SummaryPreterm birth is currently the most important problem in maternal-child health in the United States. Epidemiological studies have suggested that two factors, maternal stress and maternal urogenital tract infection, are significantly and independently associated with an increased risk of spontaneous preterm birth. These factors are also more prevalent in the population of sociodemographically disadvantaged women who are at increased risk for preterm birth. Studies of the physiology of parturition suggest that neuroendocrine and immune processes play important roles in the physiology and pathophysiology of normal and preterm parturition. However, not all women with high levels of stress and/or infection deliver preterm, and little is understood about factors that modulate susceptibility to pathophysiological events of the endocrine and immune systems in pregnancy. We present here a comprehensive, biobehavioural model of maternal stress and spontaneous preterm delivery. According to this model, chronic maternal stress is a significant and independent risk factor for preterm birth. The effects of maternal stress on preterm birth may be mediated through biological and/or behavioural mechanisms. We propose that maternal stress may act via one or both of two physiological pathways: (a) a neuroendocrine pathway, wherein maternal stress may ultimately result in premature and/or greater degree of activation of the maternal-placental-fetal endocrine systems that promote parturition; and (b) an immune/ inflammatory pathway, wherein maternal stress may modulate characteristics of systemic and local (placental-decidual) immunity to increase susceptibility to intrauterine and fetal infectious-inflammatory processes and thereby promote parturition through proinflammatory mechanisms. We suggest that placental corticotropin-releasing hormone may play a key role in orchestrating the effects of endocrine and inflammatory/immune processes on preterm birth. Moreover, because neuroendocrine and immune processes extensively cross-regulate one another, we further posit that exposure to both high levels of chronic stress and infectious pathogens in pregnancy may produce an interaction and multiplicative effect in terms of their combined risk for preterm birth. Finally, we hypothesise that the effects of maternal stress are modulated by the nature, duration and timing of occurrence of stress during gestation. A discussion of the components of this model, including a theoretical rationale and review of the available empirical evidence, is presented. A major strength of this biobehavioural perspective is the ability to explore new questions and to do so in a manner that is more comprehensive than has been previously attempted. We expect findings from this line of proposed research to improve our present state of knowledge about obstetric risk assessment for preterm birth by determining the characteristics of pregnant women who are especially susceptible to stress and/or infection, and to broaden our understanding of biological (endoc...

Residential redlining as a form institutional racism and neighborhood characteristic may be important for understanding racial/ethnic disparities in pregnancy and preterm birth.

No abstract

Accumulating evidence has associated bacterial vaginosis (BV) with serious medical complications such as premature delivery. The present article synthesizes available data on the treatment of nonpregnant and pregnant women with BV to prevent preterm delivery. A literature search identified articles published since 1976 that evaluated treatment of BV. An intention-to-treat sensitivity analysis was performed, to better compare studies. Studies that evaluated therapy efficacy varied with regard to diagnostic criteria, patient characteristics, clinicians, and laboratories. Therapies varied in efficacy for cure 4 or more weeks after therapy, from 48% to 85%. Intervention studies to reduce BV-related adverse outcomes of pregnancy differed in populations studied, medication used, type of therapy (oral or intravaginal), and timing of treatment. The benefit of treating women at high risk with oral metronidazole has been shown in several studies; however, the effect of treating women without a history of premature delivery is unclear. The use of intravaginal clindamycin therapy, especially during the latter half of the second trimester and thereafter, appears to increase infections during the neonatal period.