MON-835 - Silicone Shadows: An Unusual Cause of Hypercalcemia

A 44-year-old woman with a history of extensive cosmetic silicone injections and implants, stage IV chronic kidney disease (CKD), chronic pain, anxiety, and depression was evaluated for recurrent non–PTH-mediated hypercalcemia.
She initially presented to the emergency department with acute kidney injury (creatinine 3.9 mg/dL) and severe hypercalcemia (calcium 13.8 mg/dL). Initial evaluation demonstrated suppressed parathyroid hormone (PTH 15.8 pg/mL), low 25-hydroxyvitamin D (14.1 ng/mL), elevated 1,25-dihydroxyvitamin D (67 pg/mL), mildly elevated PTH-related peptide (PTHrP 7.1 pg/mL; normal < 3.4), normal SPEP/IFE, ESR 6, ACE 74, and negative infectious and autoimmune workup including T-Spot testing. Renal biopsy revealed nephrocalcinosis with arteriosclerosis and interstitial scarring.
She experienced recurrent hospitalizations for hypercalcemia with calcium levels ranging from 12.5–14.6 mg/dL, requiring aggressive hydration and intermittent treatment with intravenous zoledronic acid (2–3 doses over several years). She reported minimal classic hypercalcemia symptoms.
Extensive malignancy and granulomatous disease evaluation, including PET-CT revealed diffuse, symmetric FDG-avid inflammatory changes within the bilateral gluteal and proximal thigh subcutaneous tissues (SUV max 4.9–5.4), spanning approximately 31 cm craniocaudally, corresponding to sites of prior silicone injections and implants. No evidence of malignancy or systemic granulomatous disease was identified. These findings were most consistent with silicone-induced granulomatous inflammation.
Glucocorticoid therapy was initiated, resulting in consistent improvement in serum calcium and inflammatory symptoms. However, disease control was limited by inconsistent adherence and repeated steroid discontinuation, leading to recurrent hypercalcemic relapses. The patient ultimately required chronic prednisone therapy (20–40 mg daily) with PJP prophylaxis. Attempts at steroid tapering resulted in recurrent hypercalcemia. Repeat imaging with MRI demonstrated diffuse inflammatory and nodular changes consistent with granulomatous reaction to silicone.
She remains dependent on glucocorticoids for calcium control and is actively pursuing surgical consultation for implant removal and debulking as a potential definitive treatment.
Discussion
This case highlights silicone-induced granulomatous disease as a rare but important cause of chronic, steroid-responsive hypercalcemia mediated by extrarenal 1α-hydroxylase activity. Recognition of this entity is critical, as management differs from malignancy-associated hypercalcemia and often requires long-term immunosuppression or surgical intervention.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*