Sex cord stromal tumor of ovary masquerading as polycystic ovarian syndrome

Virilization is a portentous sign that suggests the possibility of an ovarian or adrenal neoplasm. Diagnosis may be delayed in some patients due to nonspecific symptoms and overlapping symptoms with that of polycystic ovarian syndrome (PCOS). However, it must be remembered that PCOS usually causes mild to moderate elevation of serum testosterone with hirsutism whereas serum testosterone levels are many times elevated in cases of androgen secreting tumors and virilization is a norm. So high testosterone level with new onset virilization rule out PCOS. Authors are reporting two cases of Sertoli Leydig cell tumor despite their similar histopathology and equivalent levels of serum testosterone had a varied clinical spectrum of virilization.

Hormonal profile in postmenopausal women: do they need androgen therapy?

The effect of androgen on women s health has not been fully elucidated. Circulating levels of testosterone and dehydroepiandrosterone sulfate (DHEA-S) gradually decrease with age in postmenopausal women, although transient increases have been observed during the menopausal transition. High testosterone level has been suggested to be associated with increased risk of cardiovascular disease, increased triglyceride, insulin resistance and increase in the risk of developing breast cancer in postmenopausal women. Female androgen insufficiency, which is characterized by the presence of reduced androgen level in circulation, leads to an impairment in sexual drive, reduced libido, depressed mood, and signs and symptoms of limited androgen exposure such as decreased muscle mass, reduced bone density and decreased sense of well-being.

319 REDUCED SUPEROVULATION EFFICIENCY BY HIGH-DOSE TREATMENT OF DEHYDROEPIANDROSTERONE IN MICE

Strain differences in in vitro fertilizability still constitute a serious problem in mouse reproduction. To improve the in vitro fertilizability of mouse oocytes, we examined the effect of implanting time-release pellets of dehydroepiandrosterone (DHEA), a testosterone precursor, in female mice on oocyte fertilizability. The DHEA pellets (0.25, 1.5, or 5 mg pellet–1, 21-day release form, Innovative Research of America, Sarasota, FL, USA) or corresponding placebo pellets were implanted subcutaneously in 9-week-old female 129X1/SvJJmsSlc mice. On Day 18 of implantation, superovulation was induced in these females by injections of pregnant mare serum gonadotropin (PMSG) and hCG 48 h apart. On Day 21, IVF was conducted using oocytes collected from the oviducal ampullae of these females and epididymal sperm from Slc : ICR male mice using TYH medium. Then, the embryos were cultured in vitro in Whitten’s medium for 96 h. Plasma steroid levels and expression of 5 ovarian proteins (PTEN and receptors for FSH, androgen, oestrogen, and progesterone) at oocyte collection were measured by enzyme immunoassay and quantitative Western blots, respectively. Embryo development into 2-cell and blastocyst stages at each dose at 24 h and 96 h after insemination, respectively, were compared between DHEA and placebo groups using weighted ANOVA with angular transformations. Other observed values were compared using Student’s t-test. Treatment with DHEA suppressed the numbers of ovulated oocytes in the 1.5 and 5 mg groups (DHEA v. placebo: 21.0 ± 2.6 v. 32.5 ± 2.8 and 19.9 ± 1.4 v. 27.1 ± 1.6, respectively, n = 10; P < 0.05), but not in the 0.25 mg group (26.6 ± 3.2 v. 24.8 ± 2.4). Treatment with DHEA did not affect the percentages of 2-cell embryo formation at any dose, ranging 50 to 60%. In the 0.25 mg group, DHEA treatment tended to increase blastocyst formation rate (1.8 ± 0.8% v. 0.4 ± 0.4%; not significant). However, the treatment at 1.5 mg suppressed the rate (0.0 ± 0.0% v. 3.1 ± 0.7%; P < 0.05) and treatment at 5 mg did not affect the rate (1.3 ± 0.9% v. 0.8 ± 0.6%). Plasma testosterone levels were increased by DHEA at 1.5 and 5 mg (338.2 ± 39.8 v. 197.0 ± 8.9 pg mL–1 and 534.9 ± 111.4 v. 241.8 ± 34.4 pg mL–1, respectively, n = 6; P < 0.05), but not at 0.25 mg (247.4 ± 22.0 v. 252.5 ± 35.6 pg mL–1, n = 6). No significant difference was induced by DHEA in plasma DHEA, progesterone, or oestradiol at any doses. Ovarian PTEN protein was more abundant in DHEA group than in placebo group at 5 mg (P < 0.05), tended to be more abundant at 1.5 mg (P ≈ 0.14), and was not different at 0.25 mg (P ≈ 0.35). The amounts of the 4 receptor proteins were not significantly changed by DHEA at any dose. These results suggest that DHEA at a low dose (e.g. 0.25 mg pellets for 21 days) might have a potential to improve in vitro fertilizability of mouse oocytes. Higher doses of DHEA reduced superovulation efficiency, perhaps because of the high testosterone level induced by the high-dose treatment of DHEA. The high testosterone level might upregulate ovarian PTEN expression, which might suppress ovarian primordial follicle activation. A more detailed study is needed to determine the optimal dose, timing, and duration of DHEA treatment for the improvement of female fertilizability.