SUN-793 Hypercalcemia Secondary to Silicone-Implant Induced Granulomatous Disease

Abstract Disclosure: M. Uppal: None. J. Khoury: None. S. Mousavi: None. K. Saardi: None. C. Baldwin: None. N. El-Asmar: None. Introduction: The introduction of silicone into soft tissue may lead to a foreign body-triggered granulomatous process that rarely results in hypercalcemia. We present a case of PTH-independent hypercalcemia due to gluteal silicone implants and offer insight into pathophysiology and therapeutic management options. Case presentation A 54-year-old man with history of HIV presented with lower extremity pain and osteomyelitis. Lab testing showed hypercalcemia with corrected serum calcium (CoCA) 11.6 mg/dL [8.5-10.5mg/dL] and acute kidney injury with serum Cr of 2.6 mg/dL. Further work-up revealed: PTH 17 pg/mL [16-80 pg/mL], phosphorous 6.1 mg/dL [2.5-4.5 mg/dL], 25-hydroxy vitamin D 27 ng/ml, and normal TSH. PTHrp was normal, while 1,25 di-hydroxy vitamin D was elevated at 169 pg/mL [24.8 - 81.5 pg/mL]. QuantiFERON TB-gold test was negative. ACE levels were normal at 55 U/L [14-82 U/L]. Serum and urine protein electrophoresis showed no evidence of multiple myeloma. CT revealed a 6 mm ureteral stone, hydronephrosis, and bilateral gluteal soft tissue changes. On further questioning, the patient reported history of street-level silicon gluteal implants decades prior. He was treated with IV fluids followed by high-dose glucocorticoids due to rise in CoCA to 13.3 mg/dL. He was given prednisone 40 mg followed by 60 mg daily. CoCA improved to 10.9 mg/dl after 6 days of steroid treatment after which patient left against medical advice. A year later, he presented with hematuria and CoCA of 14.9 mg/dL and was treated with IV fluids, calcitonin, prednisone, and zoledronic acid with minimal improvement in CoCA to 12 mg/dl. Surgery recommended against wide excision of the silicone-induced gluteal soft tissue changes given the extent of spread. Dermatology team performed a skin biopsy that showed silicone but no granulomas, likely due to patchy inflammation. During a third admission for flank pain and hypercalcemia with CoCA of 13.8 mg/dl in a one-year timeframe; the patient was treated with IV fluids and denosumab without improvement in calcium levels. He declined glucocorticoids at the time. After discussion with the Dermatology team, a single dose of TNF-alpha inhibitor infliximab 5mg/kg was given with improvement in CoCa to 11 mg/dL at discharge and a decrease in serum 1,25-di-hydroxy vitamin D from 79pg/mL to 41pg/dL. Conclusion: Silicone-induced hypercalcemia, due to granulomatous disease and consequent increased 1,25-di-hydroxy vitamin D production, can manifest years later. Treatment includes fluids and glucocorticoids. The efficacy of bisphosphonates and other anti-resorptive agents may be limited given the underlying mechanism of excessive 1,25 di-hydroxy vitamin D-induced hypercalcemia. If necessary, TNF alpha inhibitors may offer a potential therapeutic option by reducing inflammation within the granulomas thereby lowering the excessive production of active 1,25-di-hydroxy vitamin D. Presentation: Sunday, July 13, 2025