MET administration lowered LH activity in all PCOS women and in ovulatory responders and also compromised PRL stimulated secretion in the latter cases. These findings were indicative of an effect of MET on pituitary activity.

No abstract

A series of studies aiming at introducing an effective treatment for idiopathic oligozoospermia was conducted in a step-wise fashion spanning over a 20-year period. The concept was that co-administration of an accessory gland-stimulating androgen, testosterone undecanoate (40 mg t.i.d.) and the FSH raising anti-oestrogen tamoxifen citrate (10 mg b.i.d.) may improve sperm parameters. A prerequisite for such an effect was the demonstration that testosterone undecanoate had no suppressing action on pituitary-testicular axis. In this context, initial studies demonstrated no change in basal or stimulated gonadotrophin and testosterone secretion in short- or long-term protocols. Two subsequent trials with this combination showed a marked improvement of sperm parameters and pregnancy incidence, with a seasonal variation noted in response to treatment, this being higher during the cold seasons of autumn and winter. Regarding the mechanism of testosterone undecanoate's action, a recent study from our unit showed that its administration resulted in a marked rise of serum DHT levels. Because this steroid is an epididymal function promoter, it appears that its contribution in the combination is mediated mainly through its DHT raising effect. By and large, this empiric approach for the treatment of idiopathic oligozoospermia was satisfactorily documented after a 20-year investigative saga.

This study attempted to investigate the presence of seasonal variations in sperm parameters and to evaluate the season's impact on the response to treatment in men with idiopathic oligozoospermia (IO). To this end, a retrospective analysis of the records of 294 men, who participated in a controlled study, was performed. This sample included IO men (n = 106) treated with tamoxifen citrate (10 mg b.i.d.) and testosterone undecanoate (40 mg t.i.d.) or placebo (n = 106) and normozoospermic men (n = 82) serving as controls. Outcome measures included sperm parameters, functional sperm fraction (FSF) and incidence of pregnancy. Analysis showed a raised frequency of high FSF values and increased area under the response curve (AURC) for FSF mean during autumn-winter seasons in patients on active treatment compared with those in placebo (P < 0.05-P < 0.04). Moreover, receiver operation characteristics (ROC) curves for a >100% FSF rise significantly discriminated autumn-winter from other seasons (P < 0.001, all), whereas active treatment showed higher than placebo FSF values particularly during autumn and winter (P < 0.001, all). The pregnancy incidence was higher in the autumn in all groups. It is concluded that FSF values showed a better response to active treatment during autumn and winter, indicating that commencement of empirical treatment at this time in IO men may stand a better chance to succeed.

Exposure to air pollution and, in particular, to nitrogen dioxide (NO2) or particulate pollutants less than 2.5 μm (PM2.5) or 10 μm (PM10) in diameter has been linked to thyroid (dys)function in pregnant women. We hypothesized that there may be a dose—effect relationship between air pollutants and thyroid function parameters. We retrospectively evaluated thyrotropin (TSH) in 293 women, NO2, PM2.5 and PM10 levels in Athens. All the women were diagnosed with hypothyroidism for the first time during their pregnancy. Exposure to air pollution for each woman was considered according to her place of residence. Statistical analysis of age, pregnancy weight change, and air pollutants versus TSH was performed with ordinary least squares regression (OLS-R) and quantile regression (Q-R). A positive correlation for logTSH and PM2.5(r = +0.13, p = 0.02) was found, using OLS-R. Further analysis with Q-R showed that each incremental unit increase (for the 10th to the 90th response quantile) in PM2.5 increased logTSH(±SE) between +0.029 (0.001) to +0.025 (0.001) mIU/L (p < 0.01). The other parameters and pollutants (PM10 and NO2) had no significant effect on TSH. Our results indeed show a dose—response relationship between PM2.5 and TSH. The mechanisms involved in the pathophysiological effects of atmospheric pollutants, in particular PM2.5, are being investigated.