SAT-786 Abaloparatide associated calciphylaxis: a case report

Abstract Disclosure: A. Herrera Chancay: None. K.K. Soe: None. A. Bryant: None. A. Bhatnagar: None. Introduction: Calciphylaxis is a condition involving calcification of the tunica media in arterioles, leading to intimal fibroplasia and tissue necrosis. It commonly affects the skin, causing painful lesions, but can also involve areas with high adiposity. Historically linked to altered renal function, patients with normal renal function are termed non-uremic calciphylaxis. Its pathophysiology is less understood but is sometimes associated with obesity, malignancies, diabetes, and medications like warfarin, steroids, and diuretics, among others. While teriparatide is implicated in some non-uremic calciphylaxis cases, no Abaloparatide-associated calciphylaxis is reported. Abaloparatide has fewer hypercalcemia side effects than teriparatide, making this case more unique. Case presentation: A 65-year-old female was evaluated for osteoporosis after multiple fractures: a left hip fracture requiring replacement, a right tibial fracture, and an L2 compression fracture. Medical history includes GERD, chronic pancreatitis, tobacco use disorder, anxiety, and early menopause. She received no treatment except vitamin D 2000 IU daily and calcium 500 mg daily. Abaloparatide daily injection was initiated in Sept 2023. DXA showed osteoporosis (T scores: L spine -3.3, Rt femur -3.4, Rt femoral neck -3.9 ). The serum Ca value was initially at 9.5 mg/dL (Ref 8.6 -10.3 mg/dL) and trended up to 11 mg/dL after initiation of abaloparatide. Serum PTH became suppressed from 27 pg/mL to 11pg/mL (12-88 pg/mL) 24 hr urine calcium was 124 mg/24 hr (100-300). Serum phosphate, creatinine, and Vit D were normal. The patient denied taking OCT supplementations. After Calcium supplementation was discontinued, serum Calcium, PTH, and vitamin D levels became normal. Her mammogram that year showed progressively widespread bilateral calcifications, more pronounced in the left breast and significantly different from prior mammograms. The patient denied any interval illness, trauma, or infection of the breasts. The left breast biopsy showed fibroadenomatoid changes with coarse calcifications without malignancy. CT chest, abdomen, and pelvis revealed calcifications in the pancreas and aorta attributed to prior pancreatitis, elevated cholesterol, and active smoking. Since the calciphylaxis was confined to breast tissues, Abaloparatide was continued until the completion of 2 years of therapy. Conclusion: We are presenting the first case of non-uremic calciphylaxis secondary to abaloparatide. Without any other identifiable etiology for significant progression of breast calcification, abaloparatide treatment was attributed as the most likely etiology due to a strong temporal association. Presentation: Saturday, July 12, 2025