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Humoral Hypercalcemia of Malignancy in Canine Lymphosarcoma^*

Section of Comparative Medicine (E.C. W.) and the Department of Internal Medicine (A.E.B., M.A.M.), Yale University School of Medicine New Haven, Connecticut 06511
The West Haven Veterans Administration Medical Center (K.L.I.) West Haven Connecticut 06516
Animal Medical Center (R.E.M., M.B.), New York New York 10021
The Department of Pathology, Colorado State University College of Veterinary Medicine (R. W.N.) Fort Collins, Colorado 80523
The Department of Small Animal Clinical Sciences, University of Minnesota College of Veterinary Medicine (S.D.J.) St. Paul, Minnesota 55108

Address requests for reprints to: Dr. Eleanor C. Weir, Section of Comparative Medicine, Yale University, 375 Congress Avenue, P.O. Box 3333, New Haven, Connecticutt 06510.

Abstract

Studies on the pathogenesis of hypercalcemia in canine lymphosarcoma have led to conflicting results. The biochemical and bone histomorphometric findings in canine lymphosarcoma were examined in 19 hypercalcemic and 17 nonhypercalcemic dogs with lymphosarcoma. Compared to the nonhypercalcemic group, the hypercalcemic dogs demonstrated an increase in fasting and 24-h calcium excretion, an increase in fractional phosphorus excretion, and a significant increase in nephrogenous AMP excretion. Plasma 1,25-dihydroxyvitamin D and immunoreactive PTH levels were equivalent in the two groups.

Quantitative bone histomorphometry performed on iliac crest biopsies revealed increased parameters of bone resorption in those hypercalcemic dogs with no evidence of tumor at the biopsy site, without a compensatory increase in bone formation.

Acid-urea tumor tissue extracts from eight hypercalcemic and six nonhypercalcemic dogs were examined for adenylate cyclasestimulating activity (ACSA). All tumors from hypercalcemic dogs contained ACSA, whereas none of the tumors from nonhypercalcemic dogs had ACSA. Further purification of one tumor extract yielded an adenylate cyclase-stimulating protein which appeared to interact specifically with the PTH receptor.

We conclude that in some cases, hypercalcemia in canine lymphosarcoma is mediated by a tumor-derived circulating boneresorbing factor which is distinct from PTH. ACSA detected in tumor tissue appears to be a reliable marker for the syndrome in vivo. The role of this activity in the pathogenesis of the syndrome remains to be determined (Endocrinology 122: 602–608,1988)

Footnotes

^* This work was supported by Grants RR-00393 and AM-30102 from the Division of Research Resources, NIH (Bethesda, MD) and a grant from the V.A.

Received August 18, 1987.

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