Document Detail


Preterm birth and inflammation-The role of genetic polymorphisms.
MedLine Citation:
PMID:  18783866     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Daniela Holst; Yves Garnier
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Publication Detail:
Type:  Journal Article; Review     Date:  2008-09-09
Journal Detail:
Title:  European journal of obstetrics, gynecology, and reproductive biology     Volume:  141     ISSN:  0301-2115     ISO Abbreviation:  Eur. J. Obstet. Gynecol. Reprod. Biol.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-05     Completed Date:  2009-03-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375672     Medline TA:  Eur J Obstet Gynecol Reprod Biol     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  3-9     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynaecology, University Hospital of Cologne, Köln, Germany.
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MeSH Terms
Descriptor/Qualifier:
Chorioamnionitis / immunology
Cytokines / genetics
Female
Fetal Membranes, Premature Rupture / genetics*,  immunology,  microbiology
Genetic Predisposition to Disease / genetics*
Humans
Inflammation / genetics*
Matrix Metalloproteinases / genetics
Odds Ratio
Polymorphism, Single Nucleotide / genetics
Pregnancy
Premature Birth / genetics*,  immunology,  microbiology
Vaginosis, Bacterial / immunology
Chemical
Reg. No./Substance:
0/Cytokines; EC 3.4.24.-/Matrix Metalloproteinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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