Objectives This study aimed to [1] confirm that nonobese adolescents with polycystic ovary syndrome (PCOS) have higher anti-Mullerian hormone (AMH) than controls; [2] examine the relationship of AMH with PCOS features and hormonal profile; and [3] approximate an AMH value that discriminates between adolescents with PCOS and controls. Design Case-control study. Setting Subspecialty ambulatory clinic. Patients Thirty-one nonobese adolescent girls (age 13–21 years), 15 with PCOS diagnosed using the National Institutes of Health (NIH) criteria and 16 healthy control subjects. Subjects and controls were comparable for body mass index z-score, age and ethnicity. Main outcome measure(s) AMH in PCOS subjects and control groups, correlation of AMH with hormonal parameters. Results AMH was higher in PCOS subjects (4.4 ±3.4 ng/mL) than in controls (2.4 ±1.3 ng/mL), when adjusted for menstrual age. In the entire group (PCOS and controls), AMH correlated with androgens, ovarian size and the presence of polycystic ovary (PCO) appearance. There was no difference in average ovarian size between PCOS (7.1 ±2.6 cm3) and controls (6.7 ±1.8 cm3). PCOS subjects were 1.49 times more likely to have AMH >3.4 ng/mL (confidence interval 0.98–2.26 ng/mL). Conclusions Our data suggest that AMH may be a useful adjunct in the diagnosis of PCOS in adolescents.

Although the diagnostic criteria for polycystic ovary syndrome (PCOS) have become less stringent over the years, determination of the minimum diagnostic features in adolescents is still an area of controversy. Of particular concern is that many of the features considered to be diagnostic for PCOS may evolve over time and change during the first few years after menarche. Nonetheless, attempts to define young women who may be at risk for development of PCOS is pertinent since associated morbidity such as obesity, insulin resistance, and dyslipidemia may benefit from early intervention. The relative utility of diagnostic tools such as persistence of anovulatory cycles, hyperandrogenemia, hyperandrogenism (hirsutism, acne, or alopecia), or ovarian findings on ultrasound is not established in adolescents. Some suggest that even using the strictest criteria, the diagnosis of PCOS may not valid in adolescents younger than 18 years. In addition, evidence does not necessarily support that lack of treatment of PCOS in younger adolescents will result in untoward outcomes since features consistent with PCOS often resolve with time. The presented data will help determine if it is possible to establish firm criteria which may be used to reliably diagnose PCOS in adolescents.

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Background Aromatase inhibitors (AIs) have been used off-label to increase adult height in short adolescent males. Studies have shown that AIs increase the predicted adult height (PAH) while delaying bone age (BA) maturation. We sought to determine whether AI therapy increases PAH in boys with short stature or rapid pubertal progression, and to evaluate any untoward effects. Methods The charts of 27 boys with BA ≥ 13 and short stature [height ≥ 2 standard deviation (SD) below the mean or ≥ 2 SD below mid-parental target height (MPTH)] or rapid pubertal progress, treated with anastrozole were reviewed. Outcome measures included anthropomorphic, hormonal, and metabolic data. Results The AI therapy averaged 21 months (range 14–30 months) for all, with Rx group 1 receiving < 18 months therapy (n = 7) and Rx group 2 receiving 18–30 months therapy (n = 20). Post-therapy, in Rx group 1 and all subjects, there was no significant change in the PAH, height SDS, or BA/chronological age (CA). In Rx group 2, there was a small, nonsignificant increase in PAH, no change in height SDS, and a small decrease in BA/CA. Post-therapy PAH was different from MPTH in all and in both Rx groups 1 and 2, p < 0.02. Eight of them achieved near-final height, averaging 6.73 ± 1.40 cm less than MPTH and 1.91 ± 0.86 cm less than the pre-therapy PAH. Post-therapy, the initially decreased estradiol did not persist but mildly increased testosterone and decreased high-density lipoprotein were noted, as was an increase in hematocrit, and decrease in growth velocity. Conclusions We suggest that although bone age progression may be slightly delayed with longer duration of therapy, an overall short-term AI therapy does not lead to a final height that is greater than the predicted pre-therapy height.

Up to 30% of term labor deliveries experience fetal acidemia, a condition usually caused by hypoxia that is associated with adverse neonatal outcomes. The American College of Obstetricians and Gynecologists and American Academy of Pediatrics recommend assessing fetal umbilical artery (UA) blood gases at delivery when fetal metabolic status is in question. Although a UA pH of 7.24 to 7.28 is considered normal, the degree of acidemia associated with neonatal death is unclear. Recent data suggest that mild acidemia (UA pH of 7.0–7.2) and certain types of acidemia (metabolic, mixed, or respiratory) also indicate increased risk for adverse outcomes. Most cases of acidemia follow labor when the placental gas exchange is interrupted during contractions. But fetal acidemia is rare in cases of scheduled prelabor cesarean delivery (CD) and not well described in the literature. This study aims to determine if fetal acidemia at the time of scheduled, prelabor CD is associated with neonatal morbidity.This was a retrospective cohort study comparing patients with and without fetal acidemia, defined as a UA pH <7.2. Included were singleton neonates delivered via scheduled CD at a single tertiary care center from June 2004 to December 2014. Excluded were those who delivered before 37 weeks of gestation, were diagnosed with major anomalies, or underwent CD due to labor, rupture of membranes, or nonreassuring fetal status. Also excluded were cases in which data on validated umbilical cord gases were unavailable. The primary outcome was a composite of neonatal outcomes, including neonatal death, encephalopathy, therapeutic hypothermia, seizures, intubation, and respiratory distress.A total of 2081 neonates met the inclusion criteria, with fetal acidemia present at the time of delivery in 252 cases (12.1%). Acidemia occurred more frequently in breech neonates and those born to mothers with gestational diabetes mellitus or obesity. Intraoperative maternal hypotension, use of vasopressor therapy, and increased times from anesthesia induction and skin incision to delivery were also more likely to occur in cases of acidemia. The primary composite outcome was observed in 176 (8.5%) of neonates. This outcome was significantly higher in those with acidemia than those without (7.6% vs 15.1%; adjusted risk ratio [aRR], 2.95; 95% confidence interval [CI], 2.03 to 4.12). Intubation (aRR 3.50; 95% CI, 1.27–9.13) and respiratory distress (aRR, 2.93; 95% CI, 2.00–4.13) also occurred more frequently among those with acidemia. As the rate of UA pH categories decreased, the proportion of neonates with the primary outcome increased: 13.5% morbidity if UA pH was 7.0 to 7.19 versus 42.9% morbidity if UA pH was <7.0. Compared with neonates with a UA pH ≥7.2, the risk for adverse outcomes rose 3.2-fold in those with a UA pH <7.1 (aRR, 3.23; 95% CI, 1.73–5.24) and 6.6-fold in those with a UA pH <7.0 (aRR, 6.64; 95% CI, 3.23–8.96). The primary outcome was observed in 24.7% of neonates with respiratory acidemia, 27.5% with mixed, and 25% with other ac...