Body composition in infants with chronic lung disease after treatment with dexamethasone

Rj, Bolt; Weissenbruch, MM; Jc, Roos; Waal, H. Delemarre-van de; Cranendonk, Anneke; Lafeber, Harry N

doi:10.1111/j.1651-2227.2002.tb03333.x

Cited by 10 publications

(6 citation statements)

References 28 publications

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“…When corticosteroids are used, increased caloric intake during therapy may improve growth and help mitigate their bone demineralizing effects. 32 In light of our observation that postnatal growth restriction is associated with increased odds of severe MBD, these findings may be of particular importance.…”

Section: Discussionmentioning

confidence: 85%

Determinants of Severe Metabolic Bone Disease in Very Low-Birth-Weight Infants with Severe Bronchopulmonary Dysplasia Admitted to a Tertiary Referral Center

et al. 2015

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Section: Discussionmentioning

confidence: 85%

Determinants of Severe Metabolic Bone Disease in Very Low-Birth-Weight Infants with Severe Bronchopulmonary Dysplasia Admitted to a Tertiary Referral Center

et al. 2015

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“…Our study is the first to report bone mass after exposure to antenatal betamethasone. Five studies have reported bone mass in the first year of life after postnatal exposure to glucocorticoids for neonatal chronic lung disease (33–37) . Three reported no difference in bone mass after dexamethasone (33–35) .…”

Section: Discussionmentioning

confidence: 99%

“…Five studies have reported bone mass in the first year of life after postnatal exposure to glucocorticoids for neonatal chronic lung disease (33–37) . Three reported no difference in bone mass after dexamethasone (33–35) . One reported a negative association between duration of dexamethasone treatment and BMC at 3 months corrected age, (36) and the other also reported lower BMC in dexamethasone‐treated preterm infants (37) .…”

Section: Discussionmentioning

confidence: 99%

Peak Bone Mass After Exposure to Antenatal Betamethasone and Prematurity: Follow-up of a Randomized Controlled Trial

Dalziel

Fenwick

Cundy

et al. 2006

Journal of Bone and Mineral Research

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Small birth size is associated with reduced adult bone mass. We determined if antenatal betamethasone exposure, birth weight, or prematurity affects peak bone mass in 174 adults. Antenatal betamethasone exposure did not. Lower birth weight and prematurity predicted reduced adult height. Slower fetal growth rather than prematurity predicted lower bone mass, but this lower bone mass was appropriate for reduced adult height.Introduction: Small size at birth is reported to be associated with lower bone mass in adulthood. However, previous studies have not distinguished the relative contributions of length of gestation and fetal growth to size at birth. Fetal exposure to excess glucocorticoids has been proposed as a core mechanism underlying the associations between birth size and later disease risk. Antenatal glucocorticoids are given to pregnant women at risk for preterm delivery for the prevention of neonatal respiratory distress syndrome in their infants. We determined the relationship of antenatal exposure to betamethasone, birth weight, and prematurity to peak bone mass and femoral geometry in the adult survivors of the first randomized trial of antenatal glucocorticoids. Materials and Methods:We studied 174 young adults (mean age, 31 years) whose mothers participated in a randomized trial of antenatal betamethasone. Mothers received two doses of intramuscular betamethasone or placebo 24 h apart. Two thirds of participants were born preterm (<37 weeks gestation). We measured indices of bone mass and size and derived estimates of volumetric density and bone geometry from DXA assessments of the lumbar spine, femur, and total body. Results: There were no differences between betamethasone-exposed and placebo-exposed groups in any of the lumbar spine, femur, or total body DXA measures. There was no effect of antenatal betamethasone on adult height, although leg length was increased relative to trunk length (p ‫ס‬ 0.002). A lighter birth weight (p Յ 0.001) and lower gestational age (p ‫ס‬ 0.013) were associated with shorter stature (height Z scores) at age 31 years. Prematurity had no effect on peak bone mass or femoral geometry. However, lower birth weight, independent of gestational age, was associated with lower later bone mass (p < 0.001 for lumbar spine and total body, p ‫ס‬ 0.003 for femoral neck BMC). These effects on bone mass were related to bone size and not to estimates of volumetric density. In the femur, lower birth weight, independent of gestational age, was associated with narrowing of the upper shaft and narrow neck regions. Conclusions: Antenatal betamethasone exposure does not affect peak bone mass or femoral geometry in adulthood. Birth weight and prematurity predict adult height, but it is slower fetal growth, rather than prematurity, that predicts lower peak bone mass. The lower peak bone mass in those born small is appropriate for their adult height.

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“…body composition in preterm infants when it was used to treat chronic lung disease (Bolt et al, 2002). Furthermore, Gilmour et al demonstrated that Dex did not affect body composition of term gestational age infants despite the negative influences on glucose metabolism and growth patterns after drug exposure (Gilmour et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

From the Cover: Usage of Dexamethasone Increases the Risk of Cranial Neural Crest Dysplasia in the Chick Embryo

Cheng

Yan

et al. 2017

Toxicological Sciences

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Dexamethasone (Dex) is commonly used in the treatment of a variety of benign and malignant conditions. Unfortunately, although it has a variety of teratogenic effects, it remains used in clinical practice for pregnant women mainly due to limited alternatives. However, there is limited knowledge of the mechanisms that lead to the observed teratogenic effects. In this study, the effects of Dex during embryogenesis on neural crest development were evaluated in the early chick embryos. First, we demonstrated that 100 µl 10-6 M Dex treatment leads to craniofacial developmental defects, and also retards embryo growth and plausibly can cause embryo demise. Second, we demonstrated that Dex represses the production of HNK-1, PAX7, and AP-2α labeled cranial neural crest cells, the progenitor cells of the craniofacial skeleton. Third, double immunofluorescent staining of pHIS3/PAX7 and AP-2α/c-Caspase3 revealed that Dex promotes cell apoptosis but does not change cell proliferation rates. Last, fibroblast growth factor signaling molecules were inhibited by Dex treatment. Dex also inhibited neural crest cells production by repressing Msx1 expression in the developing neural tube and by altering expression of epithelial-mesenchymal transition-related adhesion molecules and cell migration genes. Overall, we obtained experimental evidence that Dex treatment during embryogenesis disrupts cranial neural crest development which in turn causes defective cranial bone development.

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Body composition in infants with chronic lung disease after treatment with dexamethasone

Cited by 10 publications

References 28 publications

Determinants of Severe Metabolic Bone Disease in Very Low-Birth-Weight Infants with Severe Bronchopulmonary Dysplasia Admitted to a Tertiary Referral Center

Determinants of Severe Metabolic Bone Disease in Very Low-Birth-Weight Infants with Severe Bronchopulmonary Dysplasia Admitted to a Tertiary Referral Center

Peak Bone Mass After Exposure to Antenatal Betamethasone and Prematurity: Follow-up of a Randomized Controlled Trial

From the Cover: Usage of Dexamethasone Increases the Risk of Cranial Neural Crest Dysplasia in the Chick Embryo

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