SAT-308 Chronic Hypophosphatemia Associated with Supraphysiologic Glucocorticoid Treatment

Abstract E. Chuki: None. K. Saleh Anaraki: None. R.I. Gafni: None. K.L. Roszko: None. I.R. Hartley: None. Background: The impact of corticosteroids on phosphate metabolism is not well understood. A potential relationship is suggested by the association between Cushing’s syndrome and hypophosphatemia, which, in some cases resolves following adrenalectomy. We report a case of chronic hypophosphatemia on supraphysiologic glucocorticoid therapy, which reversed after reducing exogenous steroid dosage. Case Presentation: A 37-year-old woman was seen for chronic hypophosphatemia. Two years prior, she underwent trans-sphenoidal resection of a non-functioning macroadenoma. Surgery was complicated by panhypopituitarism requiring replacement levothyroxine, hydrocortisone, HRT, and DDAVP. GH deficiency was not replaced. Blood phosphate prior to surgery was in the normal range. Four months following surgery, the patient developed fatigue and palpitations after starting prednisone 40 mg for inflammatory arthritis and was found to have severe hypophosphatemia. Initial work up showed blood phosphate of 1.8 mg/dL (2.5-4.5 mg/dL), 1,25(OH)2-Vitamin D (1,25D) of 51 pg/mL (18-72 pg/mL), and C-terminal FGF23 (cFGF23) elevated at 200 RU/mL(<180 RU/mL). PTH and calcium were within normal limits. Urine phosphate was uninterpretable. Over a year, hypophosphatemia persisted despite phosphate supplementation, and the patient experienced debilitating bone pain, muscle weakness, and fatigue. While steroids were titrated down, there was a strong negative correlation (r=-0.7) between the patient’s steroid dosage and phosphate level. Once hydrocortisone was decreased to physiologic dosing (10.64 mg/m2 BSA), the patient reported increased energy levels and reduced fatigue. Follow up labs off all phosphate supplements showed resolution of hypophosphatemia with serum phosphate of 3.0 mg/dl, undetectable urine phosphate (TRP exceeding 80%) 1,25D 75 pg/mL (18-72 pg/mL), and cFGF23 77 RU/mL. Conclusion: In this case, a patient experienced apparent FGF23-mediated hypophosphatemia on exogenous steroids, with a strong negative correlation between steroid dosage and phosphate levels. The impact of glucocorticoids on serum phosphate concentration is speculated to be due to glucocorticoid effects on FGF23 production and/or direct renal tubular effects. Growth hormone deficiency, which can be associated with hypophosphatemia, may have been an additional contributory factor, given GH was not replaced. Further studies are needed to understand the relationship between glucocorticoids and phosphate handling. Saturday, June 1, 2024