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Rickets and Secondary Craniosynostosis Associated With Long-term Antacid Use in an Infant

Avinash K. Shetty, MD; Tal Thomas, MD; Jayashree Rao, MD; Alfonso Vargas, MD
Arch Pediatr Adolesc Med. 1998;152(12):1243-1245. doi:10.1001/archpedi.152.12.1243.
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Oral antacids are occasionally prescribed for infantile colic, gastroesophageal reflux, esophagitis, and other peptic disorders.1 It has long been known that prolonged treatment with nonabsorbable antacids such as aluminum-magnesium hydroxides can limit gastrointestinal absorption of phosphorus.2 Hypophosphatemic bone disease, either rickets or osteomalacia, is a well-known complication of impaired renal tubular resorption of phosphate,3 but is rarely caused by nutritional phosphate deprivation. Although antacid-induced hypophosphatemic osteomalacia has been extensively reported in adults,49 very few reports exist in the pediatric literature.10,11 We report a case of rickets and secondary craniosynostosis in an infant following long-term administration of an aluminum-containing antacid.

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Figure 1.

Anteroposterior radiograph of the knees showing active rickets with severe osteopenia with evidence of metaphyseal fraying, cupping, and widening of the distal epiphyses.

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Figure 2.

Computed tomographic scan of the face (left) and brain (right) with 3-dimensional reconstruction revealing secondary craniosynostotic changes in the sagittal, lambdoid, and squamosal sutures. There is no evidence of increased intracranial pressure, and the orbits appear normal with no significant proptosis.

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