cosyntropin and Amenorrhea

Anorexia nervosa is a primarily psychiatric syndrome of self-induced weight loss due to an intense fear of becoming obese. Numerous endocrine abnormalities occur in anorexia nervosa patients, and in many respects these alterations reflects the endocrinology of reduced energy intake. However, the basic mechanisms of those alterations are far from being understood. In an attempt to understand the disrupted mechanisms of the hypogonadotropic hypogonadism of the anorectic state, we studied 10 anorectic women in the acute phase of their illness; all met the DSM III criteria. On each patient, two tests were performed with either saline as control or infusion of the opioid antagonist naloxone, and both LH and FSH levels were measured. Four mg of naloxone as bolus was used, followed by a naloxone infusion of 2 mg/h for 4 h. Compared with the pattern of normal women, naloxone did not increase in the anorectic patients either LH or FSH levels nor pulsatility. This result suggests that endogenous opioid peptides are not implicated in the low gonadotropic situation of anorexia nervosa. An alternative explanation could be that the low estrogenic "milieu" of these patients could mask the opioid action. To test this second possibility, another group of 7 anorectic women after partial weight recovery were challenged with estrogen administration. Compared with the pattern of normal women volunteers, all the anorectic patients but one presented an abnormal response in both LH and FSH levels after estrogen administration. In fact, the negative feedback and the delayed positive feedback of LH after estrogen were absent in these patients. Interestingly enough, the only patient with near-normal LH response to estrogen was considered fully recovered by the Psychiatric Unit. Several alterations in the hypothalamic-pituitary-adrenal axis has been reported in anorexia nervosa. Seven anorectic patients and 7 aged-matched women were challenged by ACTH 1-24, 250 micrograms (i.v.) and the ratio of increments in adrenal steroid products to precursors monitored. ACTH-induced increments in cortisol with respect to increments in 17-OH-progesterone was similar in anorectics and controls. On the contrary, the ratio of increments of androstenedione with respect to increments in 17-OH-progesterone were greater in anorexia nervosa than controls. These results suggest that in anorexia nervosa the 11-beta-21-alpha-hydroxylase system is normal but a deficient 17-20 desmolase system is present. Fi

Topics: Amenorrhea; Anorexia Nervosa; Corticotropin-Releasing Hormone; Cosyntropin; Endorphins; Estradiol Congeners; Feedback; Female; Gonadotropin-Releasing Hormone; Growth Hormone-Releasing Hormone; Humans; Hypothalamo-Hypophyseal System; Hypothalamus; Naloxone; Ovary; Pituitary Hormones, Anterior; Pituitary-Adrenal System

To explore possible changes in adrenal steroid metabolism and androgenic-anabolic status in female endurance athletes as a mechanism for their hypercortisolism.. Adrenal steroids and androgenic-anabolic factors were studied during basal conditions and in response to ACTH stimulation related to menstrual status.. Department of Obstetrics and Gynecology, Karolinska Hospital, Stockholm, Sweden.. Thirteen female elite middle to long distance runners (six eumenorrheic, seven oligoamenorrheic) and seven regularly menstruating controls.. Blood samples were collected before and after an injection of 250 micrograms IV synthetic ACTH 1-24. Body weight, height, and body fat were measured.. Basal serum concentrations of cortisol, androstenedione (A), DHEA, DHEAS, 17 alpha-hydroxyprogesterone (17-OHP), T, steroid-binding proteins, and insulin-like growth factor I and ACTH-induced response (area under the curve) of cortisol, DHEA, and 17-OHP.. Oligoamenorrheic athletes had higher basal cortisol and A concentrations compared with healthy controls, whereas basal levels of DHEA and DHEAS were normal. Important findings in the oligoamenorrheic athletes were a significantly lower ratio between the ACTH-induced increments of DHEA and 17-OHP and an increased ratio between basal A and DHEAS. Insulin-like growth factor I was correlated negatively to sex hormone-binding globulin and to the amount of body fat in the combined material.. The results indicate a redistribution of adrenal steroid metabolism in favor of glucocorticoid production in female endurance athletes. We suggest that hypercortisolism in female endurance athletes is a physiological adaptation to maintain adequate blood glucose levels during a condition of energy deficiency.

