Two cases of paraneoplastic hypercalcemia secondary to ovarian tumors are presented. Both cases were secondary to ectopic parathormone (PTH) production. Other mediators postulated to cause this syndrome are prostaglandins, vitamin D-like sterols, non-vitamin D sterols, vitamin A, cortisol, and "osteoclast-activating factor.' The key treatment modalities for acute hypercalcemia are hydration and diuresis with furosemide; phosphates, steroids, antiprostaglandins, and hemodialysis may also be of value. Calcitonin is theoretically the most attractive treatment modality, but the rapid development of resistance limits its use to acute management. Mithramycin is most effective for long-term palliation of hypercalcemia if tumor-directed therapy is unsuccessful. Review of the literature confirms the previously made observation that mesonephromas are disproportionaately represented in association with this syndrome.