Journal ArticleDOI
The fetal inflammatory response syndrome.
TLDR
The fetal systemic inflammatory response as a mechanism of disease is reviewed and potential interventions to control an exaggerated inflammatory response in utero are also described.About:
This article is published in American Journal of Obstetrics and Gynecology.The article was published on 1998-07-01. It has received 1019 citations till now. The article focuses on the topics: Premature rupture of membranes & Neonatal sepsis.read more
Citations
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Journal ArticleDOI
Epidemiology and causes of preterm birth
TL;DR: A short cervical length and a raised cervical-vaginal fetal fibronectin concentration are the strongest predictors of spontaneous preterm birth.
Journal ArticleDOI
Preterm labor: One syndrome, many causes
TL;DR: The current understanding of the mechanisms of disease implicated in preterm labor are summarized and advances relevant to intra-amniotic infection, decidual senescence, and breakdown of maternal-fetal tolerance are reviewed.
Journal ArticleDOI
The preterm parturition syndrome
Roberto Romero,Jimmy Espinoza,Juan Pedro Kusanovic,Francesca Gotsch,Sonia S. Hassan,Offer Erez,Tinnakorn Chaiworapongsa,Moshe Mazor +7 more
TL;DR: The evidence indicating that the pathological processes implicated in the preterm parturition syndrome include: intrauterine infection/inflammation; uterine ischaemia; (3) uterine overdistension; (4) abnormal allograft reaction; (5) allergy; (6) cervical insufficiency; and (7) hormonal disorders (progesterone related and corticotrophin‐releasing factor related).
Journal ArticleDOI
Diagnosis and Management of Clinical Chorioamnionitis
TL;DR: Clinical research into better methods for diagnosing, treating, and preventing chorioamnionitis is likely to have a substantial impact on short and long-term outcomes in the neonate.
References
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Journal ArticleDOI
The Natural History of the Systemic Inflammatory Response Syndrome (SIRS): A Prospective Study
TL;DR: This prospective epidemiologic study of SIRS and related conditions provides the first evidence of a clinical progression from SirS to sepsis to severe sepsi and septic shock, and stepwise increases in mortality rates in the hierarchy.
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Infection and labor V. Prevalence, microbiology, and clinical significance of intraamniotic infection in women with preterm labor and intact membranes
Roberto Romero,Marina Sirtori,E. Oyarzun,Cecilia Avila,Moshe Mazor,Robert Callahan,Virginia Sabo,Apostolos P. Athanassiadis,John C. Hobbins +8 more
TL;DR: Amniotic fluid retrieved by amniocentesis from 264 patients with preterm labor and intact membranes admitted to Yale-New Haven Hospital from Jan. 1, 1985, to July 31, 1988 had a higher incidence of respiratory distress syndrome and infectious complications than preterm neonates born after negative amniotics fluid cultures.
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Infection and labor. III. Interleukin-1: a signal for the onset of parturition.
Roberto Romero,Dan T. Brody,E. Oyarzun,Moshe Mazor,Ying King Wu,John C. Hobbins,Scott K. Durum +6 more
TL;DR: The hypothesis that interleukin-1 may play a role in the initiation of preterm labor associated with intraamniotic infection is supported.
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Interleukin-6 concentrations in umbilical cord plasma are elevated in neonates with white matter lesions associated with periventricular leukomalacia
Bo Hyun Yoon,Roberto Romero,Soon Ha Yang,Jong Kwan Jun,In-One Kim,Jung Hwan Choi,Hee Chul Syn +6 more
TL;DR: In this article, the authors examined the relationship between umbilical cord plasma levels of tumor necrosis factor-α, interleukin-1β, intra-cellular leukomalacia-associated lesion and the occurrence of periventricular leucomalacia in preterm neonates.
Journal ArticleDOI
A fetal systemic inflammatory response is followed by the spontaneous onset of preterm parturition
Roberto Romero,Ricardo Gomez,Fabio Ghezzi,Bo Hyun Yoon,Moshe Mazor,Samuel S. Edwin,Stanley M. Berry +6 more
TL;DR: In this article, the authors proposed that preterm labor in the setting of infection results from the actions of proinflammatory cytokines secreted as part of the fetal and/or maternal host response to microbial invasion.