ABSTRACT
Endometriosis is a common condition among women and can cause complications such as abdominal pain, dysmenorrhea, and infertility. One of the potential causes of this disease is autoimmunity. However, evidence regarding the role of autoimmunity is conflicting and inconclusive. The aim of this study was to investigate whether autoantibodies, a sign of autoimmunity, are present in people suffering from endometriosis. Relevant studies up to April 14, 2023 were identified by systematically searching Scopus, PubMed, Web of Science, Embase, and Google Scholar. This meta-analysis includes all qualified case-control studies of human populations that analyzed the association between serum autoantibodies and endometriosis. The odd ratios and 95% confidence intervals were calculated. In addition, heterogeneity and publication bias were examined, and subgroup analyses were performed based on region and target antigens. Forty-one studies were included, comparing 2,825 endometriosis patients with 4,158 healthy controls. The meta-analysis findings indicated a significant association between the presence of autoantibodies in the serum and an increased susceptibility to endometriosis (odds ratio: 4.242, confidence interval 95%: 3.824-4.706, p<0.001). In addition, there was a significant correlation between the presence of endometriosis and serum levels of anti-nuclear antibodies, B2 glycoprotein 1, CA125, carbonic anhydrase 1, cardiolipin, endometrial, laminin-1, smooth muscle, and syntaxin autoantibodies. Upon further analysis, it was found that the serum levels of these autoantibodies were higher in patients with endometriosis from North America than in those from other regions (p=0.001). The study revealed a significant correlation between serum autoantibodies and susceptibility to endometriosis, highlighting autoimmunity as a potential cause.
ABSTRACT
Endometriosis is a prevalent condition in women that causes pelvic pain and fertility issues due to the growth of endometrial tissue outside the uterus during menstrual cycles. Steroid hormones play a crucial role in the development and growth of endometriosis lesions; therefore, researchers have investigated several effective drugs that target hormones for treating this disease. One such drug is bazedoxifene, but despite several animal studies, there has yet to be a comprehensive evaluation of their combined results. A systematic search was conducted across several databases (Embase, PubMed, Scopus, and Web of Sciences) to identify studies investigating the effectiveness of bazedoxifene in animal models of endometriosis. Meta-analysis was performed using the size of endometriosis implants before and after drug administration in the case and control groups, along with the p-value of the associations. Begg's and Egger's tests were used to assess publication bias. This study included four eligible studies consisting of 45 endometrial animal models and 35 control subjects. The meta-analysis showed that bazedoxifene significantly reduced the size of endometriosis implants in animal models compared with the control group (odds ratio: 0.122, 95% confidence interval: 0.050-0.298, p<0.001). Detailed investigation determined that there was no significant heterogeneity between the studies (I2=38.81, and p-value of the Q test=0.179). However, according to Egger's test, the study showed publication bias (p=0.035). This study found that bazedoxifene is a promising treatment option for endometriosis in animal models. However, more research on animals and humans is required to confirm these results.
ABSTRACT
This study aimed to understand the relationship between two specific genetic variations (GSTT1 and GSTM1 polymorphisms) and the risk of developing polycystic ovarian syndrome (PCOS). PCOS is a common endocrinologic disorder that affects women. Oxidative stress may play a significant role in the development of PCOS. Certain enzymes, such as glutathione S-transferases, help protect cells against oxidative stress. However, previous research on the correlation between these specific genetic variations and PCOS risk has produced inconsistent findings. To address this, a meta-analysis was conducted to examine the potential impact of these genetic variations on PCOS. We conducted a thorough search of the Embase, PubMed, Scopus, Web of Science, and Google Scholar databases to find studies that met our criteria. We used fixed-effects or random-effects models to determine the pooled odds ratios (ORs) and 95% confidence intervals (CIs) of the GSTT1 and GSTM1 polymorphisms related to PCOS. We also performed subgroup analyses based on ethnicity, mean age of participants, and PCOS diagnostic protocols. After screening, we found five studies with 1.607 participants (872 in the PCOS group and 735 in the control group) to be suitable for our meta-analysis. Our analysis showed that GSTM1 and GSTT1 null genotypes were not linked to an increased risk of PCOS (OR: 0.925, 95% CI: 0.755-1.134; OR: 1.175, 95% CI: 0.614-2.247 respectively). Additionally, both Begg's and Egger's tests revealed no publishing bias. This meta-analysis confirmed that there is no association between GSTM1 and GSTT1 polymorphisms and an increased risk of PCOS. However, further studies are required to validate this conclusion.
