PITUITARY-ADRENAL SUPPRESSION AND RECOVERY IN PRETERM VERY-LOW-BIRTH-WEIGHT INFANTS AFTER DEXAMETHASONE TREATMENT FOR BRONCHOPULMONARY DYSPLASIA

Citation
Pc. Ng et al., PITUITARY-ADRENAL SUPPRESSION AND RECOVERY IN PRETERM VERY-LOW-BIRTH-WEIGHT INFANTS AFTER DEXAMETHASONE TREATMENT FOR BRONCHOPULMONARY DYSPLASIA, The Journal of clinical endocrinology and metabolism, 82(8), 1997, pp. 2429-2432
Citations number
19
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
82
Issue
8
Year of publication
1997
Pages
2429 - 2432
Database
ISI
SICI code
0021-972X(1997)82:8<2429:PSARIP>2.0.ZU;2-4
Abstract
High dose dexamethasone is frequently used for the treatment of neonat al respiratory conditions and to facilitate weaning from mechanical ve ntilation in preterm, very low birth weight infants. However, very lit tle is known about the severity, site, and duration of steroid-induced hypothalamic-pituitary-adrenal axis suppression in this category of p atients. Twenty-three preterm, very low birth weight infants who recei ved a full 3-week dose-tapering course of dexamethasone were prospecti vely studied, with a human CRH stimulation test performed at three dif ferent times: before the start of steroid treatment (week 0), immediat ely after the course (week 3), and 4 weeks after stopping dexa methaso ne (week 7). Plasma ACTH and serum cortisol concentrations were measur ed at 0 (baseline), 15, 30, and 60 min. Immediately after the steroid course (week 3), both basal and poststimulation plasma ACTH and serum cortisol concentrations were markedly suppressed. The hormone concentr ations at 0, 15, 30, and 60 min in week 3 were significantly lower tha n their corresponding levels in week 0 (P < 0.0001 for both ACTH and c ortisol) and week 7 (P < 0.0001 and P < 0.005 for ACTH and cortisol, r espectively). In contrast, when the hormone levels in week 7 were comp ared to their corresponding concentrations in week 0, only the 60 min serum cortisol concentration in week 7 was significantly lower (P = 0. 02). The currently used dosage of dexamethasone caused severe pituitar y-adrenal suppression immediately after treatment, but substantial rec overy of the endocrine axis was observed 4 weeks after discontinuation of therapy. Although the recovery appeared to be earlier with the pit uitary center, both pituitary and adrenal glands were capable of mount ing a biochemically adequate response to exogenous human CRH stimulati on at this stage. Steroid replacement therapy may be desirable at a ti me of stress in the immediate posttreatment period, but it would seem unnecessary 1 month after stopping dexamethasone treatment.