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Apollo Medicine 2011 DecemberCase Report

Volume 8, Number 4; pp. 315–316

© 2011, Indraprastha Medical Corporation Ltd

Preventable cause of dilated cardiomyopathy in children

Latha Vishwanathan*, M Sridhar**Consultant Paediatrician, Apollo Children’s Hospital, Thousand Lights, Chennai – 600006, India.

ABSTRACT

We present a 2-month-old infant with dilated cardiomyopathy (DCM) secondary to vitamin D deficient rickets. This case highlights a treatable and preventable cause of DCM which arose because of maternal vitamin D deficiency. Early identification of this problem in mother would have prevented this condition occurring in the infant.

Keywords: Cardiomyopathy, children, maternal vitamin D deficiency, vitamin D

Correspondence: Dr. Latha Vishwanathan, E-mail: latha_vish2000@yahoo.comdoi: 10.1016/S0976-0016(11)60018-5

INTRODUCTION

Early onset of vitamin D deficient rickets is recognized in many breast-fed infants across the globe. This condition presents more acutely when there is a concurrent maternal vitamin D deficiency. This study highlights this condition which occurred in the infant early in his life resulting in a seri-ous complication namely dilated cardiomyopathy (DCM), due to the maternal deficiency. This is a preventable, and once identified it is a treatable cause of DCM and in most cases a complete recovery of cardiorespiratory function.

CASE REPORT

A 2-month-old male infant was presented to our hospital following a brief febrile illness with cardiorespiratory fail-ure requiring ventilator support and intensive care. Chest X-ray analysis revealed a dilated heart and an echocardio-graphical study confirmed DCM with severe left ventricu-lar dysfunction (ejection fraction of 20%). His laboratory workup showed serum calcium—4.9 mg/dL (8.5–10.5 mg/dL), serum phosphorous—7.6 mg/dL (3–4.5 mg/dL), alkaline phosphatase—2576 IU/mL (50–650 IU/mL), vitamin D 11.3 ng/mL (7.6–75 ng/mL), parathormone (PTH)—414 pg/mL (10–69 pg/mL), and urine calcium—6.9 mg/dL (normal < 10). His renal function was normal. Maternal laboratory results showed calcium 8.4 mg/dL, vitamin D 6.32 ng/mL and PTH 60 pg/mL. There was radiological evidence of rickets in the infant. After diagnosis of vitamin D deficiency, both

mother and child were started on vitamin D supplemen-tation along with calcium correction for the baby. The infant’s calcium levels normalized with the above man-agement with a significant improvement in the cardiac sta-tus with the ejection fraction normalizing over the next 2 months.

DISCUSSION

There are a few case reports of vitamin D deficient rickets presenting as an early onset cardiomyopathy.1,2 We believe that the abovementioned patient is the youngest to present with this condition. In India, despite plenty of sunshine, this vitamin deficiency is common because of dietary reasons as opposed to poor exposure to sunlight as in colder conti-nents. There seems to be a paucity of reference to cardio-myopathy as a result of vitamin D deficiency in Indian literature. There are many complications of rickets that can occur in infants such as bony abnormalities, respiratory dif-ficulties, fractures, bone pain, late or abnormal dentition, frequent infections, to name a few. The DCM has been reported in few cases of vitamin deficient rickets and is known to present very early in life. The exact mechanism of DCM in rickets is poorly understood, although calcium ions have a key role in the excitation as well as in the contraction of the cardiac muscle fibers, and reduction in serum cal-cium level may affect ventricular contraction.3 Vitamin D deficiency in utero and early life leads to delayed matura-tion and subsequent enhanced growth (proliferation and

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316 Apollo Medicine 2011 December; Vol. 8, No. 4 Vishwanathan and Sridhar

© 2011, Indraprastha Medical Corporation Ltd

hypertrophy) of cardiomyocytes in the left ventricle. This may lead to altered cardiac function later in life, a finding suggestive by animal study.4 A prospective study investigat-ing cardiac functions in patients with rickets done by Uysal et al showed that the heart may be affected in rickets although none of the patients showed symptoms of cardiac dysfunction.5 It is important to point out that this poor car-diac function secondary to hypocalcemia is completely reversible and should always be suspected in children who are refractory to traditional methods of treatment.

Although vitamin D is present in breast milk in suffi-cient quantities, a pre-existing deficiency of this vitamin in the mother, as in this case, would most likely result in early onset rickets and resultant complications for the baby. Vitamin D deficiency is common in pregnant women (5–50%) and in breast-fed infants (10–56%), despite the widespread use of prenatal vitamins, because these are inad-equacies to maintain normal vitamin D levels (≥ 32 ng/mL).6 Adverse health outcomes such as pre-eclampsia, low birth weight, neonatal hypocalcemia, poor postnatal growth, bone fragility, and increased incidence of autoimmune dis-eases have been linked to low vitamin D levels during preg-nancy and infancy. Onal et al makes a case in a study for increasing the recommended daily maternal allowance of vitamin D from the usual 400 IU/day to 600 IU/day during the breast-feeding period. He found that up to 27.2% of exclusively breast-fed children born to mother with this supplementation had inadequate vitamin D level in blood.7 Apart from dietary reasons, the attire worn by some mothers due to religious considerations also plays a part in poor exposure to ultraviolet light, as this is necessary to convert vitamin D present in the skin to its active form, so that the body can use its existing store appropriately. A combination of such factors had resulted in this mother having significant

vitamin D deficiency although a clinical diagnosis of this deficiency is often difficult to identify in pregnant mothers. This case highlights the need for a regular blood–bone pro-filing and diet counseling for such pregnant mothers who have poor exposure to sunlight and dietary inadequacy so as to prevent a rare but serious complication in young infants in the form of DCM.

REFERENCES

1. Brown J, Nunez S, Russell M, Spurney C. Hypocalcemic rick-ets and dilated cardiomyopathy: case reports and review of literature. Pediatr Cardiol 2009;30:818–23.

2. Maiya S, Sullivan I, Allgrove J, et al. Hypocalcemia and vitamin deficiency: an important, but preventable, cause of life-threatening infant heart failure. Heart 2008;94:581–4.

3. Olgun H, Ceviz N, Ozkan B. A case of dilated cardiomyopathy due to nutritional vitamin D deficiency rickets. Turk J Pediatr 2003;45:152–4.

4. Gezmish O, Tare M, Parkington HC, et al. Maternal vitamin D deficiency leads to cardiac hypertrophy in rat offspring. Reprod Sci 2010;17:168–76.

5. Uysal S, Kalayci AG, Baysal K. Cardiac functions in children with vitamin D deficiency rickets. Pediatr Cardiol 1999;20:283–6.

6. Mulligan ML, Felton SK, Riek AE, Bernal-Mizrachic. Implication of vitamin D in pregnancy and fetal outcome. Am J Obstet Gynecol 2010;202:429.e1–9.

7. Onal H, Adal E, Alpaslan S. Is daily 400 IU of vitamin D sup-plementation appropriate for every country: a cross-sectional study. Eur J Nutr 2010;49:395–400.

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