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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8072
pubmed:dateCreated
1978-6-28
pubmed:abstractText
Hypercalcaemia is often associated with malignant disease. Causes of elevated serum-calcium levels in the absence of bony metastases include parathyroid-hormone production by the tumour, osteolytic factors made by the tumour, and coexistent primary hyperparathyroidism. By measuring nephrogenous cyclic-A.M.P. excretion to assess parathyroid-hormone function, we have determined the mechanism of such hypercalcaemia in 15 patients. Nephrogenous cyclic A.M.P. ranges from 0.05 to 2.40 mumol/g of creatinine in normal subjects, from 2.27 to 8.45 mumol/g in patients with primary hyperparathyroidism, and from 0.50 to 1.30 mumol/g in patients with proven non-hyperparathyroid hypercalcaemia without malignancy. 9 patients (60%) with hypercalcaemia and malignancy had normal levels of nephrogenous cyclic A.M.P. (range 0.35-2.07 mumol/g creatinine). The other 6 (40%) had elevated nephrogenous cyclic A.M.P. (range 2.70-5.55 mumol/g) consistent with increased parathyroid-hormone secretion. Surgical exploration of the neck in these patients showed that the increased parathyroid-hormone secretion was secondary to primary hyperparathyroidism, not ectopic hyperparathyroidism. Thus, the data indicate that coexistent hyperparathyroidism may be common in patients with hypercalcaemia and malignancy and that the measurement of nephrogenous cyclic A.M.P. is very useful in identifying patients at risk for hyperparathyroidism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0140-6736
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1004-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1978
pubmed:articleTitle
Primary hyperparathyroidism in paraneoplastic hypercalcaemia.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.