Abstract
Hypercalcemia presents difficult problems of diagnosis and therapy. Recent studies in adults and animal tumor models have established that prostaglandin excess can be etiologic. The resultant hypercalcemia is responsive to inhibitors of prostaglandin synthetase.
A 6 week old female with subcutaneous fat necrosis and hypercalcemia was unresponsive to treatment with furosemide-saline diuresis, corticosteroids, low calcium feedings, and vitamin D elimination. Rather than using more toxic therapy, a trial of aspirin (ASA) at 100 mg/kg/d was initiated. Serum calcium fell in 2 days to 10 mg/dl from a high value of 15. It remained in the normal range thereafter except during attempts to lower ASA dosage at 14 days. A similar effect was noted in a second infant with subcutaneous fat necrosis. Calcium fell only to 13 mg/dl from 18, however, and diuretic therapy was successfully added. In both patients, elevated serum triglyceride levels also responded rapidly. A third infant with hypercalcemia, nephrocalcinosis and trisomy 21-22 mosaicism was treated. ASA rapidly lowered serum calcium to normal. ASA was discontinued after 13 days without exacerbation. Despite extensive clinical studies in each case, no definitive mechanism for hypercalcemia was found. These preliminary case studies suggest a role for prostaglandins in certain hypercalcemic states as well as a potentially safe form of therapy.
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Ward, R., Sockalosky, J., Dolan, L. et al. 901 HYPERCALCEMIA RESPONSIVE TO ASPIRIN. Pediatr Res 12 (Suppl 4), 514 (1978). https://doi.org/10.1203/00006450-197804001-00906
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DOI: https://doi.org/10.1203/00006450-197804001-00906