Background: As its name indicates, anti-Müllerian hormone (AMH) is primarily found as an inhibitor of the Müllerian duct in male fetus. On the other hand, AMH may act as a mediator of Müllerian duct-derived female tissue, such as endometrium in normal and pathological conditions. However, the role of AMH in the functional regulations of endometriosis is not well understood. It can be hypothesized that AMH in peritoneal fluids may affect the activity of peritoneal endometriosis. In this study, we investigated the levels of AMH in peritoneal fluids (PF) in women with and without endometriosis. Methods: PF were collected during laparoscopy from 90 women diagnosed as having advanced endometriosis (rASRM stage III, n = 30; stage IV, n = 60), and 32 women without endometriosis were served as control. Paired serum samples were also collected before the surgery. AMH in PF and serum were measured by ELISA. Individual clinical information was collected. AMH levels were compared according to the presence of endometriosis. The expression of AMHR2 in peritoneal endometriotic lesions obtained during laparoscopy was examined by immunohistochemistry. Results: AMH levels in PF were positively and significantly correlated with serum AMH levels in both women with and without endometriosis ( R 2 = 0.17, P < 0.0001; R 2 = 0.30, P = 0.001, respectively). Serum AMH levels were inversely and significantly correlated with age in women with endometriosis ( R 2 = 0.092, P = 0.004) and in control women without statistical significance ( R 2 = 0.078, P = 0.12). AMH levels in PF were also inversely but not significantly correlated with age in women with and without endometriosis ( R 2 = 0.029, P = 0.11 and R 2 = 0.027, P = 0.37, respectively). Mean age and serum AMH levels were not significantly different between two groups. On the other hand, AMH levels in PF were significantly lower in women with endometriosis compared to those of control women [2.15 ± 2.13 (mean ± SD) vs. 4.40 ± 4.77 ng/mL, P = 0.0001]. AMHR2 are localized at glandular epithelium and stromal cells in the ectopic endometrium of peritoneal endometriosis. Conclusions: Women with endometriosis may present lower PF AMH levels even if they retain serum levels similar to women without disease. As peritoneal endometriosis expresses a specific receptor for AMH, lower AMH levels in PF of women with advanced endometriosis may be involved in the pathophysiology of peritoneal endometriosis.

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Background Androgen-producing granulosa cell tumor in adolescent girl is rare condition and clinical characteristics are not fully elucidated. Case presentation Seventeen years old girl complained of secondary amenorrhea was referred to our out-patient consultation. Markedly elevated serum testosterone, LH, and AMH levels were noted. Mild hirsutism and clitoromegaly were presented. Transabdominal ultrasonography and MRI revealed cystic mass occupied pelvic cavity probably originated from left ovary. Right ovary showed polycystic appearance. Laparoscopic left ovarian cystectomy was performed. After the surgery, her menstruation resumed along with normalized hormonal parameters, and clinical hyperandrogenism were improved. Since the scarcity of cellular lining of inner cyst wall, definitive pathological diagnosis was difficult. After the consultation with gynecological pathologist, the tumor was diagnosed as sex cord stromal tumor, highly suspicious for adult granulosa cell tumor. Residual left salpingo-oophorectomy was performed by additional laparoscopic surgery. Her serum testosterone and AMH levels were remained low with regular menstrual cycles and no evidence of recurrence. Conclusions Androgen-producing cystic granulosa cell tumor is rare gynecological disorders, which need both gynecologic oncological and endocrinological approach. Its clinical manifestations may bring some clues to the pathogenesis of ovulatory dysfunctions, such as polycystic ovary syndrome.

Infertility is a main manifestation of endometriosis, though the exact pathogenesis of endometriosis-associated infertility remains unclear. Compromised ovarian functions may be one of the causes of endometriosis related infertility. The ovarian function can be classified into three basic elements, (1) production of ovarian hormones, (2) maintenance of follicular development until ovulation, and (3) reservoir of dormant oocytes (ovarian reserve). The effects of endometriosis on ovarian hormone production and follicular development are inconclusive. Ovarian endometrioma is common phonotype of endometriosis. Development of endometrioma per se may affect ovarian reserve. Surgery for endometriomas further diminish ovarian reserve, especially women with bilateral involvement. Early intervention with surgery and/or medical treatment may be beneficial, though firm evidence is lacking. When surgery is chosen in women at reproductive age, specific techniques that spare ovarian function should be considered.

Objective: We investigated the clinical characteristics of patients with ruptured ovarian endometrioma and examined the role of serum D-dimer levels in ruptured and unruptured ovarian endometrioma. Design: Retrospective and prospective studySetting: Department of Gynecology of Saiseikai Nagasaki Hospital, Japan. Patient(s):Women who had laparoscopic surgery for ovarian endometrioma from April 2009 to April 2017 were enrolled in the study. We classified these women into three groups: those with ruptured endometrioma (n=61), emergency surgery for unruptured ovarian endometrioma (n=13), and elective surgery for unruptured ovarian endometrioma (n=26). Intervention(s): NoneMain outcome measure(s): The clinical characteristics and serum D-dimer levels of women with ruptured and unruptured ovarian endometrioma were evaluated. Result(s):In the ruptured group, the mean age was 33.8 years, mean ruptured cyst size was 6.4 cm, and rupture occurred on the right side in 27 patients and on the left side in 30 patients. Almost all patients had no definite trigger, and 30 patients (49%) had rupture during the menstrual period. We compared patients in the ruptured and unruptured groups; significant differences were observed in the rebound tenderness (79% vs. 42%,p<0.05), white blood cell count (10,536 ± 4,412/µL vs. 7,269 ± 2,650/µL, put p<0.05), and C-reactive protein level (4.0 ± 5.4 mg/dL vs. 0.5 ± 0.9 mg/dL, p<0.05). In the ruptured group, 55% of ovarian endometriomas were detected preoperatively by transvaginal ultrasonography and 74% by magnetic resonance imaging. We measured serum D-dimer levels in the ruptured group (n=24) and unruptured group with elective surgery (n=26). The mean serum D-dimer level (cut-off level is less than 1.0 μg/mL) was 2.2±1.9 μg/mL in the ruptured group, which was significantly higher than that in the unruptured group (put D-dimer value and p<0.05). In the ruptured group, 79% of patients showed higher serum D-dimer levels, and all patients in the unruptured group with elective surgery showed D-dimer values less than the cut-off levels. Conclusion(s):In addition to routine measurement of conventional parameters, our findings further suggested the clinical usefulness of measuring D-dimer levels in distinguishing patients with ruptured and unruptured ovarian endometrioma.