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Right arrow Premature & Newborn

PEDIATRICS Vol. 107 No. 3 March 2001, pp. 494-498

Association of Plasma Cortisol and Chronic Lung Disease in Preterm Infants

Received Feb 16, 2000; accepted Jul 13, 2000.

Beverly A. Banks, Nicole Stouffer, Avital Cnaan, Yue Ning, Jeffrey D. Merrill, Roberta A. Ballard, Philip L. Ballard, and the North American Thyrotropin-Releasing Hormone Trial Collaborators

From the Department of Pediatrics, University of Pennsylvania and Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, and the North American Trial Collaborators.

Background.  It has been suggested that preterm infants may have developmental immaturity of the hypothalamic-pituitary-adrenal axis, and that decreased cortisol response to stress increases risk of chronic lung disease (CLD) secondary to inflammatory lung injury.

Methods.  To investigate the relationship between endogenous corticosteroid and CLD, we measured plasma cortisol during the first 28 days of life in a subset of neonates in the North American Thyrotropin-Releasing Hormone (TRH) Collaborative Trial. Analyses were performed on 314 infants, 24 to 32 weeks' gestation, whose mothers received 1 or 2 courses of antenatal corticosteroids plus TRH or placebo.

Results.  Mean cortisol was 3.1 µg/dL (range: 0.1-17.9) at birth, reached maximal levels at 24 hours (19.4 µg/dL, range: 0.8-124.6), and decreased to 5.9 µg/dL (range: 0.2-24.7) at 14 to 28 days of age; levels during the first week were not associated with gestational age. The Clinical Risk Index for Babies (CRIB), a neonatal assessment tool that is correlated with risk of mortality, was positively associated with cortisol level on days 1 and 3 through 7. TRH versus placebo treatment did not influence cortisol levels at any time point. To examine the relationship between cortisol and adverse outcome of death or CLD at 36 weeks' postmenstrual age (CLD36), logistic regression models adjusting for known contributing clinical factors (gestational age and CRIB score) were fit. There was a statistically borderline negative association between median cortisol level at 3 to 7 days and CLD36. After adjusting for gestational age and CRIB score, the predicted probability of CLD36 was only minimally influenced by the cortisol concentration.

Conclusion.  In preterm infants, basal plasma cortisol concentration during the first week is a weak predictor for CLD36. Possible benefits as well as risks of supplemental, low-dose cortisol treatment of high-risk preterm infants remain to be determined.  Key words:  cortisol, premature infant, bronchopulmonary dysplasia, infant chronic lung disease, CRIB score.




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