8298 PrimaryHyperparathyroidism after Initiation of Burosumab in a Patient with X-linked Hypophosphatemic Rickets

Abstract Disclosure: A. Melhim: None. S. Samarasinghe, MD: None. P. Camacho, MD: None. Title: Primary Hyperparathyroidism after Initiation of Burosumab in a Patient with X-linked Hypophosphatemic Rickets Abdullah Melhim, MD; Shanika P Samarasinghe, MD; Pauline M. Camacho, MD FACE Introduction: X-linked hypophosphatemic rickets is an autosomal dominant disease that is characterized by high phosphate wasting at the proximal tubule resulting in slow growth, rickets and osteomalacia. It is usually associated with low serum phosphate, normal calcium, and either normal or modestly elevated levels of parathyroid hormone (PTH). We present a case of a male patient who developed primary hyperparathyroidism after initiation of Burosumab, a new monoclonal antibody directed against fibroblast growth factor 23 (FGF23). Clinical Case A 47-year-old man with a history of juvenile X-linked hypophosphatemic rickets and confirmed PHEX mutation presented to our clinic. He previously had normal to low-normal PTH levels, normal calcium and vitamin D levels with persistently low phosphorus, despite being on calcitriol and phosphate supplements. Patient was started on Burosumab on 7/2021 and 2 months later was noted to have rising PTH levels up to 104 pg/ml (14 – 67) with high normal calcium of 10.3 mg/dL (8.9 - 10.3), albumin of 4.5 gm/dL, vitamin D, 25- Hydroxy of 34 ng/ml (30 – 80) and low phosphorus of 1.9 mg/dL (2.5 - 4.7) consistent with primary hyperparathyroidism. Initially the patient was normocalcemic with high PTH but eventually developed frank hypercalcemia. After further discussion, the patient reported urinary frequency, constipation, and worsening fatigue, but denied any history of nephrolithiasis. Sestamibi scan completed on 8/2023 revealed increased uptake in a right inferior nodule suggestive of a parathyroid adenoma. He subsequently underwent subtotal parathyroidectomy on 11/2023 confirming enlarged hypercellular right superior and inferior and left inferior parathyroid glands. Few reports have described increasing PTH levels after prolonged anti-FGF23 treatment, however our patient started developing primary hyperparathyroidism only a few months after starting treatment. Some recent studies suggest that FGF23 and PTH could have an interdependent phosphaturic effect, this can explain the development of primary hyperparathyroidism in the setting of suppressed FGF23 levels with Burosumab. Conclusion: Burosumab is a new monoclonal antibody directed against FGF23 re