Enhanced responsiveness to selective serotonin reuptake inhibitors during lactation.

The physiology of mood regulation in the postpartum is poorly understood despite the fact that postpartum depression (PPD) is a common pathology. Serotonergic mechanisms and their dysfunction are widely presumed to be involved, which has led us to investigate whether lactation induces changes in central or peripheral serotonin (5-HT) systems and related affective behaviors. Brain sections from lactating (day 10 postpartum) and age-matched nulliparous (non-pregnant) C57BL/6J mice were processed for 5-HT immunohistochemistry. The total number of 5-HT immunostained cells and optical density were measured. Lactating mice exhibited lower immunoreactive 5-HT and intensity in the dorsal raphe nucleus when compared with nulliparous controls. Serum 5-HT was quantified from lactating and nulliparous mice using radioimmunoassay. Serum 5-HT concentrations were higher in lactating mice than in nulliparous controls. Affective behavior was assessed in lactating and non-lactating females ten days postpartum, as well as in nulliparous controls using the forced swim test (FST) and marble burying task (MBT). Animals were treated for the preceding five days with a selective serotonin reuptake inhibitor (SSRI, citalopram, 5mg/kg/day) or vehicle. Lactating mice exhibited a lower baseline immobility time during the FST and buried fewer marbles during the MBT as compared to nulliparous controls. Citalopram treatment changed these behaviors in lactating mice with further reductions in immobility during the FST and decreased marble burying. In contrast, the same regimen of citalopram treatment had no effect on these behaviors in either non-lactating postpartum or nulliparous females. Our findings demonstrate changes in both central and peripheral 5-HT systems associated with lactation, independent of pregnancy. They also demonstrate a significant interaction of lactation and responsiveness to SSRI treatment, which has important implications in the treatment of PPD. Although recent evidence has cast doubt on the effectiveness of SSRIs, these results support their therapeutic use in the treatment of PPD.

Endometrial thickness predicts endometrial hyperplasia in patients with polycystic ovary syndrome.

Body mass index is predictive of sonographic endometrial stripe thickness, which in turn is predictive of endometrial hyperplasia in patients with polycystic ovary syndrome. For every 1-mm increase in endometrial stripe, the odds ratio of hyperplasia increased by 1.48 (95% confidence interval, 1.04-2.10).

Effects of polycystic ovarian syndrome on in vitro fertilization-embryo transfer outcomes are influenced by body mass index.

OBJECTIVE: To determine whether polycystic ovary syndrome (PCOS) adversely impacts IVF-embryo transfer outcomes in obese compared to lean patients. DESIGN: Retrospective chart review. SETTING: University-affiliated infertility program. PATIENT(S): Lean non-PCOS (n = 52), lean PCOS (n = 6), obese non-PCOS (n = 18), and obese PCOS (n = 10). INTERVENTION(S): Ninety-four fresh nondonor IVF-embryo transfer cycles analyzed. MAIN OUTCOME MEASURE(S): Cycle characteristics, clinical pregnancy (PR) and live birth rates. RESULT(S): Lean PCOS had more dominant follicles (12.2 +/- 6.0 vs. 7.7 +/- 3.6), retrieved oocytes (22.2 +/- 9.2 vs. 12.6 +/- 5.8), and frozen embryos (5 +/- 4.6 vs. 1.4 +/- 2.6) than lean non-PCOS. Lean PCOS also used fewer gonadotropin ampules (18.8 +/- 6.0 vs. 29.2 +/- 14.2), but had more retrieved oocytes (22.2 +/- 9.2 vs.14.3 +/- 4.9) than obese PCOS. Obese non-PCOS had better-grade embryos (2.1 +/- 0.8 vs. 2.7 +/- 0.8) and fewer embryos transferred (2.4 +/- 0.6 vs. 2.9 +/- 0.6) than obese PCOS, but more embryos frozen than lean non-PCOS (3.2 +/- 3.2 vs. 1.4 +/- 2.6). Implantation rates trended downward in obese patients with PCOS, but no other differences were observed. CONCLUSION(S): Patients with PCOS with a body mass index (BMI) in the lean rather than the obese range have more favorable assisted reproductive technology (ART) cycle characteristics but show no clinical outcome differences.