The regulation of calcitonin in normal human plasma as assessed by immunoprecipitation and immunoextraction.

Parthemore, Jacqueline G.; Deftos, Leonard J.; Bronzert, Diane A.

doi:10.1172/jci108162

Cited by 39 publications

(12 citation statements)

References 18 publications

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“…To further assess the effect of hyperparathyroidism on C-cell function, repeat calcium infusions were performed in six 10HPT patients (Nos. 2,5,8,9,13,22) between 5 and 15 mo after their recovery from parthyroid surgery. The patients then had normal basal Ca and iPTH values and received no vitamin D or calcium supplements for several weeks before the repeat studies.…”

Section: Resultsmentioning

confidence: 99%

“…Increased degradation of calcitonin by tissue in hyperparathyroid patients could explain our results, but the studies of Baylin et al (27) have excluded increased degradation by plasma enzymes. In normal individuals CT secretion is known to be responsive to acute perturbations of serum calcium concentrations (2,4,5,28). Therefore, calcium infusion would appear to be an ideal means for testing hypercalcemic patients with 10HPT.…”

Section: Discussionmentioning

confidence: 99%

“…Calcium infusion is known to stimulate calcitonin secretion in normal man (1)(2)(3)(4), an observation that is in accord with the belief that one function of calcitonin is to combat hypercalcemia. Furthermore, some patients with hypercalcemia not caused by hyperparathyroidism have high basal serum or plasma immunoreactive calcitonin (iCT)l concentrations (5,6).…”

Section: Introductionmentioning

confidence: 91%

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Pre- and Postoperative Studies of Plasma Calcitonin in Primary Hyperparathyroidism

Lambert¹,

Heath²,

Sizemore³

1979

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

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Pre- and Postoperative Studies of Plasma Calcitonin in Primary Hyperparathyroidism

Lambert¹,

Heath²,

Sizemore³

1979

J. Clin. Invest.

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“…Consequently, the antiserum appeared to require primarily a major antigenic site within sequence positions 29-32 at the COOH-terminus of hCT monomer, and a minor antigenic site in the middle of the molecule within sequence positions [11][12][13][14][15][16]. Whether the residues within these sites interact directly with antibody sequences or produce a molecular conformation appropriate for antibody recognition could not be distinguished by these studies.…”

Section: Resultsmentioning

confidence: 99%

“…In view of the absence of binding of the immunoreactive material to the lectin agarose, carbohydrate side chains, at least of INTRODUCTION Calcitonin in several species is known to be a 32-amino acid polypeptide hormone (1)(2)(3)(4)(5)(6) containing an intrachain disulfide bridge between sequence positions 1 and 7 at the NH2-terminal end of the molecule and an amide group on the COOH-terminal proline. The human hormone (hCT)' is secreted by normal (7)(8)(9)(10)(11)(12) and neoplastic C cells (7)(8)(9)(10)(11)(12)(13)(14)(15), as well as by non-C cell neoplasms (16)(17)(18). It has been established that immunochemical heterogeneity of calcitonin exists (19)(20)(21) in body fluids of patients with medullary thyroid carcinoma and non-C cell neoplasms.…”

mentioning

confidence: 99%

Characterization of the Immunochemical Forms of Calcitonin Released by a Medullary Thyroid Carcinoma in Tissue Culture

Goltzman¹,

Tischler²

1978

J. Clin. Invest.

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Williams syndrome: An historical perspective of its evolution, natural history, and etiology

Jones

2005

Am. J. Med. Genet.

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This review examines the Williams syndrome (WS) from an historical perspective, beginning with the early descriptions of idiopathic infantile hypercalcemia (IIH) and ending with some speculative ideas about a possible causative function of a recently discovered neuropeptide. The earliest reports of W S individuals are probably those which describe a "severe" subgroup of IIH and separate it from the epidemic of milder IIH reported in Post-WWII Great Britain and Europe. Most of these latter cases apparently resulted from hypervitaminosis D produced by excessive supplementation of government-supplied infant foods. With more extensive recognition and reporting of this "severe" subgroup, the diagnostic constellation of IIH, mental deficiency, elfin face, and supravalvular aortic stenosis (SVAS) evolved as WS. More of these reports emphasized the physical and behavioral manifestations as the key diagnostic features, and the frequency of occurrence and relative importance of SVAS and IIH in WS decreased.Despite the diminished consequence of hypercalcemia, calcium and vitamin D have continued to dominate the investigation of the cause of infantile hypercalcemia and led to the proposal and confirmation of deficient calcitonin secretion in individuals with WS. Though calcitonin is probably pertinent only to infantile hypercalcemia, its alternative gene product, calcitonin-gene-related product, is an important neuropeptide with physiological effects in the central nervous system and cardiovascular systems which raise the Received for publication February 27, 1989; revision received July 5, 1989. Address reprint requests to Kenneth Lee Jones, M.D., Professor of Pediatrics, University of California, San Diego, M-009-C, La Jolla, CA 92093.This manuscript was not an official contribution to the meeting.0 1990 Wiley-Liss, Inc.possibility that it may be responsible for some of the manifestations of WS. KEY WORDS: hypercalcemia, vitamin D,calcitonin, calcitonin-generelated peptide, supravalvular aortic stenosis INTRODUCTION The Williams syndrome (WS) is a well-defined symptom complex which is usually recognized and diagnosed by physicians who care for children. The list of associated findings in individuals with this diagnosis has grown beyond those originally described and continues to expand as reviews appear [Preus, 1984; Morris et al., 19881. As recognized patients with previously undescribed manifestations age and die, we expand our knowledge by postmortem information. Despite the increase of information about and interest in this condition, our understanding of its cause and pathogenesis has advanced little since its identification.The search for the etiology of WS has primarily pursued the causes and effects of the abnormalities of calcium metabolism which led to its original description as idiopathic infantile hypercalcemia (IIH). This may seem curious at this time, for though there is still controversy, many investigators now think that hypercalcemia is not a predominant or even frequent manifestation of WS [Jones and...

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The regulation of calcitonin in normal human plasma as assessed by immunoprecipitation and immunoextraction.

Cited by 39 publications

References 18 publications

Pre- and Postoperative Studies of Plasma Calcitonin in Primary Hyperparathyroidism

Pre- and Postoperative Studies of Plasma Calcitonin in Primary Hyperparathyroidism

Characterization of the Immunochemical Forms of Calcitonin Released by a Medullary Thyroid Carcinoma in Tissue Culture

Williams syndrome: An historical perspective of its evolution, natural history, and etiology

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