Rickets in low birth weight infants receiving total parenteral nutrition.

Development of rickets in association with parenteral nutrition is described in four premature infants having gestational ages of 26-31 wk. In the first two infants there was a documented deficiency of vitamin D, but in the second two adequate supplementation was achieved. Vitamin D, whose primary action is to facilitate intestinal absorption of calcium, may also be a hormone of prime necessity in infant bone formation. Conversion of precursor cholecalciferol to the active form of hormone, 1,25-DHCC, requires intermediate hydroxylation by the liver. The premature infant liver may be deficient in its ability to carry out this step of metabolism, and in normal intrauterine existence the fetus may receive 1,25-DHCC, the active metabolite, from the mother. Calcium intake in these infants was far below that achieved by fetuses of comparable age in utero, even though in excess of that provided by usual premature infant oral formulas. Although calcium deficiency has not been incriminated as a cause of rickets in the past, it is possible that in very tiny premature infants rapid growth requirements lead to a relative calcium deficiency which may be manifested as uncalcified osteoid. Until the mechanism of the formation of rickets in small premature infants is clarified it is recommended that supplemental calcium and vitamin D be given to all premature infants receiving parenteral nutrition, and that periodic x-rays be obtained to detect the development of rickets.