The preterm parturition syndrome

Abstract

The implicit paradigm that has governed the study and clinical management of preterm labor 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 labor results from physiological activation of the components of the common pathway, preterm labor arises from pathological signaling 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 characterized by: (1) multiple etiology; (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 ischemia; (3) uterine over-distension; (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 labor are discussed.