Furosemide-Induced Severe Hypocalcemia in Latent Hypoparathyroidism SUN-454 Furosemide-Induced Severe Hypocalcemia in Latent Hypoparathyroidism Robin Koshy MD and Lisa Ceglia MD MS Tufts Medical Center, Boston, MA Date: Sunday, March 18, 2018 Time: 1:00 – 3:00 PM Poster Board Number: SUN-454 Room: ENDOExpo Hall, McCormick Place West Due to inadequate volume diuresis with furosemide, Cardiology switched to a continuous bumetanide drip. Within 24 hours, the patient’s ionized Ca markedly improved to 4.3 mg/dL (ref 4.2-5.2) and IV calcium infusion was discontinued. Oral Ca and calcitriol requirements decreased within 72 hours. Bumetanide IV was switched to oral torsemide and the patient was discharged on oral Ca supplementation 500 mg BID and calcitriol 0.25 mcg daily. After discharge, serum total Ca level was 9.4 mg/dL. Introduction Loop diuretics (e.g. furosemide) promote renal calcium (Ca) excretion. Their calciuric effect stimulates a rise in serum parathyroid hormone (PTH) levels to maintain normocalcemia. However, use of loop diuretic therapy in patients with an impaired PTH response may pose a significant risk of hypocalcemia. Case Summary Case Description We describe a case of latent hypoparathyroidism (etiology presumed postsurgical ± postradiation) who developed symptomatic refractory hypocalcemia on furosemide. The severity of hypocalcemia and the amount of treatment required were dependent on the dose of furosemide. Notably, a switch to bumetanide and torsemide, which are other potent loop diuretics, markedly reduced the treatment required for hypocalcemia. This finding indicates that these alternative loop diuretics have lesser calciuric effects compared to furosemide, as described in only two prior case reports.1, 2 Bumetanide and torsemide may be preferable loop diuretics in the management of volume overload in patients with latent hypoparathyroidism. A 54-year-old female with a history of thyroid cancer status post total thyroidectomy (2007) and a restrictive cardiomyopathy secondary to radiation therapy for Hodgkin’s lymphoma (1990s), presented with acute on chronic heart failure. On admission, serum total Ca levels were 8.1-8.3 mg/dL (ref 8.5-10.5) and serum phosphorus levels were 5.7-6.5 mg/dL (ref 2.7-4.5). She denied a history of hypoparathyroidism. She was not taking calcium supplements. Her hospital course was complicated by worsening cardiac function requiring orthotopic cardiac transplantation (OHT). She was initiated on IV furosemide. Serum total Ca levels declined as low as 6.3 mg/dL when furosemide dose was increased to a high continuous drip (40 mg/hr). Serum total Ca levels improved as the furosemide dose was reduced. Endocrine was consulted when the patient’s serum total Ca levels dropped to 6.3 mg/dL with positive Trousseau’s and Chvostek’s signs on exam. Of note, when Ca level was 6.3 mg/dL, serum PTH level was 35 pg/mL (ref 11-95), magnesium was 2.1 mg/dL (ref 1.5-2.6), 25-hydroxyvitamin D was 18 ng/mL, phosphorus level was 5.7 mg/dL and eGFR was 42 ml/min/m2. Despite oral Ca supplementation of 3-4 g/day, vitamin D2 50,000 IU/week, and calcitriol 2 mcg/day, she had refractory severe hypocalcemia requiring a Ca gluconate intravenous infusion. References 1. Shankaran S., et al. Mineral excretion following furosemide compared with bumetanide therapy in premature infants. Pediatric Nephrology 1994. Vol 9(2): 159-162. 2. Abrams J. Intramuscular Bumetanide and Furosemide in Congestive Heart Failure. Journal of Clinical Pharmacology 1981. Vol 21(11): 673-679.