Uterine leiomyomas are one of the most common and yet understudied diseases in women. These tumors, commonly known as fibroids, affect women mainly during their reproductive years and are diagnosed in up to 70% of white women and more than 80% of women of African ancestry during their lifetime. This disease has a profound impact on health care delivery and costs worldwide. Though most women with fibroids are asymptomatic, approximately 30% of them will present with severe symptoms which can include abnormal uterine bleeding, anemia, pelvic pain and pressure, back pain, urinary frequency, constipation, or infertility, and will require intervention. Furthermore, fibroids have been associated with poor obstetrical outcomes. The current options for symptomatic fibroid treatment include expectant, medical, and surgical management, and interventional radiology procedures. This article reviews the recent progress and available management strategies for uterine fibroids and highlights areas where further research is needed to find new therapeutic targets and better personalize treatments.

Problem Uterine natural killer cells (uNK) have been thought to play a key role in endometriosis and infertility. We investigated the expression of CD56, CD16 and NKp46 in endometrial tissues from 61 women with unexplained recurrent pregnancy loss (uRPL) or infertility (UI), and correlated this with the presence or absence of endometriosis. The results from the patients with sub-fertility were compared to those from 10 fertile patients. Method of study Mid-secretory phase endometrial biopsies were obtained and the endometrial expression of CD56, CD16 or NKp46 was identified by immunohistochemistry and quantified (ImageJ Software). Results The percentage of CD16+ cells was higher in women with uRPL (7.9±3.2) and UI (9.0±5.5), even when these conditions were associated with endometriosis (8.9±5.3), compared to fertile patients (5.6±2.4, p<0.05). Likewise, the ratio of NKp46+:CD56+ cells was higher in women with uRPL (0.28±0.25) and UI (0.21±0.2), even when these conditions were associated with endometriosis (0.19±0.14), compared to fertile patients (0.1±0.1, p<0.05). No differences were observed when comparing CD56. Conclusions Women, with or without endometriosis, who have larger populations of cytotoxic CD16+ uNK cells and/or higher populations of NKp46+CD56+ cells may be at greater risk for infertility disorders resulting from an inflammtory environment occuring during implantation or later during decidualization.

Antithyroid autoantibodies, particularly TG-Ab, are associated with RM and could be an expression of a more general maternal immune system abnormality leading to RM. ATA could have a role in RM irrespective of thyroid hormone status.

BackgroundEndometriosis is a common condition associated with growth of endometrial-like tissue beyond the uterine cavity. Previous reports have suggested a role for uNK cells in the pathogenesis of endometriosis postulating that survival and accumulation of menstrual endometrial tissue in the peritoneal cavity may relate to a reduction in the cytotoxic activity of peripheral blood NK cells. We aimed to assess the differences in percentage of uNK cells and their phenotypical characterization in eutopic and ectopic endometrial samples from women with and without endometriosis and baboons with induced endometriosis.MethodsEutopic and ectopic endometrial samples from 82 women across the menstrual cycle with/without endometriosis and from 8 baboons before and after induction of endometriosis were examined for CD56 and NKp30 expression with immunohistochemistry, quantified using computer assisted image analysis. Curated secretory phase endometrial microarray datasets were interrogated for NK cell receptors and their ligands. In silico data was validated by examining the secretory phase eutopic endometrium of women with and without endometriosis (n = 8/group) for the immuno-expression of BAG6 protein.ResultsThe percentage of uNK cells increased progressively from the proliferative phase with the highest levels in the late secretory phase in the eutopic endometrium of women with and without endometriosis. The percentage of uNK cells in ectopic lesions remained significantly low throughout the cycle. In baboons, induction of endometriosis increased the percentage of uNK in the ectopic lesions but not NKp30. Published eutopic endometrial microarray datasets demonstrated significant upregulation of NKp30 and its ligand BAG6 in women with endometriosis compared with controls. Immunohistochemical staining scores for BAG6 was also significantly higher in secretory phase eutopic endometrium from women with endometriosis compared with the endometrium of healthy women (n = 8/group).ConclusionsThe dynamic increase in the percentage of uNK cells in the secretory phase is preserved in the endometrium of women with endometriosis. The low number of uNK cells in human and baboon ectopic lesions may be due to their exaggerated reduction in hormonal responsiveness (progesterone resistance).Electronic supplementary materialThe online version of this article (10.1186/s12958-018-0385-3) contains supplementary material, which is available to authorized users.