Limited response to <scp>CRH</scp> stimulation tests at 2 weeks of age in preterm infants born at less than 30 weeks of gestational age

Niwa, Fusako; Kawai, Masahiko; Kanazawa, Hoshinori; Iwanaga, Kougoro; Matsukura, Tadashi; Shibata, Minoru; Hasegawa, Takeshi; Heike, Toshio

doi:10.1111/cen.12049

Cited by 20 publications

(21 citation statements)

References 41 publications

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“…If the HPA axis in extremely preterm infants is established within the early neonatal period, relative adrenal insufficiency is unlikely to be the main cause of LCC. In order to address this question, we carried out CRH tests in infants born at <30 weeks of gestational age, and found that the response to CRH test at 2 weeks of age was significantly lower than that at the term equivalent age . Based on these findings, relative adrenal insufficiency is likely even after the transitional period in extremely preterm infants.…”

Section: Hypothalamic‐pituitary‐adrenal Axis In Lccmentioning

confidence: 99%

“…The efficacy of antenatal corticosteroids is established, but they also have unfavorable effects. Infants exposed to antenatal glucocorticoids may have lower response to CRH tests at approximately 2 weeks' postnatal age . It is controversial, but based on the previous reports, antenatal corticosteroids may increase the risk of relative adrenal insufficiency for preterm infants beyond the transitional period.…”

Section: Recent Trends and Newly Introduced Treatments That May Lead mentioning

confidence: 99%

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Late‐onset circulatory collapse of prematurity

Kawai

2017

Pediatrics International

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Late-onset circulatory collapse (LCC) is a refractory hypotension occurring after the early neonatal period (>day 7), in very low-birthweight infants. Typically, infants stabilized within the early neonatal period develop sudden onset of circulatory collapse after the early neonatal period. The underlying pathophysiology of LCC is considered to be relative adrenal insufficiency, which is well known in Japan, but is not widely accepted in North America or Europe. The current increase in LCC in Japan suggests that the principal trigger is related to recent trends in neonatal medicine and/or newly introduced treatments for preterm infants, but the pathophysiology has not been fully elucidated. In this review, based on current knowledge regarding LCC, the pathophysiology is discussed.

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Section: Hypothalamic‐pituitary‐adrenal Axis In Lccmentioning

confidence: 99%

Section: Recent Trends and Newly Introduced Treatments That May Lead mentioning

confidence: 99%

Late‐onset circulatory collapse of prematurity

Kawai

2017

Pediatrics International

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“…In better-nourished mothers, the placental surface may expand to compensate for varying degrees of nutrition during fetal development. Indeed, among men in the Helsinki Birth Cohort Study (103) who were thin at birth, different materno-placentalfetal phenotypes (defined by mother's height and body mass index) were associated with coronary heart disease and were thought to be suggestive of fetal undernutrition (230). Whether placental area associates with changes in circulating glucocorticoids is presently unknown but is an area of great research interest.…”

Section: A Placental Size and Morphologymentioning

confidence: 99%

Early-Life Glucocorticoid Exposure: The Hypothalamic-Pituitary-Adrenal Axis, Placental Function, and Long-term Disease Risk

et al. 2013

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An adverse early-life environment is associated with long-term disease consequences. Adversity early in life is hypothesized to elicit developmental adaptations that serve to improve fetal and postnatal survival and prepare the organism for a particular range of postnatal environments. These processes, although adaptive in their nature, may later prove to be maladaptive or disadvantageous if the prenatal and postnatal environments are widely discrepant. The exposure of the fetus to elevated levels of either endogenous or synthetic glucocorticoids is one model of early-life adversity that contributes substantially to the propensity of developing disease. Moreover, early-life glucocorticoid exposure has direct clinical relevance because synthetic glucocorticoids are routinely used in the management of women at risk of early preterm birth. In this regard, reports of adverse events in human newborns have raised concerns about the safety of glucocorticoid treatment; synthetic glucocorticoids have detrimental effects on fetal growth and development, childhood cognition, and long-term behavioral outcomes. Experimental evidence supports a link between prenatal exposure to synthetic glucocorticoids and alterations in fetal development and changes in placental function, and many of these alterations appear to be permanent. Because the placenta is the conduit between the maternal and fetal environments, it is likely that placental function plays a key role in mediating effects of fetal glucocorticoid exposure on hypothalamic-pituitary-adrenal axis development and long-term disease risk. Here we review recent insights into how the placenta responds to changes in the intrauterine glucocorticoid environment and discuss possible mechanisms by which the placenta mediates fetal hypothalamic-pituitary-adrenal development, metabolism, cardiovascular function, and reproduction.

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“…In the congenital diaphragm hernia (CDH) animal model, vitamin A had pro-healing effects by inducing the expression of different GFs [73,117,142] . In other studies with lambs, rats and mice, vitamin A induces VEGF, EGF, and EGFR expression [21,96] . However, two large meta-analyses on epidemiological studies did not find an effect of antenatal vitamin A on RDS incidence [6,142] .…”

Section: Vitamin Amentioning

confidence: 84%

Avoiding the prenatal programming effects of glucocorticoids: are there alternative treatments for the induction of antenatal lung maturation?

Justus¹,

Sloboda²,

Henrich

et al. 2015

Journal of Perinatal Medicine

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Limited response to CRH stimulation tests at 2 weeks of age in preterm infants born at less than 30 weeks of gestational age

Abstract: VLBW infants showed a characteristic pattern in the HPA axis at 2 weeks of age: higher basal cortisol values and lower response to CRH tests. This study suggested that AG was related to the lower response to CRH tests, at least partly.

Cited by 20 publications

References 41 publications

Late‐onset circulatory collapse of prematurity

Late‐onset circulatory collapse of prematurity

Early-Life Glucocorticoid Exposure: The Hypothalamic-Pituitary-Adrenal Axis, Placental Function, and Long-term Disease Risk

Avoiding the prenatal programming effects of glucocorticoids: are there alternative treatments for the induction of antenatal lung maturation?

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