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
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.