No abstract

The relative potency in the hypothalamic-pituitary-adrenal (HPA) suppression of both prednisolone and betamethasone was examined in an acute study with normal volunteers and in a chronic study with glucocorticoid-treated patients. Circadian rhythm of plasma cortisol was studied after a single dose administration of 5 to 30 mg prednisolone or 0.5 to 3.0 mg betamethasone at 08 : 00 hr. Morning-rise of plasma cortisol occurred on the morning after the administration of 30 mg or less prednisolone but no morning rise was noted after the administration of 1.0 mg or more betamethasone. Plasma ACTH was slightly elevated on the morning after 30 mg prednisolone administration but showed low levels throughout the night after 3.0 mg betamethasone administration.Plasma cortisol responsiveness to ACTH was examined in patients before and during therapy with either prednisolone or betamethasone.The basal cortisol level was not suppressed and the responsivenessto ACTH remained nearly normal during long-term 5 mg prednisolone therapy, but these were completely suppressed during long-term 0.5 mg betamethasone therapy.The responsiveness to ACTH was nearly normal in patients receiving alternate-day therapy with prednisolone in such large doses as 50 or 60 mg every other day, but was completely suppressed in patients receiving 1.0 mg betamethasone every other day. The relative potency of betamethasone in acute and chronic suppressive effects on the HPA system seems to be much stronger than that of prednisolone inequivalent doses with comparable anti-inflammatory effects. It is also suggested that the alternate-day therapy with such long-acting steroids as betamethasone are useless in preventing HPA suppression.

Seventeen women with anorexia nervosa were studied before and during weight gain. The mean body weight was 93.8% before onset of illness, 82.9% at the beginning of amenorrhea and 61.8% at the minimum weight, each expressed as a percentage of the standard weight (SW). Basal serum LH and FSH level were significantly low in the lower weight patients, and increased with weight gain, with a linear correlation to the percent of SW. The LH response to100ug of LH-RH was impaired in the lower weight group, and was improved with weight gain. The LH response in those whose weight had increased to 70% or more of the SW was often excessive and the maximum levels were significantly higher than in normal women.The FSH response to LH-RH was well maintained even in the lower weight group, but the maximum response was delayed. There was a significant correlation between improvement in the LH response and weight gain, but no significant correlation was found between FSH response and body weight. Menstrual cycles were restored in some who showed 100mIU/ml or more of the maximum LH response, but no definite relationship was found between the LH or FSH response and the resumption of menstruation.Though the weights at the cessation and at the resumption of menstruation differed from case to case, the two weight levels were almost the same in each individual.These results indicate that the critical body weights for maintaining menstrual cycle are inconsistent and that the resumption of menstruation may not be accounted for only by the recovery of such a tonic regulation as seen in the responsiveness to LH-RH following weight gain but by the restoration of the individual critical weight.

No abstract

No abstract