Uterine arteriovenous malformation: a case report with proposal for pathogenesis.

Uterine arteriovenous malformation (UAM) is a rare medical condition. Even though UAM can cause abnormal and life-threatening uterine hemorrhage, there is no consensus on the clinical guideline on its treatments, most likely due to its low incidence, unknown etiology, and distinct fertility demands by different patients. Here, we present one elderly woman with uncommon UAM. We first discuss our experience regarding the diagnoses and treatments of UAM and then propose a hypothesis for the pathogenesis of UAM.

Increased NKG2A+CD8+ T-cell exhaustion in patients with adenomyosis.

Immune dysregulation has long been proposed to be associated with adenomyosis, but the underlying mediators and mechanisms remain largely unexplored. Here, we used flow cytometry to investigate the alterations in immune cell subsets in adenomyotic uteri and analyze the phenotype and function of abnormal immune cells. We found that an increase in cluster of differentiation (CD)8+ T-cell number was the predominant alteration in ectopic lesions in patients with adenomyosis and was significantly associated with the severity of adenomyosis. Importantly, we identified an exhausted natural killer group protein 2A (NKG2A)+CD8+ T-cell subset that was associated with the severity of adenomyosis and found that the number of these cells was significantly increased in the eutopic endometrium and ectopic lesions. In addition, the increases in the expression of NKG2A ligand histocompatibility leucocyte antigen E and interleukin-15 in glandular epithelial cells in the adenomyotic microenvironment might contribute to CD8+ T-cell exhaustion by promoting NKG2A expression on CD8+ T cells or inhibiting the effector function of these cells. In conclusion, our data revealed a previously unrecognized role for NKG2A+CD8+ T-cell exhaustion in the pathogenesis of adenomyosis, indicating that therapeutic interventions designed to target and reinvigorate exhausted CD8+ T cells may be beneficial for patients with adenomyosis.

Treatment of heterotopic cervical pregnancy by ultrasound-guided hysteroscopy: A case report and literature review.

BACKGROUND: Heterotopic cervical pregnancy is a rare event of ectopic pregnancy with an incidence rate of < 1%. Herein, we report a rare case of successful treatment of heterotopic pregnancy following an in vitro fertilization-embryo transfer using ultrasound-guided hysteroscopy. In order to choose the best treatment option, we reviewed the clinical treatments and discussion of heterotopic cervical pregnancy over the last 15 years. METHODS: The heterotopic pregnancy was terminated using ultrasound-guided hysteroscopy; however, the intrauterine pregnancy was maintained. We searched for the keywords "cervical pregnancy combined with intrauterine pregnancy," "compound pregnancy," "assisted reproductive technology," "cervical pregnancy," and "ectopic pregnancy" on PubMed to include articles published in the last 15 years. RESULTS: The patient underwent an emergency cervical cerclage at 22 weeks' gestation for cervical insufficiency and delivered a healthy newborn at 38 weeks' gestation by transvaginal compliance. Twenty-one relevant case reports were selected. After analysis and discussion, we found that assisted reproductive technology is more likely to lead to heterotopic pregnancy than unassisted reproduction. Most women requesting the preservation of intrauterine embryos opted for surgical termination of cervical pregnancy and achieved the ideal outcomes. CONCLUSION: More attention should be paid to the diagnosis and treatment of heterotopic pregnancies to obtain the most optimal pregnancy outcome and long-term prognosis. Hysteroscopic surgery is a completely feasible cervical pregnancy treatment option with less postoperative impact on the mother and the intrauterine fetus.

Follicle-Stimulating Hormone Promotes the Development of Endometrial Cancer In Vitro and In Vivo.

Endocrine disruptors as risk factors for endometrial cancer (EC) are positively correlated with serum follicle-stimulating hormone (FSH) levels. Additionally, increased FSH is associated with EC. However, its exact mechanism is not yet clear. Therefore, this study investigated how FSH affects the occurrence of EC. Using immunohistochemistry (IHC), immunofluorescence (IF), and Western blot (WB), we found that FSH receptor (FSHR) was expressed in both EC tissues and cell lines. To explore the effect of FSH on EC in vitro, Ishikawa (ISK) cells were cultured in different doses of FSH, and it was found that FSH could promote the proliferation and migration of ISK cells. Furthermore, the detection of key molecules of migration and apoptosis by WB showed that FSH promoted cell migration and inhibited apoptosis. Additionally, FSH decreased AMPK activation. To clarify the effect of FSH on EC in vivo, we subcutaneously planted ISK cells into ovariectomized mice and then gave two of the groups oestradiol (E2). In comparison with the OE (ovariectomy plus E2) and sham groups, the growth rates and weights of the tumors in the OE plus FSH group were significantly higher. The findings above suggest that FSH promotes the proliferation and metastasis of EC, providing a new strategy for the treatment of EC.