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Review| Volume 141, ISSUE 1, P3-9, November 2008

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Preterm birth and inflammation—The role of genetic polymorphisms

  • Daniela Holst
    Affiliations
    Department of Obstetrics and Gynaecology, University Hospital of Cologne, Kerpener Strasse 34, 50924 Köln, Germany
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  • Yves Garnier
    Correspondence
    Corresponding author at: Klinik für Frauenheilkunde und Geburtshilfe, Klinikum Osnabrück GmbH, Am Finkenhügel 1, 49076 Osnabrück, Germany. Tel.: +49 541 405 6801/221 478 4910; fax: +49 541 405 6899/221 478 4929.
    Affiliations
    Department of Obstetrics and Gynaecology, University Hospital of Cologne, Kerpener Strasse 34, 50924 Köln, Germany
    Search for articles by this author

      Abstract

      Spontaneous preterm labour and preterm births are still the leading cause of perinatal morbidity and mortality in the developed world. Previous efforts to prevent preterm birth have been hampered by a poor understanding of the underlying pathophysiology, inadequate diagnostic tools and generally ineffective therapies.
      Clinical, epidemiological and experimental studies indicate that genito-urinary tract infections play a critical role in the pathogenesis of preterm birth. Moreover, intrauterine infection increases perinatal mortality and morbidity, such as cerebral palsy and chronic lung disease, significantly.
      It has recently been suggested that gene–environment interactions play a significant role in determining the risk of preterm birth. Polymorphisms of certain critical genes may be responsible for a harmful inflammatory response in those who possess them. Accordingly, polymorphisms that increase the magnitude or the duration of the inflammatory response were associated with an increased risk of preterm birth. In contrast polymorphisms that decrease the inflammatory response were associated with a lower risk of preterm birth. This article will review the current understanding of pathogenetic pathways in the aetiology of preterm birth.

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