Because we previously found increased basal serum cortisol levels in women runners,we examined adrenocortical function in amenorrheic running women (AR), eumenorrheic running women (R), and normal nonexercising women (NC) in further detail. Mean 24-h urinary cortisol levels were significantly elevated (P < 0.001) in six AR [45.1 ± 7.2 (±SEM) µg/24 h] andeight R (38.5 ± 6.9 µg/24 h) compared to four NC (13.9 ± 2.8 µg/24 h). After adrenal suppression with 2 mg dexamethasone, integrated responses and absolute maximal elevations in serum cortisol levels in response to 10 µg/m2 exogenous ACTH (1-24) administered as an iv bolus dose, were not significantly different among six AR,six R, and six NC. This dose of ACTH results in maximal steroid release. The disappearance ratesof cortisol (5 mg, iv) after dexamethasone suppression were similar in four AR, five R, and fourNC and corresponded to a two-compartment model with mean half-lives of 4.9 and 93.8 min, respectively. Cortisol-binding globulin levels werealso similar among the groups. These data document higher cortisol secretion and suggest increased ACTH secretion in running women.
To elucidate the relation between interpersonal trauma and subsequent urinary dysfunction, investigators conducted a cross-sectional study of data from
A select group of investigators attended a structured workshop, the Stages of Reproductive Aging Workshop (STRAW), at Park City, Utah, USA, in July 2001, which addressed the need in women for a staging system as well as the confusing nomenclature for the reproductive years.
In Brief Premature ovarian failure is the term usually used to describe women aged younger than 40 years who present with amenorrhea, hypergonadotropinism, and hypoestrogenism. Such women may ovulate and even conceive after the diagnosis is made, so it may be more appropriate to refer to these patients as having "primary ovarian insufficiency," or alternatively, as having "hypergonadotropic hypogonadism" or "primary hypogonadism." The clinical presentation is diverse, and several different disorders can lead to premature ovarian failure. Affected women should be investigated for premutations of the FMR1 gene (causing fragile X syndrome in its fullest form) and for adrenal antibodies. Thyroiditis is the most frequent autoimmune disorder associated with premature ovarian failure and should be ruled out as well. Osteopenia is increased in women with premature ovarian failure, and measures to prevent accelerated bone loss are warranted. Hormone therapy (HT) should be provided to eliminate symptoms of estrogen deficiency and help prevent osteopenia, but will not necessarily (and inexplicably) prevent pregnancy in the 5–10% of women who conceive spontaneously after the diagnosis is made. There are no data indicating that these young women are at increased risk of side effects from HT. If pregnancy is desired, use of donor oocytes with in vitro fertilization is most likely to result in pregnancy. This article reviews what is known about the clinical presentation and cause of premature ovarian failure and suggests appropriate diagnostic tests and treatment.
