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Pathogenesis to treatment: Preventing preterm birth mediated by infection
Author(s) -
McGregor James A.,
French Janice I.
Publication year - 1997
Publication title -
infectious diseases in obstetrics and gynecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.656
H-Index - 48
eISSN - 1098-0997
pISSN - 1064-7449
DOI - 10.1002/(sici)1098-0997(1997)5:2<106::aid-idog4>3.0.co;2-y
Subject(s) - bacterial vaginosis , medicine , pathogenesis , genitourinary system , premature rupture of membranes , immune system , endocrine system , immunology , premature birth , chorioamnionitis , inflammation , pregnancy , proteases , prom , fetus , hormone , obstetrics , biology , gestation , biochemistry , genetics , enzyme
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. Infect. Dis. Obstet. Gynecol. 5:106–114, 1997. © 1997 Wiley‐Liss, Inc.

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