Plasma Mineralocorticoids, Glucocorticoids, and Progestins in Premature Infants: Longitudinal Study during the First Week of Life

Doerr, H. G.; Sippell, Wolfgang G.; Versmold, Hans T.; Bidlingmaier, F.; Knorr, D

doi:10.1203/00006450-198805000-00018

Cited by 63 publications

(26 citation statements)

References 21 publications

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“…This is consistent with the finding that preterm infants have elevated levels of 17-OHP in the neonatal screening for CYP21 deficiency [22]. This is likely due to the immaturity of enzyme activities (i.e., functional 11β-hydroxylase deficiency) together with the high levels of sulfated metabolites of Δ 5 - and Δ 4 -steroids cross-reacting in the assay, thus leading to false elevated hormone assessments in the Delfia assay [23]. Immature kidney function with low excretion rate can also play a role.…”

Section: Discussionsupporting

confidence: 76%

A Case of 3β-Hydroxysteroid Dehydrogenase Type II (HSD3B2) Deficiency Picked up by Neonatal Screening for 21-Hydroxylase Deficiency: Difficulties and Delay in Etiologic Diagnosis

2007

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Background: 3β-Hydroxysteroid dehydrogenase type II deficiency, a rare form of congenital adrenal hyperplasia, is characterized by varying degrees of salt loss and incomplete masculinization in males and mild virilization or normal external genitalia in females. The clinical signs may be difficult to recognize, increasing the risk of a neonatal adrenal crisis. In addition, elevated 17α-hydroxyprogesterone and androstenedione levels due to peripheral HSD3B1 activity may lead to a delay of the correct diagnosis and even to misdiagnosis as CYP21 deficiency. Method: We report a patient who was detected on neonatal screening for 21-hydroxylase deficiency, in part because of cross-reactivity in the commonly used assay. Results: The diagnostic difficulties in this case were overcome by the use of more specific antibodies. Conclusion: This case emphasizes the importance of confirming the etiological diagnosis with molecular genetic analyses.

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Section: Discussionsupporting

confidence: 76%

A Case of 3β-Hydroxysteroid Dehydrogenase Type II (HSD3B2) Deficiency Picked up by Neonatal Screening for 21-Hydroxylase Deficiency: Difficulties and Delay in Etiologic Diagnosis

2007

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“…The reason is unclear. However, a decreased rate of metabolism due to altered enzymatic activities might play a role, as suggested also for premature infants (20,28,29).…”

Section: Discussionmentioning

confidence: 99%

Adrenocortical Steroids in Small-for-Gestational-Age Term Infants during the Early Neonatal Period1,2

et al. 1989

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ABSTRACT. We evaluated adrenocortical steroid concentrations a t birth and during postnatal adaptation (2 h until 7 days) in 10 vaginally delivered term small-for-gestational-age (SGA) infants and 1 2 term appropriate-forgestational age infants. Plasma aldosterone, ll-deoxycorticosterone, corticosterone, progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, cortisol, and cortisone were longitudinally measured by specific RIA after Sephadex LH-20 chromatography. Mean aldosterone was significantly higher in SGA than in appropriate-for-gestationalage infants (2 h to 7 days; p < 0.001). In SGA infants, cortisone and cortisol levels were significantly lower in umbilical artery (p < 0.05), and all glucocorticoid levels were significantly lower 12 h after birth (p < 0.05). Thereafter (24 h to 7 days), only 11-deoxycortisol levels remained significantly lower in SGA; corticosterone and cortisol levels were even higher @ < 0.05) in SGA 24 h after birth. The data suggest that SGA infants maintain high aldosterone levels throughout the 1st wk of life. Low cortisol and cortisone levels in umbilical artery a s well a s low glucocorticoid levels a t 2 h and/or 1 2 h compared to term appropriate-for-gestational-age infants may reflect either a less stressful postnatal adaptation or, more likely, a reduced adrenocortical synthesis in term SGA infants. (Pediatr Res 25:115-118, 1989) Abbreviations SGA, small for gestational age UA, umbilical artery AGA, appropriate for gestational age Perinatal problems in neonates with severe intrauterine growth retardation are frequent. They include asphyxia, a high neonatal mortality, electrolyte imbalance, hypoglycemia, cardiorespiratory problems, and neurologic abnormalities (1). Organ weights are significantly reduced (2); in particular, the adrenal cortex is small with respect to size and cell number (3).

