SUN-800 Hypercalcemia in Disseminated Coccidioidomycosis

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Abstract Disclosure: T. Patel: None. E. Rosario Diaz: None. D. Rosario Lora: None. T. Porter: None. Background: Hypercalcemia is a rare but serious complication of disseminated coccidioidomycosis, with its underlying mechanism remaining unclear. One case report suggests that hypercalcemia may result from the expression of parathyroid hormone-related peptide (PTHrP) by granulomatous tissue [1]. However, other studies indicate that hypercalcemia in coccidioidomycosis is not associated with the increased production of 1,25-dihydroxyvitamin D (calcitriol), a common mechanism seen in other granulomatous diseases [2]. This case illustrates that the direct destruction of bone tissue may be the underlying cause of hypercalcemia.Body: A 24-year-old man with disseminated coccidioidomycosis (C. immitis) manifesting as multiple soft tissue abscesses, multifocal osteomyelitis, and numerous lytic lesions throughout the axial and appendicular skeleton, presented with persistent hypercalcemia. His ionized calcium level was 1.52 (0.95-1.32 mmol/L), and his adjusted calcium was 12.3 (9.1-11.2 mg/dL), despite receiving various antifungal treatments. A detailed history revealed no previous use of calcium supplements, thiazides, topiramate, or lithium. Work up to determine the etiology of hypercalcemia included PTH < 4 (8.0 - 85.0 pg/mL), PTHrp < 2 ( < 2 pmol/L), 25-OH vitamin D 5 (30-80 ng/mL), 1,25-OH vitamin D 6.5 (24.8 - 81.5 pg/mL), SPEP and UPEP unremarkable. Hypercalcemia was resistant to aggressive intravenous hydration. Remarkably, calcium levels normalized within 36 hours and remained stable off intravenous fluids following a single dose of 4 mg IV zoledronic acid. Conclusion: The pathophysiology of hypercalcemia due to direct bone destruction is well established in the context of malignancies such as multiple myeloma and certain metastatic cancers, where excessive osteoclast-mediated bone resorption is the primary mechanism. In our patient, we hypothesize a similar process occurring as a result of disseminated infection. The rapid normalization of calcium levels after administration of bisphosphonates, which inhibit osteoclastic bone resorption, strongly supports this hypothesis.1. Fierer J, Burton DW, Haghighi P, Deftos LJ. Hypercalcemia in disseminated coccidioidomycosis: expression of parathyroid hormone-related peptide is characteristic of granulomatous inflammation. Clin Infect Dis. 2012;55(7): e61-e66.2. Caldwell JW, Arsura EL, Kilgore WB, Reddy CM, Johnson RH. Hypercalcemia in patients with disseminated coccidioidomycosis. Am J Med Sci. 2004;327(1):15-18. Presentation: Sunday, July 13, 2025

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