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Growth and Bone Accretion in Former Infants Exposed to Neonatal Dexamethasone« Back to Volume 23, Issue 2, June 2007 - Table of Contents The authors assessed in the late prepubertal-early pubertal years growth (height, weight) and body composition (DEXA: bone, lean tissue, and fat mass) in prematurely born, very low birth weight (VLBW <1500 g) children who had developed bronchopulmonary dysplasia (BPD) in the neonatal period and required treatment with dexamethasone ([DEX] tapering doses over 7 or more days with cumulative doses of 6 to 8 mg). They compared data from the VLBW + DEX group (n=47) to those of premature VLBW subjects who had not developed BPD or received DEX (VLBW – DEX, n=36) and to those from term-born infants ([TERM] n=36). Mean height and weight z-(standard deviation) scores were significantly lower in VLBW + DEX children than in VLBW – DEX or TERM; mean height and weight z-scores were lower in VLBW − DEX children compared to TERM subjects. Heights less than the 10th percentile were recorded in 9/47 VLBW + DEX, 1/36 VLBW − DEX, and 2/36 TERM subjects. Percentages of fat and lean tissue mass relative to total body weight were similar in all 3 subject groups. Bone mineral content (BMC) and bone area (BA) were similar in the VLBW groups and less than those of the TERM subjects. Whole body BMC z-score was below −1.5 in 12/43 VLBW + DEX, 7/36 VLBW − DEX, and 3/35 TERM subjects and significantly lower in both VLBW groups compared to TERM children. The investigators concluded that in the late prepubertal-early pubertal years, former premature VLBW neonates who developed BPD and received dexamethasone were smaller in height and weight than were VLBW subjects who had not developed BPD or received DEX and that both groups of VLBW subjects were smaller than TERM children. Factors that contributed to this growth pattern were the extremely LBW and the administration of DEX. First Editor’s CommentAs the authors point out, the association of BPD with DEX exposure likely contributes to the suboptimal growth pattern of the VLBW + DEX group. They suggest that growth in later childhood is conditioned by events encountered in utero and in the post natal period. Inasmuch as bone mineralization is reported to be normal for height in older adolescents and young adults who were born prematurely1 current data suggest that mineral acquisition is delayed but not ultimately impaired in such subjects. However, it seems likely that the degree of prematurity, birth weight, neonatal course, drug exposure, neonatal nutritional status, and many other factors interact to affect adult bone mineralization. Allen W. Root, MD Second Editor’s CommentThis study is complex, yet the findings are not altogether surprising. The VLBW children treated with DEX for BPD have growth attenuation at 5 to 10 years of age and reduced BMC. The suggestion that growth hormone given concomitantly with DEX might partially attenuate reduction in bone loss as in animal models is intriguing. Clearly as more VLBW and extremely low birth weight children survive, the frequency of the morbidity associated with their neonatal course will become more apparent. These data demonstrate that in addition to reductions in linear growth, there are also reductions in BMC. Studies are needed to determine whether such infants might benefit from growth hormone therapy not just during DEX treatment, but once they are clinically stable and discharged from the hospital. William L. Clarke, MD Editor’s Note: The prenatal dexamethasone effects on cognitive function are reviewed in this issue of GGH.2 References - (linked to
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Volume 24 Number 1
May 2008
www.GGHjournal.com
ISSN 1932-9032
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