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Recalcitrant hypocalcaemia responding to teriparatide therapy: a clinical insight
Arohi Gupta1, Preeti Dabadghao2, Amruta Sathe2
1Department of Neonatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India.
Insights
Neonatal hypocalcaemia, a common issue, has varied causes. A refractory case improved with teriparatide, a parathyroid hormone analogue, suggesting its use in difficult neonatal hypocalcaemia cases.
Area of Science:
- Neonatal Medicine
- Endocrinology
- Metabolic Disorders
Background:
- Hypocalcaemia is a frequent neonatal metabolic issue with early and late-onset forms.
- Early-onset hypocalcaemia is linked to prematurity, perinatal asphyxia, and maternal diabetes.
- Late-onset hypocalcaemia can stem from high phosphate intake, formula, vitamin D issues, hypoparathyroidism, or genetic factors.
Purpose of the Study:
- To discuss the causes and clinical manifestations of neonatal hypocalcaemia.
- To present a case of refractory neonatal hypocalcaemia.
- To highlight the potential of teriparatide in treating refractory neonatal hypocalcaemia.
Main Methods:
- Literature review of neonatal hypocalcaemia causes and treatments.
- Case report of a neonate with refractory hypocalcaemia.
- Administration of teriparatide (recombinant parathyroid hormone analogue).
Main Results:
- The reported neonate presented with refractory hypocalcaemia.
- Conventional therapies (oral calcium, vitamin D, magnesium) were insufficient.
- Teriparatide administration led to significant clinical improvement.
Conclusions:
- Neonatal hypocalcaemia requires timely diagnosis and management based on onset.
- Refractory cases may necessitate advanced therapeutic strategies.
- Teriparatide shows promise as an effective treatment for refractory neonatal hypocalcaemia.
Abstract:
Hypocalcaemia is a common metabolic abnormality in neonates, with distinct causes based on the timing of onset. Early-onset hypocalcaemia (within 72 hours of life) is typically related to transitional physiology, prematurity, perinatal asphyxia or maternal diabetes. In contrast, late-onset hypocalcaemia (after 72 hours) is less common and may result from high phosphate intake, cow's milk-based formulas, vitamin D deficiency or resistance, maternal vitamin D deficiency, hypoparathyroidism (eg, DiGeorge syndrome), magnesium deficiency or activating mutations in the calcium-sensing receptor. Clinical manifestations of late-onset hypocalcaemia can include seizures, tetany, irritability, arrhythmias or stridor. While most cases respond to oral calcium, vitamin D and magnesium supplementation, some are refractory to conventional therapy. We report a case of refractory neonatal hypocalcaemia that showed significant improvement with teriparatide, a recombinant parathyroid hormone analogue, highlighting the potential role of advanced pharmacological agents in difficult-to-treat cases of neonatal hypocalcaemia.
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