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Review
. 2006 Dec;113 Suppl 3(Suppl 3):17-42.
doi: 10.1111/j.1471-0528.2006.01120.x.

The preterm parturition syndrome

R Romero  1 , J Espinoza, J P Kusanovic, F Gotsch, S Hassan, O Erez, T Chaiworapongsa, M Mazor
Affiliations
Review

The preterm parturition syndrome

R Romero et al. BJOG. 2006 Dec.

Erratum in

  • BJOG. 2008 Apr;115(5):674-5

Abstract

The implicit paradigm that has governed the study and clinical management of preterm labour is that term and preterm parturition are the same processes, except for the gestational age at which they occur. Indeed, both share a common pathway composed of uterine contractility, cervical dilatation and activation of the membranes/decidua. This review explores the concept that while term labour results from physiological activation of the components of the common pathway, preterm labour arises from pathological signalling and activation of one or more components of the common pathway of parturition. The term "great obstetrical syndromes" has been coined to reframe the concept of obstetrical disease. Such syndromes are characterised by: (1) multiple aetiology; (2) long preclinical stage; (3) frequent fetal involvement; (4) clinical manifestations that are often adaptive in nature; and (5) gene-environment interactions that may predispose to the syndromes. This article reviews the evidence indicating that the pathological processes implicated in the preterm parturition syndrome include: (1) intrauterine infection/inflammation; (2) 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). The implications of this conceptual framework for the prevention, diagnosis, and treatment of preterm labour are discussed.

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Figures

Figure 1.
Figure 1.
Pathological processes implicated in the preterm parturition syndrome. (Reproduced with permission from reference 5.)
Figure 2.
Figure 2.
The most common pathway of intrauterine infection is the ascending route. (Reproduced with permission from reference 1.)
Figure 3.
Figure 3.
Concentrations of bacterial endotoxins are significantly higher in women with PPROM in labor than in those with PPROM not in labor. (Reproduced with permission from reference 129.)
Figure 4.
Figure 4.
Classification and procedure-to-delivery interval of women according to AF and fetal plasma (FP) IL-6 concentrations. Analysis restricted to 30 women with available AF. White in the fetal or AF compartment represents a low FP or AF IL-6 concentration, respectively. Black in the fetal or AF compartment denotes elevated fetal plasma or AF IL-6 concentration, respectively. (Reproduced with permission from reference 39).
See this image and copyright information in PMC

References

    1. Romero R, Mazor M. Infection and preterm labor. Clin Obstet Gynecol 1988;31:553–84. - PubMed
    1. Romero R, Gomez R, Mazor M, Ghezzi F, Yoon BH. The preterm labor syndrome In: Elder MG, Romero R, Lamont RF, editors. Preterm labor. New York, NY: Churchill Livingstone; 1997. p. 29–49.
    1. Romero R, Mazor M, Munoz H, Gomez R, Galasso M, Sherer DM. The preterm labor syndrome. Ann N Y Acad Sci 1994;734:414–29. - PubMed
    1. Romero R, Avila C, Brekus CA, Mazor M. The role of systemic and intrauterine infection in preterm parturition In: Garfield RE, editor. Uterine contractility. Norwell, MA: Serono Symposia, USA; 1990. p. 319–53.
    1. Romero R, Espinoza J, Mazor M, Chaiworapongsa T. The preterm parturition syndrome In: Critchely H, Bennett P, Thornton S, editors. Preterm Birth. London: RCOG Press; 2004. p. 28–60.

MeSH terms