{"paper_id":"bdf937b5-bfb1-44ba-ab1e-c265dbee7935","body_text":"Dear Editor,\nWe read with great interest by Aldardier et al.[1] The research content of this article is novel. The surveyed population is rather special and is likely to arouse readers’ interest. The credibility of the research results is relatively high, and the conclusion can provide guidance and assistance for clinical diagnosis and treatment practice. Meanwhile, we would like to focus on the following issues:\nFirstly, as mentioned by the author, this is a single-center study conducted only at King Abdulaziz University Hospital, without using a sample size calculation formula to determine the sample size, and the sample size is relatively small. This may result in insufficient statistical efficiency, large errors, limited generalizability, and inability to conduct complex multi-factor analysis. In the future, multi-center and large-sample studies that include people from different regions and ethnic groups can be adopted to enhance the universality of the results. In the future, multi-center, large-sample, regional, and ethnic group studies can be adopted to enhance the universality of the research results.\nSecondly, this study is a cross-sectional study with a sample of patients diagnosed with endometriosis. It can only reveal the correlation between endometriosis and irritable bowel syndrome (IBS), but it cannot determine the causal relationship. In order to prospectively analyze the causal relationship between the two diseases, longitudinal cohort studies can be attempted in the future.\nFinally, although the study suggests that IBS is a comorbidity of endometriosis, there has been no in-depth analysis of the possible shared pathogenesis between the two diseases. According to current theories, the common pathogenesis of endometriosis and IBS may be explored from the following aspects: On the one hand, based on the bidirectional communication network theory of the microbiota gut brain axis (MGBA), researchers have found that the gut microbiome affects the activity of microglia and astrocytes, leading to changes in neurotransmitter levels, including an increase in glutamate and a decrease in gamma aminobutyric acid, ultimately resulting in pain hypersensitivity reactions.[2,3] Dysbiosis of gut microbiota may cause central sensitization through the MGBA, leading to inflammatory pain in endometriosis and chronic visceral pain associated with IBS.[4] On the other hand, some studies have reported that dysbiosis of the gut microbiota can increase intestinal permeability, disrupt intestinal barrier function, and induce bacterial endotoxin translocation. This process involves the secretion of pro-inflammatory cytokines, leading to immune imbalance and low-grade systemic inflammation. This inflammation contributes to the pathogenesis of the IBS and ultimately creates an immunosuppressive environment that allows endometrial cells to escape, spread, and grow outside the uterus, leading to the occurrence of endometriosis.[5]\nMGBA may play a key role in the pathogenesis of endometriosis and IBS. If the hypothesis holds true, new drugs developed targeting MGBA as the therapeutic target can not only alleviate the gastrointestinal symptoms of IBS but also solve various pains and symptoms related to endometriosis.\nList of Abbreviations\nAuthor contributions\nYY: Manuscript writing. LL: Concepts, design. XJS: Definition of intellectual content.\nFinancial support and sponsorship\nNil.\nConflicts of interest\nThere are no conflicts of interest.","source_license":"CC0","license_restricted":false}