Objective-One publication reported that lower body satisfaction and lower education were independent predictors of depression in polycystic ovary syndrome (PCOS) women. This study replicates that analysis using different instruments, and adds androgen levels to the model.Methods-Cross-sectional analysis of questionnaires (Quick Inventory of Depressive Symptomatology-Self-Report, Body Esteem Scale) and serum androgens from a community cohort with (n=94) and without (n=96) PCOS, matched by BMI category. Non-parametric tests, Spearman correlations, and negative binomial regression models were analyzed.Results-Depression symptoms were common (40-60% in lean, overweight and obese BMI categories) in the PCOS cohort, albeit generally of mild severity. The PCOS women had similar depression symptom severity (P > 0.20) and similar body dissatisfaction (P ≥ 0.25) as the regularly cycling women in total and stratified by BMI category. In both the PCOS and non-PCOS cohorts, depression symptom severity was positively correlated with dissatisfaction with physical appearance and physical conditioning (P < 0.02). Body dissatisfaction (especially perception of physical conditioning) was strongly associated with more severe depression symptoms in nonobese PCOS women (BMI<30, P < 0.04) before and after controlling for age, testosterone and free testosterone. In contrast, for obese women with PCOS, depression was unrelated to body dissatisfaction after controlling for age.Conclusions-Among non-obese PCOS women, their subjective body image was strongly associated with the severity of their depression symptoms. Most of the obese PCOS cohort had low body satisfaction and depression symptoms, therefore individual differences in the body dissatisfaction scores were not helpful in identifying depression symptom severity. Neither testosterone nor free testosterone were associated with depression symptom severity in PCOS women after controlling for body dissatisfaction and age.

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How estradiol stimulates pulsatile GH secretion in the human is not well understood. Here, we test the clinical hypothesis that estradiol stimulates GH secretion, in part, by opposing somatostatin's inhibition of GH release. To this end, 13 estrogen-withdrawn postmenopausal women received placebo or 1 mg micronized estradiol-17beta orally, twice daily for 14 days, in a prospectively randomized, patient-blinded, within-subject cross-over design. For each intervention, the dose-dependent suppressive actions of somatostatin were evaluated by infusing 0 (saline), 3, 10, 30, 100, or 300 microg/1.73 m(2).h somatostatin-14 continuously, iv, for 3 h, on separate mornings, in the fasting state, 48 h apart. Blood was sampled at 10-min intervals for 2 h before, for 3 h concurrently with, and for 1 h after each infusion. Serum GH concentrations were quantitated in an ultrasensitive chemiluminescence-based assay (detection threshold, 0.005 microg/L). In the estrogen-deficient milieu, constant iv somatostatin infusions inhibited steady-state serum GH concentrations (valley mean during the last 60 min of the infusion interval) in a dose-dependent manner (P < 10(-4) interventional effect). Maximally effective doses of somatostatin reduced the latter by 89 +/- 6.1% (mean +/- SEM) below the subject-specific preinfusion baseline. Estrogen administration increased the serum estradiol concentration from 12 +/- 1 to 245 +/- 35 pg/mL [42 +/- 4 to 920 +/- 110 pmol/L] (P < 10(-4)); decreased serum concentrations of LH (P = 0.018), FSH (P < 10(-4)), and insulin-like growth factor-I (P = 0.003); and elevated the fasting (6-h mean) serum GH concentration from 0.41 +/- 0.07 to 0.87 +/- 0.27 (P = 0.011). Estradiol supplementation did not alter somatostatin's maximal suppression of GH by 89 +/- 4.7% (P < 10(-4) below subject-specific preinfusion baseline), thus signifying unchanging somatostatin efficacy. In contrast, estradiol replacement significantly elevated the half-maximally inhibitory dose of infused somatostatin by 13.5-fold, from 0.43 (0.38-0.48, 95% group statistical confidence intervals) (placebo) to 6.0 (5.2-7.0) (estradiol) microg/1.73 m(2)/h (P < 10(-4)), denoting muting of somatostatin's inhibitory potency. The latter inference was confirmed by a concomitant 4-fold decrease in the exponential steepness of the somatostatin inhibitory dose-response function; viz., mean 1.42 (1.49 to 1.33) (placebo) vs. 0.34 (0.62 to 0.26) (estradiol) slope units (P < 10(-4)). The foregoing effects were specific, because estrogen did not alter somatostatin's dose-dependent enhancement (P < 10(-4)) of the orderliness of GH release patterns, as quantitated via the approximate entropy regularity statistic. In summary, short-term replacement of estradiol to midfollicular phase levels in postmenopausal women selectively reduces the potency, but not the efficacy, of somatostatin's dose-dependent inhibition of GH release. Estrogen supplementation does not modify somatostatin's reciprocal enhancement of the quantifiable orderliness (approximate entropy) of...

ProblemThe rapid expansion of entrustable professional activity (EPA) assessment programs has led to calls to ensure fidelity in implementation and integrity in meeting the goals of competencybased medical education. Initiated in July 2017, in advance of the articulated core components of EPA implementation, this article describes the structure and outcomes of the University of Virginia (UVA) EPA Program and provides support for the identified essential components.

Bloom syndrome is a rare autosomal recessive disorder notable for increased chromosome fragility and an increased rate of somatic mutation. The clinical manifestations include small stature, a characteristic dermatologic lesion, and an excess incidence of malignancy. Fertility is generally reduced. A 19-year-old white woman with Bloom syndrome was successfully treated for preterm labor at 32 weeks' gestation, and ultimately delivered a healthy male infant at 35 weeks' gestation. Reports of pregnancy in women with Bloom syndrome are few. Despite reduced fertility, conception can occur, and women with Bloom syndrome should receive appropriate reproductive counseling to prevent unintended pregnancies and increased surveillance for preterm birth.