Circulating parathyroid hormone activity: Familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism

S. J. Marx, Allen M. Spiegel, E. M. Brown, R. Windeck, D. G. Gardner, R. W. Downs, M. Attie, G. D. Aurbach

Research output: Contribution to journalArticle

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Abstract

Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH concentration (normal, <0.2 ng/ml, urinary cAMP excretion per 100 ml glomerular filtrate (U(cAMP)/GF) (normal, 2.3/0.6 nmol/100 ml glomerular filtrate; mean, /1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (T(M)P/GFR; normal, 3.4 ± 0.4 mg/dl; mean, ± 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37/.48 vs. 0.25/.46 (P<0.05); for U(cAMP)/GF, 4.3/.53 vs. 2.6/.60 (P<0.0005); and for T(M)P/GFR, 2.0 ± 0.6 vs. 2.6 ± 0.7 (P<0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in T(M)P/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for T(M)P/GFR but not for U(cAMP)/GF. However, analysis of changes in U(cAMP)/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH vs. that in 1HPT, because at any elevation of serum calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.

Original languageEnglish (US)
Pages (from-to)1190-1197
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume47
Issue number6
StatePublished - 1978
Externally publishedYes

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Primary Hyperparathyroidism
Parathyroid Hormone
Calcium
Serum
Hypercalcemia
Kidney
Hypercalciuria
Parathyroidectomy
Parathyroid Glands
Magnesium
Minerals
Creatinine
Glomerular Filtration Rate
Phosphates
Hypocalciuric hypercalcemia, familial, type 1
Homeostasis
Plasmas

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Circulating parathyroid hormone activity : Familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. / Marx, S. J.; Spiegel, Allen M.; Brown, E. M.; Windeck, R.; Gardner, D. G.; Downs, R. W.; Attie, M.; Aurbach, G. D.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 47, No. 6, 1978, p. 1190-1197.

Research output: Contribution to journalArticle

Marx, SJ, Spiegel, AM, Brown, EM, Windeck, R, Gardner, DG, Downs, RW, Attie, M & Aurbach, GD 1978, 'Circulating parathyroid hormone activity: Familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism', Journal of Clinical Endocrinology and Metabolism, vol. 47, no. 6, pp. 1190-1197.
Marx, S. J. ; Spiegel, Allen M. ; Brown, E. M. ; Windeck, R. ; Gardner, D. G. ; Downs, R. W. ; Attie, M. ; Aurbach, G. D. / Circulating parathyroid hormone activity : Familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. In: Journal of Clinical Endocrinology and Metabolism. 1978 ; Vol. 47, No. 6. pp. 1190-1197.
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abstract = "Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH concentration (normal, <0.2 ng/ml, urinary cAMP excretion per 100 ml glomerular filtrate (U(cAMP)/GF) (normal, 2.3/0.6 nmol/100 ml glomerular filtrate; mean, /1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (T(M)P/GFR; normal, 3.4 ± 0.4 mg/dl; mean, ± 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37/.48 vs. 0.25/.46 (P<0.05); for U(cAMP)/GF, 4.3/.53 vs. 2.6/.60 (P<0.0005); and for T(M)P/GFR, 2.0 ± 0.6 vs. 2.6 ± 0.7 (P<0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in T(M)P/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for T(M)P/GFR but not for U(cAMP)/GF. However, analysis of changes in U(cAMP)/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH vs. that in 1HPT, because at any elevation of serum calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.",
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N2 - Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH concentration (normal, <0.2 ng/ml, urinary cAMP excretion per 100 ml glomerular filtrate (U(cAMP)/GF) (normal, 2.3/0.6 nmol/100 ml glomerular filtrate; mean, /1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (T(M)P/GFR; normal, 3.4 ± 0.4 mg/dl; mean, ± 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37/.48 vs. 0.25/.46 (P<0.05); for U(cAMP)/GF, 4.3/.53 vs. 2.6/.60 (P<0.0005); and for T(M)P/GFR, 2.0 ± 0.6 vs. 2.6 ± 0.7 (P<0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in T(M)P/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for T(M)P/GFR but not for U(cAMP)/GF. However, analysis of changes in U(cAMP)/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH vs. that in 1HPT, because at any elevation of serum calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.

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