Another systematic review by Bosdou et al. reports that only transdermal testosterone, but no other androgen modulating agents including DHEA achieved significantly improved clinical PRs. Recently, a systematic review and meta-analysis that reported specifically on the role of DHEA alone in women with diminished ovarian reserve, suggested that DHEA does not improve the ovarian response and pregnancy outcome. However, all these review are limited by small sample sizes.The review by Bosdou et al. on DHEA included only one study with 33 participants. Especially,the heterogeneity between the former studies is criticized, caused by the wide diversity in the definitions used to specify women with impaired response to ovarian stimulation. Recently, a consensus was reached by the ESHRE Working Group on the criteria needed to define POR 
when at least two of the following three features must be present:advanced maternal age or any other risk factor for POR;a previous POR andan abnormal ovarian reserve test. One of the most important components in the Bologna criteria is a previous POR and, therefore, one stimulated cycle is considered essential for the diagnosis of POR. However, patients over 40 years of age with an abnormal ORT may also be classified as poor responders since both advanced age and an abnormal ORT could indicate reduced ovarian reserve and act as a surrogate of ovarian stimulation cycle. Although the Bologna criteria have also been criticized for several limitations, such as the risk factors for POR were not clearly defined. However, it is the only internationally accepted universal definition of POR, so that it is amenable for use in future clinical trials. Here we presented DHEA data by using these uniform inclusion criteria. The results showed significantly higher implantation rates and ongoing PRs were noted in the DHEA group, although there were no obvious beneficial effects of DHEA on oocytes yield in poor responders. These findings imply that DHEA may exert its positive effect by improving oocytes and embryo quality. In addition, our study shows that DHEA administration resulted in a significant increase in the total number of follicles that develop to a size $14 mm in response to FSH stimulation, while the total FSH dose required was significantly decreased in DHEA group. These suggest that exogenous DHEA increases the ovarian sensitivity to gonadotrophin stimulation in poor responders. The mechanism of DHEA action on the Nortriptyline ovaries remains speculative. Numerous hypotheses have been proposed on how DHEA may enhance fertility. One mechanism that has been suggested is a direct effect of DHEA on ovarian folliculogenesis by Alprostadil increasing primordial follicle pool up to the pre-antral and antral follicle stages. Androgens may act on ovarian follicular development by increasing the number of FSH receptors expressed in the granulosa cells, and the increasing intrafollicular androgens could augment granulose cell antiMu��llerian hormoneproduction, thus stimulating early stages of follicular growth. It was recently proven in an animal experimental model that DHEA exposure stimulated initiation of primordial follicles and development of gonadotrophin-responsive preantral and early antral follicles through promoting granulosa cell proliferation. Besides, oral DHEA administration has been demonstrated to increase serum IGF-I concentrations, which are known to have a positive effect on follicular development and oocyte quality.