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“…Although we are not informed about the amount of crossreactivity between baseline cortisol and cortisone, we know from other studies that the levels of cortisone can be in the same range as the cortisol levels (8,23,24). This may have contributed to the measured baseline cortisol levels, especially when the baseline cortisol levels are low.…”

Section: Adrenal Function In Very Preterm Infantsmentioning

confidence: 99%

Adrenal Function in Sick Very Preterm Infants

et al. 2000

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Some very preterm neonates admitted to the neonatal intensive care unit show circulatory and respiratory problems that improve after administration of steroids. It is unclear whether these symptoms could be caused by adrenal insufficiency. The objective of our study was to investigate the cortisol levels and the cortisol release from the adrenals after ACTH in very preterm infants with and without severe illness and to find whether a relation exists between adrenal function and outcome. An ACTH test (0.5 g) was performed on d 4 in 21 very preterm infants (gestational age, 25.6 -29.6 wk; birth weight, 485-1265 g). Baseline cortisol and 17-hydroxyprogesterone (17OHP) levels and the cortisol levels 30, 60, and 120 min after ACTH administration were measured. The Score for Neonatal Acute Physiology was used to measure illness severity. All infants showed an increase in cortisol levels after ACTH, but the cortisol levels were significantly lower in the ventilated more severely ill infants. After adjusting for birth weight and gestational age, the mean baseline cortisol levels and cortisol/17OHP ratios were significantly lower and the 17OHP levels significantly higher in the ventilated infants compared with the nonventilated infants. Patients with an adverse outcome had significantly lower baseline cortisol/ 17OHP ratios and 60-min cortisol levels during ACTH testing (p ϭ 0.002 and p ϭ 0.03, respectively). These data suggest an insufficient adrenal response to stress in sick ventilated very preterm infants with gestational ages younger than 30 wk compared with nonventilated less sick preterm infants. Further studies are required to investigate whether supplementation with physiologic doses of hydrocortisone may benefit the outcome. With increasing neonatal and obstetric treatment modalities, younger and smaller neonates are admitted to neonatal intensive care units (NICU). Some of these infants show not only respiratory but also circulatory problems such as systemic hypotension resistant to volume expansion and cardiotonic drugs but reactive to the administration of corticosteroids (1). Declining cortisol levels in the first week of life in patients with ongoing respiratory problems are reported (2), and a higher incidence of bronchopulmonary dysplasia (BPD) in patients with an insufficient cortisol response to ACTH has been found (3).In the 1970s, the adrenal function of preterm neonates was investigated after administration of a short course of corticosteroids during gestation, and no signs of adrenal insufficiency were found (4). These preterm neonates, however, were born after a greater gestational age, had a higher birth weight than the infants presently seen in the NICU, and were tested with a relatively high dose of ACTH (15 g/kg) on the first day of life. In infants exposed to long courses of corticosteroids during gestation, no evidence of adrenal insufficiency was found when tested with a higher dose of ACTH (36 g/kg) (5). These infants, however, were of greater gestational age compared with the very preterm...

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Plasma Mineralocorticoids, Glucocorticoids, and Progestins in Premature Infants: Longitudinal Study during the First Week of Life

Cited by 63 publications

References 21 publications

A Case of 3β-Hydroxysteroid Dehydrogenase Type II (HSD3B2) Deficiency Picked up by Neonatal Screening for 21-Hydroxylase Deficiency: Difficulties and Delay in Etiologic Diagnosis

A Case of 3β-Hydroxysteroid Dehydrogenase Type II (HSD3B2) Deficiency Picked up by Neonatal Screening for 21-Hydroxylase Deficiency: Difficulties and Delay in Etiologic Diagnosis

Adrenocortical Steroids in Small-for-Gestational-Age Term Infants during the Early Neonatal Period1,2

Adrenal Function in Sick Very Preterm Infants

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