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August 1982

Rickets and Deficiency of Vitamin D Metabolites-Reply

Author Affiliations

Department of Pediatrics UCLA School of Medicine Los Angeles, CA 90024
Department of Biochemistry University of California, Riverside Riverside, CA 92502
Department of Medicine UCLA School of Medicine Los Angeles, CA 90024

Am J Dis Child. 1982;136(8):754-755. doi:10.1001/archpedi.1982.03970440098036

In Reply.—We agree that the biochemical findings were not the same in each of the three children described, but we do not believe that this necessarily indicates different pathogeneses for the condition. All the infants receiving TPN were given the same amounts of calcium and phosphate on a body-weight basis. The three affected children had similar roentgenographic changes and elevated levels of serum alkaline phosphatase. None showed features of malnutrition when the rickets appeared. The lesions shown on roentgenograms improved in each in association with the same therapy, ie, larger doses of ergocalciferol, given intramuscularly. Thus, a single pathogenic process seems as likely as multiple ones.

We agree that the principal function of 1,25-(OH)2-D is to enhance intestinal absorption of calcium and phosphate; however, it cannot be concluded that 1,25-(OH)2-D may not have other functions during treatment with TPN when patients do not receive oral calcium. In

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