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Treatment with metformin is indicated in all hyperinsulinaemic overweight patients with PCOS, especially in those with NAFLD. These data appear even more interesting considering their increased risk to develop metabolic and hepatic complications.

For the first time, we have identified a genetic variant that is strongly associated with PCOS in an isolated population. These results, if confirmed in other cohorts, may provide the opportunity to test the S312N genotype at the LHCGR locus in fertile women to assess the risk of PCOS. The avoidance of triggering factors like weight increase may improve the reproductive outcome of potentially at-risk subjects.

Objective To assess the effectiveness of an antispasmodic drug, hyoscine-N-butylbromide, in reducing pain during hysterosalpingo-contrast sonography (HyCoSy). Methods

Objective To evaluate the role of mean ovarian volume (MOV) in the diagnosis of polycystic ovary syndrome (PCOS) during adolescence, and its relationship with metabolic and endocrine parameters. Design Observational study. Patients A total of 134 young girls, including 86 adolescents with PCOS and 48 controls, were studied. Measurements During the early follicular phase, a pelvic ultrasound examination was performed to measure the ovarian volume of both ovaries and to calculate the MOV. All subjects underwent hormonal assessment and an ultrasound examination. PCOS subjects were submitted to an oral glucose tolerance test. The homeostasis model assessment for insulin resistance (HOMA‐IR) and several insulin resistance indexes were also determined. Results Androgens, free androgen index (FAI), LH and insulin resistance indexes were higher in the PCOS group. MOV was significantly different between the two groups: control group 4·6 ± 1·9 cm3, adolescent PCOS group 9·6 ± 4·4 cm3. The MOV threshold of 5·596 cm3 offered the best compromise between sensitivity and specificity based on the characteristics of the operating receiver curve analysis. Therefore, an ovarian volume higher than 5·6 increased the risk of PCOS by about 15 times (OR 16·25 IC 95% 6·3–41·3). In adolescent PCOS girls, the ovarian volume was significantly associated with circulating testosterone and insulin, and indices of insulin resistance. Conclusions During early adolescence MOV evaluation may offer an effective means to screen and follow up young girls with irregular cycles in order to prevent the long‐term metabolic disturbances of the polycystic ovary syndrome.

We investigated the effect of nicotine and its methylated metabolite, N-methyl-nicotine (M-nicotine), on human luteal cells by measuring release of progesterone and prostaglandins (PGs) from cultured cells and by testing gene expression of vascular endothelial growth factor (VEGF), an angiogenic factor strictly involved in luteal pathophysiology. Primary cultures of human luteal cells were treated for 24 h with nicotine and M-nicotine (from 10(-6) to 10(-11) M) either alone or combined with hCG (25 ng/ml); progesterone and PGs were assayed in the culture medium. In another group of experiments, luteal cells were treated for 24 h with nicotine and M-nicotine (10(-7) M) to perform reverse transcriptase-polymerase chain reaction on VEGF mRNA. Nicotine and M-nicotine negatively affected basal luteal steroidogenesis at all tested concentrations, but neither was able to affect hCG-induced progesterone release. Both substances were able to significantly increase PGF2alpha release from luteal cells, with a dose-related efficacy for M-nicotine. On the contrary, PGE2 release was significantly inhibited by both nicotine and its metabolite. Finally, nicotine was able to increase VEGF mRNA expression significantly, whereas M-nicotine was not. In conclusion, nicotine and M-nicotine can induce a sort of luteal insufficiency by inhibiting progesterone release, probably through modulation of the PG system.

No abstract

The oral low dose of unopposed estradiol therapy had a favorable effect on glycoinsulinemic metabolism in healthy postmenopausal women; however, the standard dose caused a slight but significant deterioration in insulin sensitivity.