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Rickets secondary to phosphate depletion. A sequela of antacid use in infancy

E K Pivnick1, N C Kerr, R A Kaufman

  • 1Department of Pediatrics, University of Tennessee, Memphis 38105, USA.

Clinical Pediatrics
|February 1, 1995
PubMed

Insights

Prolonged use of aluminum antacids in infants can cause phosphate depletion, leading to rickets and bone disease. Caution and monitoring are essential when using these medications in children.

Area of Science:

  • Pediatric Gastroenterology
  • Pediatric Endocrinology
  • Neonatology

Background:

  • Infantile colic is often treated with medications, including antacids.
  • Aluminum-containing antacids are sometimes used for gastrointestinal issues in infants.
  • Prolonged use of certain medications can have unintended consequences on infant development.

Observation:

  • Two infants experienced growth failure and were diagnosed with generalized osteomalacia (rickets).
  • Phosphate depletion was identified as the cause, linked to prolonged administration of aluminum-containing antacids for colic.
  • One infant developed bilateral proptosis secondary to craniosynostosis, a complication of the metabolic bone disease.

Findings:

  • Chronic administration of aluminum-containing antacids poses a significant risk to the developing skeletal system in infants.
  • Phosphate depletion from antacid use can lead to severe metabolic bone disease, including rickets and craniosynostosis.
  • The observed cases highlight a direct correlation between aluminum antacid exposure and severe bone abnormalities in infants.

Implications:

  • Aluminum-containing antacid therapy in infants requires extremely cautious use and low dosages.
  • Routine monitoring of serum calcium and phosphorus levels is crucial for infants receiving medications that may impair phosphate absorption.
  • Healthcare providers should be aware of the potential skeletal risks associated with aluminum antacid use in pediatric patients.

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