IN THIS issue of the ARCHIVES is an important case report describing an infant in whom phosphate depletion due to aluminum and magnesium hydroxide gel therapy (Maalox, Rhone-Poulenc Rorer Pharmaceuticals Inc, Collegeville, Pa) for colic resulted in radiological evidence of rickets and secondary craniosynostosis.1 This article and another recent report of 2 similar cases2 support the conclusion that therapy with phosphate-binding agents can result in the "phosphate depletion syndrome" during infancy.3 Prior to the appearance of these 2 articles, the phosphate depletion syndrome had not been described in infants. This observation of phosphopenia during infancy is particularly noteworthy, because dietary phosphate intake was ample and renal phosphate reclamation was markedly enhanced.4 The resorption of phosphate by the proximal renal tubule of the neonate or infant is so avid that there exists at the tubule a relative resistance to the phosphaturic action of parathyroid hormone. Also, the prevailing concentration of phosphate in the serum of infants is significantly higher than in that of children or adults.5 Hence, the infant is remarkably protected against phosphate depletion. The finding of phosphate depletion–induced rickets in 3 infants is, therefore, quite remarkable.
Chesney RW. A New Form of Rickets During Infancy: Phosphate Depletion–Induced Osteopenia Due to Antacid Ingestion. Arch Pediatr Adolesc Med. 1998;152(12):1168–1169. doi:10.1001/archpedi.152.12.1168
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