
Primary Hyperparathyroidism
Calcium
Calcitonin
Reference Values
Hypocalciuric hypercalcemia, familial, type 1
Immunoradiometric Assay
Hypercalcemia
Biological Assay
Radioimmunoassay
Immune Sera
Healthy Volunteers

ASJC Scopus subject areas

  • Surgery

Cite this

Calcium regulation fo parathyroid and C cell function in familial benign hypercalcemia. / Rajala, M. M.; Klee, G. G.; Heath, H.

In: Journal of Bone and Mineral Research, Vol. 6, No. 2, 1991, p. 117-124.

Research output: Contribution to journalArticle

Rajala, M. M. ; Klee, G. G. ; Heath, H. / Calcium regulation fo parathyroid and C cell function in familial benign hypercalcemia. In: Journal of Bone and Mineral Research. 1991 ; Vol. 6, No. 2. pp. 117-124.
@article{e6c1ad7bc46945aca9c0d5f673d68a76,
title = "Calcium regulation fo parathyroid and C cell function in familial benign hypercalcemia",
abstract = "The roles of parathyroid hormone (PTH) and calcitonin (CT) in the pathogenesis of familial benign hypercalcemia (FBH, or hypocalciuric hypercalcemia) are uncertain. Thus we performed studies in 26 patients with FBH, 12 patients with primary hyperparathyroidism (HPT), and 20 normal volunteers, to answer these questions: are plasma levels of intact or biologically active PTH frequently elevated in FBH? Is plasma intact PTH nonsuppressible during calcium infusion? Is there blunting of the C cell CT response to calcium infusion as occurs in primary HPT? We used three methods for measurement of PTH: a mid region-specific radioimmunoassay (iPTH, antiserum GP-1M), an extraction-concentration bioassay (bioPTH, stimulation of cAMP generation in osteoblastlike cells), and a two-site immunoradiometric assay (IRMA) for intact PTH. PTH levels were significantly elevated in primary HPT by all three methods, but mean PTH was normal in FBH and 85-92{\%} of values overlapped the normal range. During 5 minute calcium infusions (2 mg Ca2+ per kg) iPTH values fell little, but bioPTH and intact PTH fell sharply in all three groups. Mean calcium-induced decreases of intact and bioPTH were indistinguishable from normal in FBH, but PTH levels generally remained elevated at 5 minutes in primary HPT. In FBH basal and postinfusion CT levels were normal. The data show that, in the majority of patients with FBH, PTH concentrations and bioactivity in blood are within the normal range and are suppressed rapidly to very low levels with further increases of calcium. The data suggest that the abnormality of parathyroid function in FBH differes from that in primary HPT. There was no deficiency of CT or C cell responsiveness in FBH, another difference from primary HPT. Nonetheless, in 8-15{\%} of cases, measurement of PTH could not discriminate FBH from primary HPT.",
author = "Rajala, {M. M.} and Klee, {G. G.} and H. Heath",
year = "1991",
language = "English (US)",
volume = "6",
pages = "117--124",
journal = "Journal of Bone and Mineral Research",
issn = "0884-0431",
publisher = "Wiley-Blackwell",
number = "2",

}

TY - JOUR

T1 - Calcium regulation fo parathyroid and C cell function in familial benign hypercalcemia

AU - Rajala, M. M.

AU - Klee, G. G.

AU - Heath, H.

PY - 1991

Y1 - 1991

N2 - The roles of parathyroid hormone (PTH) and calcitonin (CT) in the pathogenesis of familial benign hypercalcemia (FBH, or hypocalciuric hypercalcemia) are uncertain. Thus we performed studies in 26 patients with FBH, 12 patients with primary hyperparathyroidism (HPT), and 20 normal volunteers, to answer these questions: are plasma levels of intact or biologically active PTH frequently elevated in FBH? Is plasma intact PTH nonsuppressible during calcium infusion? Is there blunting of the C cell CT response to calcium infusion as occurs in primary HPT? We used three methods for measurement of PTH: a mid region-specific radioimmunoassay (iPTH, antiserum GP-1M), an extraction-concentration bioassay (bioPTH, stimulation of cAMP generation in osteoblastlike cells), and a two-site immunoradiometric assay (IRMA) for intact PTH. PTH levels were significantly elevated in primary HPT by all three methods, but mean PTH was normal in FBH and 85-92% of values overlapped the normal range. During 5 minute calcium infusions (2 mg Ca2+ per kg) iPTH values fell little, but bioPTH and intact PTH fell sharply in all three groups. Mean calcium-induced decreases of intact and bioPTH were indistinguishable from normal in FBH, but PTH levels generally remained elevated at 5 minutes in primary HPT. In FBH basal and postinfusion CT levels were normal. The data show that, in the majority of patients with FBH, PTH concentrations and bioactivity in blood are within the normal range and are suppressed rapidly to very low levels with further increases of calcium. The data suggest that the abnormality of parathyroid function in FBH differes from that in primary HPT. There was no deficiency of CT or C cell responsiveness in FBH, another difference from primary HPT. Nonetheless, in 8-15% of cases, measurement of PTH could not discriminate FBH from primary HPT.

AB - The roles of parathyroid hormone (PTH) and calcitonin (CT) in the pathogenesis of familial benign hypercalcemia (FBH, or hypocalciuric hypercalcemia) are uncertain. Thus we performed studies in 26 patients with FBH, 12 patients with primary hyperparathyroidism (HPT), and 20 normal volunteers, to answer these questions: are plasma levels of intact or biologically active PTH frequently elevated in FBH? Is plasma intact PTH nonsuppressible during calcium infusion? Is there blunting of the C cell CT response to calcium infusion as occurs in primary HPT? We used three methods for measurement of PTH: a mid region-specific radioimmunoassay (iPTH, antiserum GP-1M), an extraction-concentration bioassay (bioPTH, stimulation of cAMP generation in osteoblastlike cells), and a two-site immunoradiometric assay (IRMA) for intact PTH. PTH levels were significantly elevated in primary HPT by all three methods, but mean PTH was normal in FBH and 85-92% of values overlapped the normal range. During 5 minute calcium infusions (2 mg Ca2+ per kg) iPTH values fell little, but bioPTH and intact PTH fell sharply in all three groups. Mean calcium-induced decreases of intact and bioPTH were indistinguishable from normal in FBH, but PTH levels generally remained elevated at 5 minutes in primary HPT. In FBH basal and postinfusion CT levels were normal. The data show that, in the majority of patients with FBH, PTH concentrations and bioactivity in blood are within the normal range and are suppressed rapidly to very low levels with further increases of calcium. The data suggest that the abnormality of parathyroid function in FBH differes from that in primary HPT. There was no deficiency of CT or C cell responsiveness in FBH, another difference from primary HPT. Nonetheless, in 8-15% of cases, measurement of PTH could not discriminate FBH from primary HPT.

UR - http://www.scopus.com/inward/record.url?scp=0025924409&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025924409&partnerID=8YFLogxK

M3 - Article

VL - 6

SP - 117

EP - 124

JO - Journal of Bone and Mineral Research

JF - Journal of Bone and Mineral Research

SN - 0884-0431

IS - 2

ER -