Department Development and Regeneration, Cluster Urogenital Surgery, Biomedical Sciences, and Clinical Department Obstetrics and Gynaecology, University Hospitals Leuven, KU Leuven, Herestraat 49, B-3000, Leuven, Belgium.
Department of Epidemiology & Biostatistics, Imperial College London, Norfolk Place, London and Department of Urogynaecology, LNWH NHS Trust, London, UK.
Int Urogynecol J. 2022 Jul;33(7):1699-1710. doi: 10.1007/s00192-022-05081-0. Epub 2022 Mar 10.
This manuscript is the International Urogynecology Consultation (IUC) on pelvic organ prolapse (POP) chapter one, committee three, on the Pathophysiology of Pelvic Organ Prolapse assessing genetics, pregnancy, labor and delivery, age and menopause and animal models.
An international group of urogynecologists and basic scientists performed comprehensive literature searches using pre-specified terms in selected biomedical databases to summarize the current knowledge on the pathophysiology of the development of POP, exploring specifically factors including (1) genetics, (2) pregnancy, labor and delivery, (3) age and menopause and (4) non-genetic animal models. This manuscript represents the summary of three systematic reviews with meta-analyses and one narrative review, to which a basic scientific comment on the current understanding of pathophysiologic mechanisms was added.
The original searches revealed over 15,000 manuscripts and abstracts which were screened, resulting in 202 manuscripts that were ultimately used. In the area of genetics the DNA polymorphisms rs2228480 at the ESR1 gene, rs12589592 at the FBLN5 gene, rs1036819 at the PGR gene and rs1800215 at the COL1A1 gene are significantly associated to POP. In the area of pregnancy, labor and delivery, the analysis confirmed a strong etiologic link between vaginal birth and symptoms of POP, with the first vaginal delivery (OR: 2.65; 95% CI: 1.81-3.88) and forceps delivery (OR: 2.51; 95% CI: 1.24-3.83) being the main determinants. Regarding age and menopause, only age was identified as a risk factor (OR : 1.102; 95% CI: 1.02-1.19) but current data do not identify postmenopausal status as being statistically associated with POP. In several animal models, there are measurable effects of pregnancy, delivery and iatrogenic menopause on the structure/function of vaginal support components, though not on the development of POP.
Genetics, vaginal birth and age all have a strong etiologic link to the development of POP, to which other factors may add or protect against the risk.
本文是国际尿妇科咨询（IUC）关于盆腔器官脱垂（POP）一章的第三节，主要探讨 POP 的发病机制，包括遗传学、妊娠、分娩、年龄和绝经以及动物模型。
一组国际泌尿妇科医生和基础科学家使用预先指定的术语在选定的生物医学数据库中进行了全面的文献检索，以总结 POP 发展的发病机制的现有知识，专门探讨了以下因素：（1）遗传学；（2）妊娠、分娩；（3）年龄和绝经；（4）非遗传动物模型。本文代表了三项系统评价和一项叙述性评价的总结，其中增加了对当前发病生理机制理解的基础科学评论。
原始搜索显示，最初搜索显示有超过 15000 篇手稿和摘要被筛选，最终使用了 202 篇手稿。在遗传学领域，ESR1 基因的 rs2228480、FBLN5 基因的 rs12589592、PGR 基因的 rs1036819 和 COL1A1 基因的 rs1800215 的 DNA 多态性与 POP 显著相关。在妊娠、分娩和分娩领域，分析证实阴道分娩与 POP 症状之间存在很强的病因联系，首次阴道分娩（OR：2.65；95%CI：1.81-3.88）和产钳分娩（OR：2.51；95%CI：1.24-3.83）是主要决定因素。关于年龄和绝经，只有年龄被确定为危险因素（OR：1.102；95%CI：1.02-1.19），但目前的数据并未表明绝经后状态与 POP 有统计学关联。在几种动物模型中，妊娠、分娩和医源性绝经对阴道支持结构的功能有可测量的影响，但对 POP 的发展没有影响。
遗传学、阴道分娩和年龄与 POP 的发展都有很强的病因联系，其他因素可能会增加或降低风险。
