Dilated Cardiomyopathy due to Vitamin D Deficiency

C l i n M e d International Library Citation: Karabayir N, Kelesoglu E, Bornau H, Oztarhan K, Aktas D, et al. (2016) Dilated Cardiomyopathy due to Vitamin D Deficiency. Int J Clin Cardiol 3:084 Received: May 30, 2016: Accepted: August 04, 2016: Published: August 06, 2016 Copyright: © 2016 Karabayir N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Karabayir et al. Int J Clin Cardiol 2016, 3:084


Introduction
Dilated cardiomyopathy (DCM), which mostly has an idiopathic etiology, or is caused by genetic inheritance or infection, can cause irreversible congestive heart failure.Although hypocalcemia secondary to vitamin deficiency is an important cause of DCM in infants, cardiogenic shock as a presenting feature without clinical or radiological features of rickets is very rarely reported in the literature [1][2][3][4].
Here, we report two cases of DCM secondary to hypocalcemia that originated from a nutritional vitamin D deficiency induced rickets both were exclusively breastfed by mothers who had vitamin D deficiency.

Case 1
Five month-old boy who had cyanosis and respiratory difficulty was admitted to our emergency department.He was born at 38 weeks of gestational age with a birth weight of 3,850 kg and he had been exclusively breastfed.There were no medical or familial histories.He was not taking any medications or vitamin supplements.Family history was unremarkable.was added to treatment at 50 µg/kg parenterally.Echocardiographic exam conducted 3 days after the initiation of therapy showed an EF of 65% (Figure 4), and a Ca value of 7.2 mg/dL, which allowed for oral calcium supplementation.After a further 1-week follow up, the Ca level was 8.78 mg/dL.The patient was discharged on current treatment and advised to return for follow up.

Discussion
Dilated cardiomyopathy in children have been well studied.The most common cause of DCM is an idiopathic etiology (> 60%), followed by familial cardiomyopathy and acute myocarditis.Other causes of DCM include viral infections, endocrine disorders and metabolic diseases.Cardio toxic drugs and systemic diseases can also cause DCM [5,6].Calcium ions have a key role in the excitation of the cardiac muscle fibers, and reduction in serum calcium level may affect ventricular contraction [7,8].Hypocalcemia causes decreased myocardial contractility, leading to congestive heart failure, hypotension, and angina [9].Rickets is a metabolic disorder of the bone that develops due to in sufficient mineralization of the bone tissue and present strikingly in the skeletal system [10].Hypocalcemia is present in the majority of patients with vitamin D deficiency rickets and may cause convulsions [4].Consequently, it has been considered that the leading cause cardiomyopathy in patients with rickets was longstanding hypocalcemia, but the exact mechanism of cardiomyopathy has not been understood [4].
Many reports of with hypocalcemia-associated reversible heart failure and dilated cardiomyopathy have appeared in international publications.Yilmaz et al. showed that eight patients who developed dilated cardiomyopathy and congestive heart failure because of marked rickets-associated hypocalcaemia were described between 1999 and 2012 in our country [9].Brown et al. reported four patients with signs of dilated cardiomyopathy related to rickets and congestive heart failure at the ages of 4-10 months [10].At admission, extremely low calcium and vitamin D levels were revealed in our patients.After calcium and vitamin D replacement, abnormal findings of calcium and vitamin D were corrected rapidly with the normalization of parathyroid hormone and left ventricular function improved.
Rachitic hypocalcemic cardiomyopathy is a serious life threatening complication of infantile vitamin D deficiency rickets which is a growing community health problem, among breastfed infants born to vitamin D deficient mothers.In a study reported that maternal D vitamin status had a crucial effect on rickets development in babies [11].Mother of our patients had very low vitamin D levels.
Although hypocalcemia secondary to vitamin D deficiency is an important cause of DCM in infants, cardiogenic shock as a presenting feature without clinical or radiological features of rickets is very rarely reported in the literature [12,13].Kumar et al. noted that dilated cardiomyopathy and cardiogenic shock developed in a 2-month-old patient with severe hypocalcaemia as a result of vitamin D deficiency.Rickets caused a clinical picture characterised by a dL, RDW: 17.2%, WBC: 7.12 x 103/µL, HCT: 27.9%, PLT: 407 x 103/ µL, ALB: 3.75 g/dL, ALP: 438 U/L, Ca: 5.82 mg/dL (9-11), P: 10.4 mg/ dL (3.5-6.6),PTH: 93.92 pg/mL (15-65), 25OHD: 3.53 ng/mL and ionized Ca: 3.16 mg/dL.Therapy was initiated with Ca 50 mg/kg/day IV and vitamin-D 2,000 IU/day po.Electrocardiological assessment revealed a QTc interval of 380 ms with no pathology.Upon detection of a spheric left ventricle and EF 38% in echocardiography (Figure 3), furosemide and captopril treatments were initiated.The mother's biochemical tests obtained Ca: 9.3 mg/dL, P: 3.57 mg/dL, 25OHD: 3.0 ng/mL and PTH: 61.1 pg/mL.In addition, the patient's anemia work up revealed iron: 129 µg/dL (50-150), iron binding capacity: 239 µg/ dL, and vitamin-B12: 255 pg/mL (211-946).Therefore, vitamin B12    decline in cardiac function with progression to cardiogenic shock [1].Our first patient had clinical, biochemical and radiological signs of rickets in conjunction with signs of cardiogenic shock secondary to severe DCM.Also, our second patient aged 48 days old is one of the youngest patients in the literature.
Paediatricians should recognize risk factors for rickets and prescribe appropriate vitamin supplementation in infants at risk.Plans for prevention by antenatal supplementation of vitamin D to pregnant mothers with 1000 -2000 IU of vitamin D3 is vital.Also, pediatric cardiologists should include hypocalcemia in the differential diagnosis of children with DCM.