TY - JOUR
T1 - Mechanisms of hypercalcemia in patients with head and neck cancer
AU - Angel, Michael F.
AU - Stewart, Andrew
AU - Pensak, Myles L.
AU - Pillsbury, Harold R.C.
AU - Sasaki, Clarence T.
PY - 1982
Y1 - 1982
N2 - Hypercalcemia associated with head and neck malignancy is not an uncommon occurrence; its causes are multiple. Eight hypercalcemic patients with head and neck malignancy were studied. Serum calcium, serum phosphorus, tubular phosphorus threshold, fasting calcium excretion, plasma 1,25‐dihydroxyvitamin D, nephrogenous cyclic adenosine monophosphate (AMP), and immunoreactive parathyroid hormone were measured. Excessive dietary calcium administration in the form of an oral hyperalimentation preparation appeared to be the cause of hypercalcemia in 2 patients. Six patients demonstrated humorally mediated hypercalcemia. These patients resembled patients with primary hyperparathyroidism in having elevated nephrogenous cyclic AMP excretion and reduced proximal tubular phosphorus reabsorption, but they differed from patients with primary hyperparathyroidism by having normal levels of immunoreactive parathyroid hormone, MA rkedly increased fasting calcium excretion, and strikingly reduced mean plasma levels of 1,25‐dihydroxyvitamin D. These data strongly suggest that the humoral factor responsible for hypercalcemia in patients with head and neck cancer is not parathyroid hormone, and that patients with hyperparathyroidism can now be distinguished with confidence from those with malignancy‐associated hypercalcemia.
AB - Hypercalcemia associated with head and neck malignancy is not an uncommon occurrence; its causes are multiple. Eight hypercalcemic patients with head and neck malignancy were studied. Serum calcium, serum phosphorus, tubular phosphorus threshold, fasting calcium excretion, plasma 1,25‐dihydroxyvitamin D, nephrogenous cyclic adenosine monophosphate (AMP), and immunoreactive parathyroid hormone were measured. Excessive dietary calcium administration in the form of an oral hyperalimentation preparation appeared to be the cause of hypercalcemia in 2 patients. Six patients demonstrated humorally mediated hypercalcemia. These patients resembled patients with primary hyperparathyroidism in having elevated nephrogenous cyclic AMP excretion and reduced proximal tubular phosphorus reabsorption, but they differed from patients with primary hyperparathyroidism by having normal levels of immunoreactive parathyroid hormone, MA rkedly increased fasting calcium excretion, and strikingly reduced mean plasma levels of 1,25‐dihydroxyvitamin D. These data strongly suggest that the humoral factor responsible for hypercalcemia in patients with head and neck cancer is not parathyroid hormone, and that patients with hyperparathyroidism can now be distinguished with confidence from those with malignancy‐associated hypercalcemia.
UR - http://www.scopus.com/inward/record.url?scp=0020263288&partnerID=8YFLogxK
U2 - 10.1002/hed.2890050207
DO - 10.1002/hed.2890050207
M3 - Article
C2 - 7169331
AN - SCOPUS:0020263288
SN - 0148-6403
VL - 5
SP - 125
EP - 129
JO - Head and Neck
JF - Head and Neck
IS - 2
ER -