Decreased Calcium Tolerance in Nongoitrous Cretins

Anast, Constantine S.; Guthrie, Rufus K.

doi:10.1203/00006450-197112000-00003

Cited by 10 publications

(1 citation statement)

References 16 publications

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“…DISCUSSION Our results demonstrate that children with CNC have lower than normal levels of plasma CT in the basal state and during provocative testing with two known CT secretagogues, calcium and pentagastrin. Because CT can act to lower blood calcium, this CT deficiency may explain why the children with congenital cretinism are less able than the normal children to rapidly correct the hypercalcemia induced by the calcium infusion, an observation similar to that of Anast and Guthrie (7). In addition, the pattern of stimulated CT secretion in the congenital cretin group was also different from that observed in the normal children.…”

Section: Introductionmentioning

confidence: 56%

Calcitonin secretion in congenital nongoitrous cretinism.

Carey¹,

Jones²,

Parthemore³

et al. 1980

J. Clin. Invest.

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A B S T R A C T Plasma calcitonin (CT) was measured in the basal state and/or during provocative tests of hormone secretion in 11 children with congenital nongoitrous cretinism (CNC), in 1 girl with a lingual thyroid, and in 11 normal children. Basal and stimulated CT concentrations were significantly lower in the patients with CNC than in the normal subjects. Mean basal CT (± SE) was 41±4 pg/ml in the normal children, 24±3 pg/ml in the children with CNC, and 20±2 pg/ml in the patient with the lingual thyroid. The mean incremental CT responses to calcium infusion were 7.0±2 pg/ml in the children with CNC, 6.0 pg/ml in the patient with the lingual thyroid, and 146±47 pg/ml in the normal children. The children with CNC also demonstrated a significant delay in the return of the total serum calcium to basal level after the calcium infusion. The mean incremental CT response after infusion of pentagastrin was 7.6+2 pg/ml in the children with CNC, 10.0 pg/ml in the child with the lingual thyroid, and 34.4±11 pg/ml in the normal children. These data indicate that CT deficiency is present in children with CNC and suggest that the deficiency is a consequence of the defective embryologic development of the thyroid gland.

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Section: Introductionmentioning

confidence: 56%

Calcitonin secretion in congenital nongoitrous cretinism.

Carey¹,

Jones²,

Parthemore³

et al. 1980

J. Clin. Invest.

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

Rajala

Klee

Heath

1991

Journal of Bone and Mineral Research

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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 differs from that in primary HPT.(ABSTRACT TRUNCATED AT 250 WORDS)

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Calcium Homeostasis

Parfitt¹

1993

Physiology and Pharmacology of Bone

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Decreased Calcium Tolerance in Nongoitrous Cretins

Cited by 10 publications

References 16 publications

Calcitonin secretion in congenital nongoitrous cretinism.

Calcitonin secretion in congenital nongoitrous cretinism.

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

Calcium Homeostasis

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