EFFICACY OF ACNE THERAPY IN PATIENTS WITH OVARIAN HYPERANDROGENISM

The aim of the study was to show the effectiveness of treatment of acne with moderate severity in women with ovarian hyperandrogenism. A total of 25 female reproductive voerast patients with moderate acne and ovarian hyperandrogenism who were not planning pregnancy were examined. All patients were examined, which included a consultation with a gynecologist with a gynecological examination, ultrasound examination of the pelvic organs, a study of the hormonal status, a biochemical blood test, as well as a dermatological examination with the determination of the dermatological index of acne (DIA). After the examination, the patients underwent complex therapy using the external treatment recommended by the dermatovenerologist (skin cleansing, gel with azelaic acid and / or gel with adapalene), as well as the appointment of a combined oral contraceptive (COC) Jes Plus. Based on this study, it can be concluded that complex therapy, including local treatment and taking Jes Plus, is the first choice in the treatment of androgen-dependent dermopathy, manifested by moderate acne, in patients with ovarian hyperandrogenism due to PCOS. Such therapy contributes not only to the formation of a pronounced clinical result, but also causes a low probability of side effects. The administration of COC containing drospirenon and the active form of folate, in the form of the calcium salt levomefolate, allows a favorable effect on the metabolic processes in the body as a whole, and in particular, provides a positive effect on the skin, the cardiovascular system, reduces the risk of systemic and local inflammation, relieving the state of hyperhomocysteinemia, providing prevention of cardiometabolic risks.

Ovarian Steroid Cell Tumor (Not Otherwise Specified): A Case Report of Ovarian Hyperandrogenism

Steroid cell tumors (SCTs) (not otherwise specified (NOS)) are rare sex cord-stromal tumors of the ovary. These are associated with hormonal disturbances resulting in menstrual bleeding patterns and androgenic effects. We report the case of a 36-year-old female presented with hirsutism, signs of virilization, and elevated androgen levels. Transvaginal ultrasound showed a solid-appearing right ovarian mass. She underwent fertility-sparing surgery with a laparoscopic left oophorectomy. Histological examination showed a benign steroid cell tumor, NOS. These tumors often small can then present a problem of positive diagnosis responsible for a delay in the diagnosis.

OR31-05 Emergence of Ovarian Hyperandrogenism and Luteal Insufficiency Following ESR1 Knockdown in the Mediobasal Hypothalamus of Adult Female Rhesus Monkeys

Diminished estradiol (E2) negative feedback action by neuronal ESR1 in the arcuate nucleus (ARC) of the mediobasal hypothalamus (MBH) is hypothesized to cause gonadotropin-releasing hormone (GnRH) hypersecretion, and thus LH excess, contributing to ovarian hyperandrogenism in polycystic ovary syndrome (PCOS). In primates, including humans, however, the mediating estrogen receptor is unknown. Thus, to test the hypothesis that diminished E2 action on ARC ESR1 contributes to female primate ovarian hyperandrogenism, eleven, ovary intact, adult female rhesus macaques, pair housed with female peers, received five 12µl MRI-guided MBH infusions into the rostral-to-caudal extent of both right and left ARC. Each infusion comprised gadolinium contrast agent and ~3-4 x 1010 adeno-associated virus 8 (AAV8) particles containing either a shRNA specific for ESR1 (n=6, ERaKD) or scrambled shRNA (n=5, control). Mid-surgery MRI scans identified targeting accuracy. 2-2.5 years following AAV8 infusion, EIA-determined P4 values were obtained from twice weekly serum samples; samples obtained during the follicular phase of menstrual cycles or anovulatory periods were submitted to liquid chromatography, tandem mass spectrometry (LCMS) for additional steroid hormones. LCMS-determined values were also obtained 0 hours (h) and 24 h following an IM injection of 200IU hCG. Both ERaKD (28.5 ± 1.3 days, mean ± SEM) and control (34.0 ± 3.3 days) female groups exhibited comparably regular menstrual cycles. ERaKD exhibited higher circulating levels of LH (2.8 ± 0.2 ng/ml, p=0.03), androstenedione (A4, 0.43 ± 0.03 ng/ml, p=0.03) and testosterone (T, 0.23 ± 0.03 ng/ml, p=0.09), and LH/FSH ratio (1.7 ± 0.2, p=0.05) compared to controls (LH, 2.1 ± 0.4; A4, 0.30 ± 0.05; T, 0.18 ± 0.01 ng/ml; LH/FSH 1.3 ± 0.2). Following an ovarian androgen-stimulating hCG injection, ERaKD 24-h peak levels for T (0.28 ± 0.01 ng/ml) were higher (p=0.03) compared to controls (0.21 ± 0.01 ng/ml). In addition, luteal insufficiency emerged in ERaKD females, with mean (2.4 ± 0.3 ng/ml), peak (3.6 ± 0.4 ng/ml) and area-under-the-curve (AUC, 23.2 ± 4.2 ng/ml/days) P4 values diminished compared to controls (mean, 3.6 ± 0.1, p=0.01; peak 5.7 ± 0.1 ng/ml, p=0.01; AUC, 43.7 ± 6.7 ng/ml/days, p=0.03). Taken together, these results suggest that knockdown of ARC ESR1 disrupts Gn stimulation of ovarian function, contributing to female monkey ovarian hyperandrogenism and menstrual cycle impairment emulating PCOS in women.

Severe hyperandrogenism due to ovarian hyperthecosis in a young woman

Hyperandrogenism is a relatively common clinical problem. However, severe hyperandrogenism causing virilisation is rare. A 27-year-old woman presented with generalised hirsutism, clitoromegaly, breast atrophy and secondary amenorrhoea. She had serum testosterone levels elevated to the adult male range. Administration of gonadotropin-releasing hormone (GnRH) analogue resulted in >50% suppression of serum testosterone which was suggestive of luteinising hormone-dependent ovarian hyperandrogenism. Imaging studies of abdomen and pelvis were normal, and ovarian venous sampling failed to show a gradient between the two sides. A presumptive diagnosis of ovarian hyperthecosis was, therefore, considered. Medical treatment with GnRH analogue and combined oral contraceptive pills was initiated to which an excellent clinical and biochemical response was noted. This case highlights a rare presentation of ovarian hyperthecosis in a young woman with severe hyperandrogenism mimicking a virilising neoplasm.