Section of Molecular Pathology and Human Genetics, Department of Internal Medicine, School of Medicine, University of Crete, 71403 Heraklion, Greece.
First Department of Obstetrics and Gynecology, School of Medicine, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.
Int J Mol Med. 2024 Feb;53(2). doi: 10.3892/ijmm.2024.5344. Epub 2024 Jan 8.
Patients with a history of endometriosis have an increased risk of developing various autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, multiple sclerosis and celiac disease. There is a potential association between endometriosis and an increased susceptibility for Sjögren's syndrome (SS). SS is a common chronic, inflammatory, systemic, autoimmune, multifactorial disease of complex pathology, with genetic, epigenetic and environmental factors contributing to the development of this condition. It occurs in 0.5‑1% of the population, is characterized by the presence of ocular dryness, lymphocytic infiltrations and contributes to neurological, gastrointestinal, vascular and dermatological manifestations. Endometriosis is an inflammatory, estrogen‑dependent, multifactorial, heterogeneous gynecological disease, affecting ≤10% of reproductive‑age women. It is characterized by the occurrence of endometrial tissue outside the uterine cavity, mainly in the pelvic cavity, and is associated with pelvic pain, dysmenorrhea, deep dyspareunia and either subfertility or infertility. It is still unclear whether SS appears as a secondary response to endometriosis, or it is developed due to any potential shared mechanisms of these conditions. The aim of the present review was to explore further the biological basis only of the co‑occurrence of these disorders but not their association at clinical basis, focusing on the analysis of the partially shared genetic background between endometriosis and SS, and the clarification of the possible similarities in the underlying pathogenetic mechanisms and the relevant molecular pathways.
患有子宫内膜异位症病史的患者发生各种自身免疫性疾病的风险增加，如类风湿关节炎、强直性脊柱炎、系统性红斑狼疮、多发性硬化症和乳糜泻。子宫内膜异位症与干燥综合征（SS）易感性增加之间存在潜在关联。SS 是一种常见的慢性、炎症性、系统性、自身免疫性、多因素疾病，具有复杂的病理生理学，遗传、表观遗传和环境因素共同促成了这种疾病的发生。它发生在 0.5-1%的人群中，其特征为眼睛干燥、淋巴细胞浸润，并导致神经、胃肠道、血管和皮肤表现。子宫内膜异位症是一种炎症性、雌激素依赖性、多因素、异质性妇科疾病，影响≤10%的育龄妇女。其特征是子宫内膜组织出现在子宫腔外，主要在盆腔内，并伴有盆腔疼痛、痛经、深部性交痛以及生育力降低或不孕。目前尚不清楚 SS 是作为子宫内膜异位症的继发反应出现，还是由于这些疾病的任何潜在共同机制而发展。本综述的目的是进一步探讨这些疾病同时发生的生物学基础，但不探讨其临床相关性，重点分析子宫内膜异位症和 SS 之间部分共享的遗传背景，并阐明潜在发病机制和相关分子途径中的可能相似性。
