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NEONATAL HYPOCALCEMIA AND THE MATERNAL-NEONATAL VITAMIN D AXIS: A TERTIARY NICU CROSS-SECTIONAL STUDY

Sep 2026 · International Journal of Advanced Research · Vol 14, pp. 382-388 · 0 citations

TL;DR

Early detection and prompt management are indispensable, as untreated neonatal hypocalcemia can adversely affect neurodevelopment and skeletal mineralization.

Abstract

Neonatal hypocalcemia, a frequently encountered metabolic disorder in the Neonatal Intensive Care Unit (NICU), can pose serious health risks to newborns. It is typically defined by reduced serum calcium levels, with threshold values varying based on gestational age and birth weight. In term infants and preterm neonates weighing more than 1500 g, hypocalcemia is considered when total serum calcium falls below 8 mg/dL (2 mmol/L) or ionized calcium below 4.4 mg/dL (1.1 mmol/L). In very low birth weight infants (1500 g), lower cutoff values are used [1]. Based on time of onset, neonatal hypocalcemia is broadly categorized into Early-onset hypocalcemia (EOH) and Late-onset hypocalcemia (LOH). Early-onset hypocalcemia usually develops within the first 72 hours of life and is associated with a physiological decline in calcium levels after birth, along with a delayed parathyroid hormone response. In contrast, late-onset hypocalcemia typically presents after the initial 3 days, often toward the end of the first postnatal week, and is more likely to be symptomatic.[2]. The clinical presentation can vary widely. Some neonates may exhibit mild features such as irritability, tremors, or increased neuromuscular excitability, while others may develop more severe complications including seizures, apnea, or cardiac dysfunction [3,4]. Hence, early detection and prompt management are indispensable, as untreated neonatal hypocalcemia can adversely affect neurodevelopment and skeletal mineralization.

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