Hypocalcemic cardiomyopathy-different mechanisms in adult and pediatric cases

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Abstract

Background: Hypocalcemic cardiomyopathy (CMP) is a rare but potentially reversible cause of heart failure. However, the mechanism of hypocalcemia seems to differ between infants and adults. Although severe vitamin D deficiency alone is the usual cause of hypocalcemic CMP in infants, in adult patients significant cardiac dysfunction usually occurs as a result of hypoparathyroidism, either isolated or in combination with vitamin D deficiency.Wepresent two cases of hypocalcemic CMP-one adult and one pediatric-to highlight these differences. Case Presentation: The first patient was a 47-year-old female who presented with progressive dyspnea and fatigue and was found to have severe left ventricular (LV) systolic dysfunction (LV ejection fraction, 25%). Her serum calcium level was 3.5 mg/dL, serum phosphorus level was 5.7 mg/dL, and serum 25-hydroxyvitamin D level was 14.1 ng/mL, along with a serum PTH level of 11.8 pg/mL. Her LV ejection fraction normalized completely over 6 months with calcium and calcitriol treatment. In contrast, the second patient was an infant who had presented in cardiogenic shock. Investigations revealed serum calcium of 4.5 mg/dL, serum phosphorus of 11.9 mg/dL, 25-hydroxyvitamin D of 8.9 ng/mL, and serum PTH level of 670 pg/mL. Calcium and calcitriol supplementation resulted in rapid and complete clinical and hemodynamic recovery. Conclusion: Hypocalcemia is a rare but treatable cause of dilated CMP. In infants, hypocalcemia is usually due to maternal vitamin D deficiency and is accompanied by compensatory hyperparathyroidism. In contrast, in adult patients, hypocalcemic CMP is usually a result of hypoparathyroidism, with or without concomitant vitamin D deficiency. Copyright © 2014 by the Endocrine Society.

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APA

Bansal, B., Bansal, M., Bajpai, P., & Garewal, H. K. (2014). Hypocalcemic cardiomyopathy-different mechanisms in adult and pediatric cases. In Journal of Clinical Endocrinology and Metabolism (Vol. 99, pp. 2627–2632). Endocrine Society. https://doi.org/10.1210/jc.2013-3352

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