Topics: 17-alpha-Hydroxyprogesterone; Adrenal Cortex Hormones; Adrenocortical Hyperfunction; Adult; Amenorrhea; Androstenedione; Cosyntropin; Dehydroepiandrosterone; Dehydroepiandrosterone Sulfate; Female; Humans; Hydrocortisone; Hydroxyprogesterones; Insulin-Like Growth Factor I; Physical Endurance; Running; Testosterone

To investigate mechanisms of blunted adrenocortical responsiveness to exercise and mild hypercortisolism in amenorrheic runners, adrenocorticotropic hormone [ACTH-(1-24) 0.25 mg Cortrosyn] stimulation tests were performed in the presence and absence of overnight dexamethasone (1 mg) suppression (DX and NDX condition, respectively) in six eumenorrheic sedentary women (ES), nine eumenorrheic runners (ER), and nine amenorrheic runners (AR). Before the NDX stimulation test, plasma cortisol was higher (P < 0.001) in AR than in ER and ES. The cortisol response to the NDX stimulation test was blunted (P < 0.001) in AR but reached similar (P > 0.7) peak levels in all groups. Dexamethasone suppressed (P < 0.001) cortisol to similar (P > 0.5) levels (approximately 20 nmol/l) in all groups. In AR, cortisol responses to the DX test were larger (P < 0.03) than to the NDX test and similar (P > 0.6) in the three groups, again reaching comparable (P > 0.8) peak levels. The blunted cortisol response to stimulation in AR in the presence of their mild hypercortisolism appears to be due to a normal limitation in maximal adrenal secretory capacity. Extrapituitary modulators of adrenal responsiveness to ACTH may explain the mild hypercortisolism observed in AR, but limitations of these tests prevent a central negative-feedback defect or an intrinsic adrenal abnormality from being excluded until results of additional studies with even lower doses of dexamethasone and submaximal doses of ACTH-(1-24) are available.

Topics: Adolescent; Adrenal Cortex; Adrenal Cortex Hormones; Adult; Amenorrhea; Body Composition; Cosyntropin; Dexamethasone; Female; Gonadal Steroid Hormones; Humans; Hydrocortisone; Menstrual Cycle; Running

Late-onset congenital adrenal hyperplasia is a mild genetic defect in steroidogenesis that presents with hirsutism and menstrual irregularities and responds to specific treatment with dexamethasone sodium phosphate. Its incidence as a significant cause of hirsutism or amenorrhea is controversial because it cannot be distinguished clinically from other causes. However, it is readily diagnosed by a marked increase in 17 alpha-hydroxyprogesterone levels after adrenocorticotropic hormone stimulation. Seventy-seven randomly selected women with hirsutism or amenorrhea were tested, and eight women (10.4%) were found to have late-onset congenital adrenal hyperplasia. Plasma levels of other hormones were similar in patients with and without late-onset congenital adrenal hyperplasia and were of no benefit in making the diagnosis. It is concluded that the adrenocorticotropic hormone stimulation test should be more widely utilized in patients presenting with hirsutism or menstrual dysfunction.

Topics: 17-alpha-Hydroxyprogesterone; Adolescent; Adrenal Hyperplasia, Congenital; Adult; Amenorrhea; Cosyntropin; Female; Hirsutism; Humans; Hydroxyprogesterones; Mass Screening

The occurrence of uterine bleeding following administration of Metyrapone in cases of secondary amenorrhoea and oligomenorrhoea led the authors to measure pituitary, gonadal and adrenal hormone levels, before and after the oral administration of this drug in sixteen patients, in an attempt to provide an interpretation of this phenomenon. There were expected changes in plasma ACTH and urinary 17-hydroxycorticosteroids, but no variations were noted in serum FSH and LH, plasma oestradiol and urinary oestrogens; the most important alterations occurred in plasma progesterone and urinary pregnanetriol levels. It is suggested that bleeding occurs because of the changes which are induced in plasma progesterone levels.

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Adult; Amenorrhea; Cosyntropin; Estradiol; Estrogens; Female; Follicle Stimulating Hormone; Humans; Luteinizing Hormone; Menstruation; Metyrapone; Oligomenorrhea; Pituitary Function Tests; Pregnanediol; Pregnanetriol; Progesterone