Amenorrhea: an approach to diagnosis and management.

Although amenorrhea may result from a number of different conditions, a systematic evaluation including a detailed history, physical examination, and laboratory assessment of selected serum hormone levels can usually identify the underlying cause. Primary amenorrhea, which by definition is failure to reach menarche, is often the result of chromosomal irregularities leading to primary ovarian insufficiency (e.g., Turner syndrome) or anatomic abnormalities (e.g., Müllerian agenesis). Secondary amenorrhea is defined as the cessation of regular menses for three months or the cessation of irregular menses for six months. Most cases of secondary amenorrhea can be attributed to polycystic ovary syndrome, hypothalamic amenorrhea, hyperprolactinemia, or primary ovarian insufficiency. Pregnancy should be excluded in all cases. Initial workup of primary and secondary amenorrhea includes a pregnancy test and serum levels of luteinizing hormone, follicle-stimulating hormone, prolactin, and thyroid-stimulating hormone. Patients with primary ovarian insufficiency can maintain unpredictable ovarian function and should not be presumed infertile. Patients with hypothalamic amenorrhea should be evaluated for eating disorders and are at risk for decreased bone density. Patients with polycystic ovary syndrome are at risk for glucose intolerance, dyslipidemia, and other aspects of metabolic syndrome. Patients with Turner syndrome (or variant) should be treated by a physician familiar with the appropriate screening and treatment measures. Treatment goals for patients with amenorrhea may vary considerably, and depend on the patient and the specific diagnosis.

Effects of dehydroepiandrosterone and alprazolam on hypothalamic-pituitary responses to exercise.

CONTEXT: The hypothalamic-pituitary-adrenal axis (HPA) is restrained by activation of gamma-amino-butyric acid receptors. Alprazolam (APZ) and dehydroepiandrosterone (DHEA) are purported to be gamma-amino-butyric acid agonists and antagonists, respectively. OBJECTIVE: Our objective was to examine the effects of APZ and DHEA alone and in combination on HPA axis activity. DESIGN: This was a double-blind, crossover, placebo-controlled study. SETTING: The study setting was the general community. PARTICIPANTS: Subjects consisted of 15 men (age, 20-45 yr) with a body mass index of 20-25 kg/m2. INTERVENTIONS: DHEA (100 mg/d) or placebo was given for 4 wk, followed by a 2-wk washout; participants ingested 0.5 mg APZ or placebo 10 and 2 h before high-intensity exercise. OUTCOME MEASURES: We measured basal and exercise-induced ACTH, arginine vasopressin (AVP), cortisol, DHEA, and GH responses. It was hypothesized that DHEA would enhance and APZ would blunt exercise-induced ACTH and cortisol release. RESULTS: DHEA significantly increased the AVP response to exercise (P < 0.01). APZ treatment significantly increased basal GH and blunted plasma cortisol, ACTH, AVP, and DHEA responses to exercise (P < 0.05). DHEA and APZ in combination significantly increased the GH response to exercise (P < 0.01). CONCLUSIONS: DHEA may alter a subset of receptors involved in AVP release. Together DHEA and APZ may up-regulate GH during exercise by blunting a suppressive (HPA axis) and potentiating an excitatory (glutamate receptor) system.

Inadequacy of in-school support for diabetic children.

The level of blood glucose control needed to minimize complications in children with diabetes requires frequent blood sugar monitoring and appropriate responses to the information obtained. It is our impression that optimal support for good control is not available in all of the schools our patients attend. The objective of this study was to identify and quantify barriers to good control of diabetes in the school setting, and then use this information to target interventions to improve in-school support for children with diabetes. Two questionnaires were designed based on recommendations of the American Diabetes Association for appropriate in-school support for children with diabetes. Parental perception of in-school resources was addressed in one questionnaire. Forty-seven parents of children with diabetes in our clinic were surveyed. The second questionnaire was mailed to 222 randomly selected schools in our area inquiring about the in-school support available to children with diabetes and the types of educational materials that would be useful for school personnel. Thirty percent of the parents of children with diabetes indicated that the in-school support of their child was insufficient. Sixty-five of the 222 schools surveyed responded. The responses were variable and demonstrated inconsistency and, in some cases, inadequacy of support. A major deficiency noted in 13% of schools was lack of on-site personnel trained in diabetes management skills. From the schools' perspective, however, 50% of schools reported lack of parental communication. The care available for the child with diabetes is highly variable among schools. Targeted educational materials for both school personnel and parents would be useful to improve support for these children.