MON-776 When Electrolytes Tell the Story: Hypomagnesemia and Its Paradoxical Interaction with Parathyroid Disorders: A case report

Abstract Disclosure: R. Reguram: None. S. Neti: None. D.K. Yerasuri: None. Background: While hypomagnesemia can cause hypocalcemia, it also serves as an indicator for severity of primary hyperparathyroidism (PHPT) by contributing to hypercalcemia. This rare case presents a mixed picture of PHPT and familial hypocalciuric hypercalcemia (FHH) and the relationship between magnesium metabolism and parathyroid disorders. Presentation: A 76-year-old female with type 2 diabetes, hypertension, and chronic diarrhea presented with persistent hypomagnesemia despite oral and IV supplementation. Laboratory results showed consistently low magnesium (1.3-1.7 mg/dL), high-normal calcium (10.1-10.9 mg/dL), significantly elevated PTH (119.1-202.4 pg/mL), low 24-hour urine calcium (55-74 mg), and a high 24-hour urinary magnesium (186.9 mg) that indicated renal magnesium wasting. A Sestamibi scan identified a parathyroid adenoma. She also had a history of skeletal complications including an atraumatic radial fracture and severe osteoporosis on DEXA (radial T-score: -3.3). Despite these features pointing towards PHPT, presence of hypocalciuria and a low calcium-creatinine clearance ratio (<0.01) suggested coexisting FHH. Discussion: This case shows the complex interaction between magnesium, calcium and parathyroid (PTH) regulation. Hypomagnesemia can impair calcium-sensing receptor (CaSR) function and PTH secretion, potentially modifying PHPT presentation or mimicking FHH. Renal magnesium wasting likely exacerbated the patient's symptoms and complicated diagnosis. While FHH typically presents in younger individuals with mild hypercalcemia, this patient’s advanced age, significant osteoporosis and parathyroid adenoma supported PHPT. Hypomagnesemia is associated with more severe PHPT manifestations and increased risk of postoperative hypocalcemia. Hence comprehensive evaluation of magnesium status becomes critical, especially in patients with persistent hyperparathyroidism and atypical biochemical profiles. Conclusion: This case focuses on the importance of recognizing hypomagnesemia as both a modulator and a confounder in the diagnosis and management of parathyroid disorders. Persistent magnesium imbalance may complicate the presentation of PHPT or mimic FHH, leading to diagnostic uncertainty. Early and aggressive correction of hypomagnesemia is crucial not only for improving symptoms but also for ensuring accurate diagnosis and optimizing management. Further research is needed to clarify magnesium’s role in parathyroid pathophysiology and its impact on clinical outcomes. Presentation: Monday, July 14, 2025