Elsevier

The Journal of Pediatrics

Volume 128, Issue 2, February 1996, Pages 257-263
The Journal of Pediatrics

Adrenocortical function in the very low birth weight infant: Improved testing sensitivity and association with neonatal outcome,☆☆,,★★

https://doi.org/10.1016/S0022-3476(96)70404-3Get rights and content

Abstract

OBJECTIVE: To evaluate adrenocortical function in ill preterm infants and investigate potential relationships between plasma cortisol concentrations and major neonatal outcomes. STUDY DESIGN: Randomized trial of adrenocorticotropic hormone (1-24ACTH) stimulation testing, followed by a chart review. SETTING: Two level III neonatal intensive care units, Sacramento, Calif. PARTICIPANTS: Sixty-seven very low birth weight infants, born at 32 weeks of gestation or earlier weighing 1500 gm or less, who had endotracheal intubation and indwelling arterial access. RESULTS: Most infants (76%) had baseline cortisol concentrations <414 nmol/L (15.0 μg/dl), and of those, only 36% responded to stimulation with 1-24ACTH, 0.1 μg/kg. Raising the 1-24ACTH dose to 0.2 μg/kg resulted in a response rate of 67% (p = 0.09) but decreased the sensitivity of the test. An elevated mean 11-deoxycortisol/cortisol ratio indicated that decreased 11β-hydroxylase activity may limit cortisol production in some infants. Infants with baseline cortisol concentrations less than 414 nmol/L (15.0 μg/dl) were more likely to have chronic lung disease (p <0.002) and less likely to have severe intraventricular hemorrhage (p <0.02). Response to 1-24ACTH was not associated with a detectable difference in outcome. CONCLUSION: Many very low birth weight infants have low cortisol and ACTH concentrations and are unable to mount a cortisol response to physiologic doses (0.1 μg/kg) of 1-24ACTH. These findings suggest that delayed maturation of adrenal response may result in physiologically inadequate cortisol concentrations in stressed very low birth weight infants. This delayed maturation may contribute to the development of chronic lung disease. (J PEDIATR 1996;128:257-63)

Section snippets

Subjects

Institutional review boards at the University of California, Davis Medical Center, and Sutter Memorial Hospital, in Sacramento, Calif., approved the study. Infants admitted to the neonatal intensive care units at the Davis medical center (n = 53) and the Sutter hospital (n = 15) between May 1993 and December 1994 were considered for enrollment if their birth weight was less than 1500 gm, indwelling access was available for blood sampling, and parental approval was obtained by written informed

RESULTS

Nineteen infants were randomly assigned to receive placebo and 17 to receive 0.1 μg/kg of 1-24ACTH in the initial study phase. In the second phase, 17 received 0.1 μg/kg and 14 received 0.2 μg/kg of 1-24ACTH. Infants' weights ranged from 505 to 1490 gm (900 ± 248 gm [mean ± SD]) and gestational age from 23 to 32 weeks (27.0 ± 1.9 weeks). The randomized groups were well matched with respect to the remaining demographic, prenatal, and postnatal characteristics (data not shown).

Of the 67 infants

DISCUSSION

The use of low-dose 1-24ACTH testing is increasingly recognized as a significant improvement over the classic 250 μg 1-24ACTH stimulation test.8, 9, 10, 11 Investigators applying this newer approach in adults have employed 1-24ACTH doses from 0.5 to 14 μg/m2.7, 8, 10, 23 In infants and children, doses of 0.3 to 0.6 μg/m2 have proved successful in discriminating between adequate and inadequate adrenocortical function.9, 24 For the present study, we chose a dose of 0.1 μg/kg, which approximates a

Acknowledgements

We are grateful for the assistance of Dr. Boyd Goetzman in reviewing the manuscript and the assistance from the neonatal nursing staffs at University of California, Davis, Medical Center and Sutter Memorial Hospital, especially Jeanette Harrison, RN, who helped to obtain study consent and to collect and process the blood samples. We also thank Dr. Prabir Burman and Mr. Matthew Facer, in the Statistics Department at the University of California, Davis, for their valuable assistance with data

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  • Cited by (0)

    From the Department of Pediatrics, University of California, Davis, Sutter Memorial Hospital, Sacramento, and Endocrine Sciences, Calabasas Hills, California

    ☆☆

    aNow at the Division of Neonatology, Children's Hospital-Oakland, 747 52nd St., Oakland, CA 94609.

    Reprint requests: Cindy Korte, MD, University of California, Davis, Division of Neonatology, TB-193, Davis, CA 95616.

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    0022-3476/96/$5.00 + 0 9/23/69468

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