Serum Dehydroepiandrosterone Sulfate in Premature Infants and Infants with Intrauterine Growth Retardation

Turnipseed, Marvin R.; Bentley, Karen L. de Mesy; Reynolds, John W.

doi:10.1210/jcem-43-6-1219

Cited by 37 publications

(14 citation statements)

References 20 publications

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“…However, these infants had normal urinary levels of the metabolic products of cortisol, 6P-hydroxy cortisol and tetrahydrocortisone, which is secreted mainly by the permanent zone. In another group of IUGR newborns 36 wk gestation or greateir studied on the 1st day of life, the serum DHAS levels were found to be significantly lower than in normally grown newborn infants of the same gestational age (7).…”

Section: Discussionmentioning

confidence: 85%

Feto-Placental Steroid Metabolism in Growth Retarded Human Fetuses

1986

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ABSTRACT. The goal of the study was the determination of the relative roles of the placenta and the fetus in causing low serum estriol (E3) levels in women bearing fetuses with intrauterine growth retardation (IUGR). Umbilical venous levels of E3 and dehydroepiandrosterone sulfate (DHAS) were measured in 31 samples from fetuses with IUGR, 21 of whom were vaginally delivered and 10 who were delivered by cesarean section. In addition, estrone (El) and estradiol (E2) were measured in 11 of the samples. The results were compared with 11 samples from cesarean section delivered control term infants and 54 samples from vaginally delivered control infants. The vaginally delivered IUGR group had a significantly lower mean umbilical venous DHAS level than did their control group (2128 + 158 ng/ml S E M versus 2645 + 130, p < 0.05). Both the vaginally delivered and cesarean section delivered IUGR infants had umbilical venous E3 levels significantly lower than in their control groups (70 2 1 0 ng/ml S E M versus 144 + 10, p < 0.001, and 46 2 1 1 ng/ml S E M versus 136 2 23, p < .01, respectively). Umbilical venous El and EZ levels were not different from the control values. El, EZ, E3, and DHAS were measured in eight maternal venous samples obtained from mothers bearing fetuses with IUGR. In comparison with 11 control mothes, only E3 was significantly different (10.7 + 3.0 ng/ml S E M in mothers with IUGR fetuses versus 25.0 + 4.9 in control mothersp < 0.01). The study provides evidence for reduced DHAS secretion in one group of the fetuses with IUGR, and no evidence for decreased placental conversion of DEIAS to the estrogens El and EZ. The significantly low E3 values in both umbilical and maternal samples are postulated to result not only from the reduced fetal adrenal DHAS secretion, but also underactive 16a-hydroxylase activity in fetal liver or low efficiency of 16a-OH-DHAS, relative to DHAS, as a substrate for placental conversion to an estrogen. (Pediatr Res 20: 166-168, 1986) Abbreviations IUGR, intrauterine growth retardation DHAS, dehydroepiandrosterone sulfate E,, estrone E2, estradiol E3, estriol Women bearing fetuses with IUGR frequently have low serum E3 levels in late gestation (1, 2). One origin of the low E3 production in these pregnancies may be reduced secretion of fetal adrenal cortex-derived neutral steroid precursors of estriol synthesis in the placenta (3). However, there is evidence that placental conversion of the neutral precursors to estrogen may be low in association with a fetus with IUGR (4). In order to investigate the relative importance of these two possible causes of low Ej production, umbilical venous, and maternal venous neutral steroid and estrogen levels were assessed in a series of pregnancies in which the fetus had IUGR. MATERIALS AND METHODSPatients. All pregnant women studied in this investigation were hospitalized in the Oregon Health Sciences University Hospital. Fetuses with IUGR were diagnosed when their birth weights were more than 2 SD below the mean for gestational age, as...

