SAT-791 - A Case of Severe Recurrent Hypophosphatemia Due to Hyperventilation

Introduction: Transient hypophosphatemia may occur with hyperventilation-induced respiratory alkalosis due to phosphate redistribution from extracellular fluids into cells. We present a case of severe recurrent hypophosphatemia from hyperventilation masquerading as FGF23-mediated hypophosphatemia and primary hyperparathyroidism.

Case: A 39 year old woman was evaluated for refractory hypophosphatemia of unknown etiology. She was otherwise healthy until age 34y when she began experiencing episodic fatigue and weakness. Laboratory testing showed severely low blood phosphate (Pi), nadir < 1 mg/dL (nl 2.5-4.5), blood calcium (Ca) of 9.1-10.4 mg/dL (nl 8.5-10.2) and variable PTH of 22-128 pg/mL (nl 15-69). She underwent 2 gland parathyroidectomy for primary hyperparathyroidism with reported symptom resolution. At 38y, severe episodes of weakness, dyspnea, and chest tightness recurred, resulting in >20 emergency room visits where she was often profoundly hypophosphatemic. Despite chronic treatment with IV phosphate 976 mg daily, oral phosphate up to 5000 mg daily in divided doses, and calcitriol 0.5 mcg daily, intermittent symptomatic hypophosphatemia persisted, leading to referral to our clinical center. Since supplemental therapy confounds biochemical evaluation of hypophosphatemia, phosphate and calcitriol were discontinued at admission. Blood Pi was initially stable within the normal range for 2 days, followed by brief sporadic episodes of hypophosphatemia associated with shortness of breath and tachypnea. These hypophosphatemic bouts coincided with decreased bicarbonate (nadir 13 mmol/L; nl 22-29) and venous blood gas consistent with respiratory alkalosis and compensatory metabolic acidosis. Continuous end-tidal CO₂ monitoring confirmed concurrent hyperventilation. Episodes resolved with IV phosphate, IV lorazepam, or controlled breathing. PTH decreased from 160 pg/mL to 30-50s pg/mL, with normal blood Ca, reflecting resolution of phosphate-supplement induced secondary hyperparathyroidism. Intact FGF23 varied but was mildly elevated at 54-113 pg/mL (nl < 58). Tubular reabsorption of Pi (TRP) was initially 42% (normal 85-95%) indicating renal phosphate wasting but increased to 67-85% with decreased phosphate supplementation, suggesting physiologic responses to excessive phosphate loading. The patient was discharged off phosphate with PRN propranolol and lorazepam. Cognitive behavioral therapy and long-term anxiolytic treatment were recommended.

Conclusion: The differential diagnosis of hypophosphatemia is broad and includes proximal tubulopathies, FGF23-mediated hypophosphatemia, impaired intestinal absorption, and transcellular shifts. This case of respiratory alkalosis–induced hypophosphatemia highlights the importance of withholding phosphate and calcitriol during biochemical evaluation to ensure accurate diagnosis.

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