Dexamethasone treatment impairs calcium regulation and reduces bone mineralization in infant pigs
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Calcium and vitamin D metabolism, bone mineralization, and growth were studied in piglets randomly assigned to 15 d of dexamethasone (0.5 mg.kg-1.d-1, orally) or placebo. Growth velocity was significantly reduced by dexamethasone treatment (P < 0.001). Pigs in the dexamethasone group demonstrated lower 45Ca absorption by in situ intestinal perfusion (P < 0.01). Plasma 25-hydroxycholecalciferol (calcidiol) and 1,25-dihydroxycholecalciferol (calcitriol) were lower (P < 0.05) and the urinary ratio of calcium to creatinine was higher (P < 0.05) after 15 d of dexamethasone compared with placebo. Differences between pre- and postosteocalcin (P < 0.01) and pyridinoline (P < 0.01) were higher and wholebody, lumbar, and femur bone mineral density were lower (P < 0.05) in dexamethasone-treated piglets. Dexamethasone-induced reductions in bone mineral mass likely result from reduced vitamin D status, reduced intestinal calcium absorption, elevated urinary calcium loss and direct effects of the steroid on bone. When dexamethasone is used in premature infants to improve lung function, negative effects on growth and bone metabolism could occur.
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