Starved Bones, Failing Heart: Uncommon Yet Life Threatening Hypocalcemic Cardiomyopathy in Nutritional Rickets
https://doi.org/10.15605/jafes.041.S1
- Author:
Siti Nur Hanim Najwa binti Sheikh Osman
1
;
Sze Teik Teoh
1
Author Information
1. Paediatric Department Hospital Sultanah Bahiyah
- Publication Type:Journal Article
- MeSH:
Cardiomyopathies;
Rickets
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):142-143
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:We report an insidious presentation of hypocalcemic
dilated cardiomyopathy (HDCM) in an infant with nutritional rickets and severe hypocalcemia, highlighting
the myocardium’s strict reliance on calcium-phosphate
homeostasis.
Case:A 3-month-old, small-for-gestational-age male (birth
weight: 1.93 kg), with congenital cataracts and persistent
neonatal cholestasis (negative hepatopathy and congenital
infection screens) presented acutely with post-feeding
cyanosis, requiring intubation for aspiration pneumonia.
The mother denied prior apneic episodes, seizures,
feeding difficulties, or heart failure symptoms. Clinically,
there was no murmur or hyperactive pericardium. Chest
radiograph revealed globular cardiomegaly. Echocardiography confirmed HDCM (LVEF 41%).
Bloodwork revealed profound hypocalcemia (1.16 mmol/L;
normal 2.1–2.6), hyperphosphatemia (2.97 mmol/L), and
markedly elevated alkaline phosphatase (2,411 IU/L).
25(OH)D3 was deficient (34.08 nmol/L). Secondary
hyperparathyroidism (iPTH 19.55 pmol/L) represented an
appropriate response. The mother had introduced goat’s
milk instead of cow’s milk due to inadequate lactation.
She took no supplements during pregnancy and was also
vitamin D deficient. Management included IV calcium gluconate, targeted antifailure therapy (captopril, furosemide, spironolactone),
and mechanical ventilation. High-dose cholecalciferol
replenished depleted stores, alongside an active vitamin D
analog (alfacalcidol) to bypass impaired hepato-intestinal
pathways, stimulating calcium absorption. Extubated
after 2 weeks with stabilized serum calcium, he was discharged on anti-failure therapy, oral calcium carbonate
(54 mg/kg/day elemental), D-cure 25,000 IU 4-weekly,
Ursodeoxycholic acid (45 mg 12-hourly), and multivitamins.
Repeat echocardiography is planned at 3 months.
Conclusion:This case underscores the vulnerability to nutritional
rickets and late-onset hypocalcemia in SGA infants with
inadequate maternal nutrition and impaired GI absorption.
The calcium-phosphate axis is easily disrupted; highphosphate substitutes (goat’s milk) precipitously unmask
hypocalcemia, overwhelming compensatory hyperparathyroidism. Proactive, dual-therapy metabolic supplementation is paramount to avert catastrophic, yet reversible,
HDCM.
- Full text:2026081013475271156EP_P015.pdf