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Section: Discussionmentioning

confidence: 85%

Feto-Placental Steroid Metabolism in Growth Retarded Human Fetuses

1986

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“…The fetal zone disappears in the first few months after birth, and production of DHEA and DHEAS virtually ceases, only resuming around 6 yr later at adrenarche (15,16). Low-birthweight infants have hypoplasia of the fetal zone at birth (17), with lower plasma and urine DHEAS levels in the first 24 h of life compared with normal-birth-weight infants (18,19). Our findings together with previous case control studies (3,4,10) strongly indicate that postnatal adrenal androgen secretion may be programmed during fetal and early postnatal development.…”

Section: Discussionmentioning

confidence: 99%

Opposing Influences of Prenatal and Postnatal Weight Gain on Adrenarche in Normal Boys and Girls

Ong

Potau

Petry

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

223

147

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Associations between low birth weight and higher adrenal androgen secretion before puberty have yet only been reported in case-control studies in girls. We examined the influence of birth weight and early postnatal weight gain on overnight-fasting adrenal androgen and cortisol levels in 770 children from a large normal United Kingdom birth cohort at age 8 yr. In univariate analyses, adrenal androgen levels were inversely related to birth weight SD score in each sex [dehydroepiandrosterone sulfate in boys: regression coefficient (B) ‫؍‬ ؊2.5 g/dl/SD; 95% confidence interval (CI), ؊4.7 to ؊0.2; in girls: B ‫؍‬ ؊3.8 g/dl/SD; 95% CI, ؊6.2 to ؊1.4; androstenedione in boys: B ‫؍‬ ؊0.15 nmol/liter/SD, 95% CI, ؊0.25 to ؊0.6; in girls: B ‫؍‬ ؊0.13 nmol/liter/SD; 95% CI, ؊0.24 to ؊0.02). In multivariate analyses, both lower birth weight and larger current body weight predicted higher adrenal androgen levels (P < 0.005 for all comparisons). Allowing for current weight, children who showed rapid postnatal weight gain between 0 and 3 yr had higher dehydroepiandrosterone sulfate (P ‫؍‬ 0.002) and androstenedione (P ‫؍‬ 0.004) levels at 8 yr. In contrast, cortisol levels were unrelated to birth weight or current body size. In summary, the relationship between lower birth weight and higher childhood adrenal androgen levels was continuous throughout the range of normal birth weights, and was similar in boys and girls. Adrenal androgen levels were highest in small infants who gained weight rapidly during early childhood. We suggest that higher adrenal androgen secretion could contribute to links between early growth and adult disease risks, possibly by enhancing insulin resistance and central fat deposition. (J Clin Endocrinol

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“…[22][23][24] Low birth weight is commonly associated with fetal adrenal hypoplasia, and correspondingly low serum DHEA-S levels. 25,26 However, adrenarche has been found to be most dramatic in children who were small for gestational age at birth, and, in particular, in those that exhibit postnatal catch-up growth. In this regard, it has been demonstrated in pairs of discordant siblings with similar weights in childhood that DHEA-S levels were higher in those of low birth weight compared with those born with normal weight.…”

Section: Excessive Androgen Productionmentioning

confidence: 99%

Reproductive endocrinology of adolescent polycystic ovary syndrome

Shayya

Chang

2009

BJOG

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Polycystic ovary syndrome (PCOS) is the most common endocrinopathy among reproductive-aged women, and it typically presents during adolescence. The objective of this review is to describe the clinical manifestations of PCOS in adolescent girls and the underlying basis for the altered reproductive physiology. Recognising adolescents at risk for PCOS and taking the appropriate steps to reduce circulating androgen levels is critical in reducing the clinical symptomatology of this disorder, and the development of adulthood infertility, diabetes, and metabolic syndrome in patients with PCOS.

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Serum Dehydroepiandrosterone Sulfate in Premature Infants and Infants with Intrauterine Growth Retardation

Cited by 37 publications

References 20 publications

Feto-Placental Steroid Metabolism in Growth Retarded Human Fetuses

Feto-Placental Steroid Metabolism in Growth Retarded Human Fetuses

Opposing Influences of Prenatal and Postnatal Weight Gain on Adrenarche in Normal Boys and Girls

Reproductive endocrinology of adolescent polycystic ovary syndrome

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