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Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection
Prevention of preterm birth and subsequent newborn immaturity is a primary goal of obstetrical care worldwide. Accumulated evidence shows that 1) as many as 25–50% of preterm births are caused by common genital tract infections and subsequent maternal/fetal inflammatory responses; 2) microbial and m...
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
1997
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364559/ https://www.ncbi.nlm.nih.gov/pubmed/18476162 http://dx.doi.org/10.1155/S1064744997000173 |
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author | McGregor, James A. French, Janice I. |
author_facet | McGregor, James A. French, Janice I. |
author_sort | McGregor, James A. |
collection | PubMed |
description | Prevention of preterm birth and subsequent newborn immaturity is a primary goal of obstetrical care worldwide. Accumulated evidence shows that 1) as many as 25–50% of preterm births are caused by common genital tract infections and subsequent maternal/fetal inflammatory responses; 2) microbial and maternal host factors (phospholipases, proteases, etc.) play roles in preterm labor and preterm premature rupture of membranes (pPROM); 3) integrated aspects of maternal and fetal host responses (inflammation, altered immune adaptations, endocrine and paracrine mechanisms) play increasingly understood roles in premature activation of parturition; and 4) identification and systemic treatment of common genitourinary infections, most importantly bacterial vaginosis (BV), reduce the risks of preterm delivery and PROM. |
format | Text |
id | pubmed-2364559 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1997 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-23645592008-05-12 Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection McGregor, James A. French, Janice I. Infect Dis Obstet Gynecol Research Article Prevention of preterm birth and subsequent newborn immaturity is a primary goal of obstetrical care worldwide. Accumulated evidence shows that 1) as many as 25–50% of preterm births are caused by common genital tract infections and subsequent maternal/fetal inflammatory responses; 2) microbial and maternal host factors (phospholipases, proteases, etc.) play roles in preterm labor and preterm premature rupture of membranes (pPROM); 3) integrated aspects of maternal and fetal host responses (inflammation, altered immune adaptations, endocrine and paracrine mechanisms) play increasingly understood roles in premature activation of parturition; and 4) identification and systemic treatment of common genitourinary infections, most importantly bacterial vaginosis (BV), reduce the risks of preterm delivery and PROM. Hindawi Publishing Corporation 1997 /pmc/articles/PMC2364559/ /pubmed/18476162 http://dx.doi.org/10.1155/S1064744997000173 Text en Copyright © 1997 Hindawi Publishing Corporation. http://creativecommons.org/licenses/by/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article McGregor, James A. French, Janice I. Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection |
title | Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection |
title_full | Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection |
title_fullStr | Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection |
title_full_unstemmed | Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection |
title_short | Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection |
title_sort | pathogenesis to treatment: preventing preterm birth mediated by infection |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364559/ https://www.ncbi.nlm.nih.gov/pubmed/18476162 http://dx.doi.org/10.1155/S1064744997000173 |
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