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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1989-11-21
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pubmed:abstractText |
We sought an explanation for prior findings of high plasma chromogranin-A (Chr-A) in primary hyperparathyroidism. Chr-A was measured in plasma samples from 55 controls and 73 patients with primary hyperparathyroidism caused by adenoma (n = 14), sporadic or familial hyperplasia (n = 10), or familial multiple endocrine neoplasia type 1 (FMEN1; n = 49). Serum or plasma samples were also tested for calcium, PTH, gastrin, pancreatic polypeptide, CG alpha, and PRL. Plasma Chr-A was 34 +/- 10 in parathyroid adenoma, 55 +/- 33 in parathyroid hyperplasia without FMEN1, 63 +/- 88 in FMEN1, and 25 +/- 8 in controls (mean +/- SD; nanograms per ml; FMEN1 or parathyroid hyperplasia vs. control, P less than 0.05). Plasma Chr-A did not correlate with other hormonal variables in controls. Plasma Chr-A correlated with log serum gastrin (r = 0.43; P = 0.003) and plasma PTH (r = 0.52; P less than 0.05) only in FMEN1. In FMEN1, plasma Chr-A was highest in subjects with Zollinger-Ellison syndrome (ZES, 120 +/- 127; no ZES, 30 +/- 33 (P less than 0.0001). Parathyroidectomy did not decrease plasma Chr-A in patients with parathyroid adenoma or parathyroid hyperplasia. For FMEN1 patients with available pre- and postparathyroidectomy samples, Chr-A decreased postoperatively in four of five patients with ZES compared to none of six patients without ZES (P less than 0.05). Elevated plasma Chr-A is not a general feature of primary hyperparathyroidism. Elevated plasma Chr-A in primary hyperparathyroidism was restricted principally to patients who also had ZES. Primary hyperparathyroidism may influence the level of Chr-A by an effect of hypercalcemia or elevated PTH on Chr-A secretion from pancreatic islet tissue.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0021-972X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
69
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
950-5
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2571619-Adenoma,
pubmed-meshheading:2571619-Adult,
pubmed-meshheading:2571619-Chromogranin A,
pubmed-meshheading:2571619-Chromogranins,
pubmed-meshheading:2571619-Female,
pubmed-meshheading:2571619-Humans,
pubmed-meshheading:2571619-Hyperparathyroidism,
pubmed-meshheading:2571619-Hyperplasia,
pubmed-meshheading:2571619-Male,
pubmed-meshheading:2571619-Middle Aged,
pubmed-meshheading:2571619-Multiple Endocrine Neoplasia,
pubmed-meshheading:2571619-Nerve Tissue Proteins,
pubmed-meshheading:2571619-Parathyroid Diseases,
pubmed-meshheading:2571619-Parathyroid Glands,
pubmed-meshheading:2571619-Parathyroid Neoplasms,
pubmed-meshheading:2571619-Retrospective Studies
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pubmed:year |
1989
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pubmed:articleTitle |
Plasma chromogranin-A in primary hyperparathyroidism.
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pubmed:affiliation |
Mineral Metabolism Section, National Institute of Diabetes and Digestive and Kidney Disease, Bethesda, Maryland 20892.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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