Pathogenesis and Prediction of Preterm Delivery

蜕膜 肌层 蜕膜细胞 受体 促肾上腺皮质激素释放激素 促炎细胞因子 炎症 下调和上调 蛋白酵素 内分泌学 内科学 发病机制 趋化因子 生物 医学 胎盘 胎儿 怀孕 子宫 生物化学 遗传学 基因
作者
Anthony Kendle,Catalin S. Buhimschi,Charles J. Lockwood
标识
DOI:10.1002/9781119636540.ch40
摘要

Chapter 40 Pathogenesis and Prediction of Preterm Delivery Anthony M. Kendle, Anthony M. Kendle Department of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, FL, USASearch for more papers by this authorCatalin S. Buhimschi, Catalin S. Buhimschi Department of Obstetrics and Gynecology, University of Illinois College of Medicine, Chicago, IL, USASearch for more papers by this authorCharles J. Lockwood, Charles J. Lockwood Department of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, FL, USASearch for more papers by this author Anthony M. Kendle, Anthony M. Kendle Department of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, FL, USASearch for more papers by this authorCatalin S. Buhimschi, Catalin S. Buhimschi Department of Obstetrics and Gynecology, University of Illinois College of Medicine, Chicago, IL, USASearch for more papers by this authorCharles J. Lockwood, Charles J. Lockwood Department of Obstetrics and Gynecology, Morsani College of Medicine, University of South Florida, Tampa, FL, USASearch for more papers by this author Book Editor(s):Catherine Y. Spong, Catherine Y. Spong Professor and Chair Editor-in-Chief Contemporary OB/GYN Department of Obstetrics and Gynecology, Paul C. MacDonald Distinguished Chair in Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX, USASearch for more papers by this authorCharles J. Lockwood, Charles J. Lockwood Dean Executive Vice President Executive Vice President Professor of Obstetrics Morsani College of Medicine USF Health Tampa General Hospital Gynecology and Public Health, University of South Florida, Tampa, FL, USASearch for more papers by this author First published: 01 December 2023 https://doi.org/10.1002/9781119636540.ch40 AboutPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShareShare a linkShare onEmailFacebookTwitterLinkedInRedditWechat Summary Preterm birth (PTB) affects approximately 10% of all births in the United States. Four distinct pathways have been identified in its pathophysiology. In the idiopathic or stress-associated PTB, with premature activation of the hypothalamic-pituitary-adrenal axis pathway, fetal or maternal stress upregulate placental corticotropin-releasing hormone to accelerate cortisol release and promote expression of the progesterone receptor (PR) inhibitor, FKBP51 in the decidua. In the decidual-amnion-chorion inflammation pathway, bacteria induce an inflammatory cascade by binding to toll-like receptors. This cascade is initiated by increased levels of interleukin 1β, which enhances expression of other inflammatory chemokines, and matrix metalloproteinases while downregulating decidual PR expression. In the abruption-associated PTB pathway, decidual hemorrhage generates thrombin, which binds to protease-activated receptors to create a procontractile environment and downregulate decidual PR expression. Lastly, in the pathologic myometrial stretch pathway, uterine overdistension induces biochemical remodeling of the myometrium to activate contractions. All pathways lead to a final common PTB pathway characterized by increased levels of reproductive track prostaglandins, proteases, and proinflammatory cytokines as well as progressive withdrawal of progesterone activity. Biochemical and sonographic markers are employed for the prediction of PTB. 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