Center for Global Health, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Acta Obstet Gynecol Scand. 2024 Oct;103(10):2070-2080. doi: 10.1111/aogs.14909. Epub 2024 Jul 31.
Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder affecting salivary and lacrimal glands, while endometriosis involves uterine-like tissue growth outside the uterus, causing pelvic pain and infertility. Investigating their intricate relationship using real-world data is crucial due to limited research on their connection.
This population-based cohort study included patients with endometriosis and controls without endometriosis. Propensity score matching was used to balance baseline differences in demographic and clinic characteristics between the two groups. Cox proportional hazards model were used to estimate the effect of endometriosis on the risk of new-onset pSS over time. A symmetrical cohort study, including patients with pSS and propensity score-matched controls without pSS, was conducted to investigate the effect of pSS on the risk of endometriosis over time. To elaborate on the mechanisms linking endometriosis and pSS, Ingenuity Pathway Analysis was performed to identify activated pathways in eutopic endometrium from patients with endometriosis and parotid tissues from patients with pSS.
A total of 15 947 patients with endometriosis and 15 947 propensity score-matched controls without endometriosis were included. Patients with endometriosis presented a significantly greater risk of pSS compared to non-endometriosis controls (adjusted hazard ratio, aHR = 1.57, 95% CI = 1.29-1.91, p < 0.001). In the symmetrical cohort study, which included 4906 pSS patients and 4,906 propensity score-matched controls without pSS, patients with pSS were found to be at a significantly higher risk of endometriosis compared to non-pSS controls (aHR = 1.51, 95% CI = 1.12-2.04, p = 0.012). Ingenuity Pathway Analysis showed that the underlying cellular mechanisms involved autoimmune-related pathways, including activation of dendritic cell maturation, and chronic inflammatory pathways, including the fibrosis signaling pathway.
These findings support a bidirectional association between endometriosis and pSS, which may be driven by dendritic cell maturation and fibrosis signaling pathways.
原发性干燥综合征(pSS)是一种影响唾液腺和泪腺的慢性自身免疫性疾病,而子宫内膜异位症则涉及子宫外生长的类似子宫的组织,导致盆腔疼痛和不孕。由于对它们之间联系的研究有限,使用真实世界的数据来研究它们之间的复杂关系至关重要。
这项基于人群的队列研究包括子宫内膜异位症患者和无子宫内膜异位症的对照组。使用倾向评分匹配来平衡两组患者在人口统计学和临床特征方面的基线差异。Cox 比例风险模型用于估计随着时间的推移,子宫内膜异位症对新发 pSS 风险的影响。进行了一项对称队列研究,包括 pSS 患者和无 pSS 的倾向评分匹配对照组,以研究随着时间的推移,pSS 对子宫内膜异位症风险的影响。为了详细阐述子宫内膜异位症和 pSS 之间的联系机制,对来自子宫内膜异位症患者的在位子宫内膜和 pSS 患者的腮腺组织进行了 Ingenuity 通路分析,以鉴定激活的通路。
共纳入 15947 例子宫内膜异位症患者和 15947 例无子宫内膜异位症的倾向评分匹配对照组。与非子宫内膜异位症对照组相比,子宫内膜异位症患者发生 pSS 的风险显著增加(调整后的危险比,aHR=1.57,95%可信区间=1.29-1.91,p<0.001)。在包括 4906 例 pSS 患者和 4906 例无 pSS 的倾向评分匹配对照组的对称队列研究中,与非 pSS 对照组相比,pSS 患者发生子宫内膜异位症的风险显著增加(aHR=1.51,95%可信区间=1.12-2.04,p=0.012)。Ingenuity 通路分析显示,潜在的细胞机制涉及自身免疫相关通路,包括树突状细胞成熟的激活,以及慢性炎症通路,包括纤维化信号通路。
这些发现支持子宫内膜异位症和 pSS 之间存在双向关联,这可能是由树突状细胞成熟和纤维化信号通路驱动的。