Background. The improvement in locoregional control of head and neck carcinomas over the last decades does not appear to modify the final survival of these patients, mainly due to the appearance of distant metastases and second neoplasms. We ran a study to evaluate the incidence of second neoplasms
Mechanisms of hypercalcemia in patients with head and neck cancer
β Scribed by Angel, Michael F. ;Stewart, Andrew ;Pensak, Myles L. ;Pillsbury, Harold R. C. ;Sasaki, Clarence T.
- Publisher
- Wiley (John Wiley & Sons)
- Year
- 1982
- Weight
- 491 KB
- Volume
- 5
- Category
- Article
- ISSN
- 0148-6403
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β¦ Synopsis
Abstract
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 1,25βdihydroxyvitamin 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 1,25βdihydroxyvitamin 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 malignancyβassociated hypercalcemia.
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