MON-259 Transient PTH Resistance and Vitamin D Deficiency in a Newborn with Hypocalcemic Seizure and Bacteremia

Abstract

Background: Late onset neonatal hypocalcemia is a rare condition defined by a total calcium of <7 mg/dL after 72 hours of life. Etiologies include increased phosphate load, hypoparathyroidism, vitamin D deficiency, hypomagnesemia, and PTH resistance. Hypocalcemia has been reported in the setting of critical illness/sepsis in both adults and children, and in adults with bacteremia. Clinical case: An 18 day old full-term, formula-fed female infant was admitted with hypocalcemic seizures. Four days prior to presentation, she began experiencing brief episodes of altered mentation and rhythmic jerking with associated vomiting and decreased oral intake. She was afebrile and normotensive. She had no dysmorphic features or brachydactyly, and she was otherwise well appearing. Initial labs showed hypocalcemia (total calcium 6.4 mg/dL (9-10.9), ionized calcium 2.8 mg/dL (4.2 - 5.2)) and hyperphosphatemia (phosphorous 9 mg/dL (3.4-5.9). Magnesium and alkaline phosphatase were normal. Bicarbonate was low at 17 mEq/L (22-32) with an anion gap of 16. Lactic acid was mildly elevated at 2.2 mEq/L (0.2-1.9) with a normal pH. BUN was 5 mg/dL with a creatinine of 0.23 mg/dL. She had a witnessed seizure and was given 1 mL/kg of 10% calcium gluconate and initiated on calcium supplementation. In the setting of a total calcium of 6.8 mg/dL and phosphorous of 7.9 mg/dL, PTH was elevated at 143 pg/mL (18-80). The 25-OHD was low at 7.4 ng/mL (>30), and 1,25 OHD was 56 pg/mL (31-87 pg/mL). Urine calcium/creatinine ratio was 0.58. Random urine phosphorous was low at <10 mg/dL. TSH was normal. Initial evaluation included urine, blood, and CSF cultures which revealed Klebsiella pneumoniae bacteremia. Ionized calcium normalized by day 4 of calcium therapy, and over the following two weeks, the calcium dose was slowly reduced. She was also treated with cholecalciferol and low phosphate formula, and completed a 10 day antibiotic course. Maternal labs revealed normocalcemic vitamin D deficiency with a 25-OHD of 9.4 ng/mL. Conclusion: We describe a full-term, formula-fed newborn who presented with seizures due to late onset hypocalcemia in the setting of bacteremia, and severe vitamin D deficiency. Evaluation was consistent with transient PTH resistance, evidenced by hypocalcemia, hyperphosphatemia, low urinary phosphorous, and elevated PTH. Mechanism is likely multifactorial including excess phosphate load from formula intake, dehydration or relative renal insufficiency from bacteremia, and vitamin D deficiency. To our knowledge, this is the first report of a neonate with late onset hypocalcemia due to PTH resistance found to have concomitant bacteremia and severe vitamin D deficiency, and emphasizes the importance of evaluation for sepsis in a neonate presenting with seizure, regardless of etiology.