Abstract
Recent advances in the physiology of human pregnancy have implicated placental corticotropin-releasing hormone (CRH) as one of the primary endocrine mediators of parturition and possibly also of fetal development. The aim of this study was (1) to prospectively assess the relationship of maternal plasma concentrations of CRH in the early third trimester of gestation with two prematurity-related outcomes-spontaneous preterm birth (PTB), and small-for-gestational age birth (SGA), and (2) to determine whether the effects of CRH on each of these outcomes are independent from those of other established obstetric risk factors. In a sample of 232 women with a singleton, intrauterine pregnancy, maternal plasma was collected at 33 weeks' gestation and CRH concentrations were determined by radioimmunoassay. Each pregnancy was dated on the basis of last menstrual period and early ultrasonography. Parity, obstetric risk conditions for prematurity, mode of delivery, and birth outcomes were abstracted from the medical record. After adjusting for the effects of established obstetric risk factors, elevated CRH levels at 33 weeks' gestation were significantly associated with a 3.3-fold increase in the adjusted relative risk (RR) for spontaneous preterm birth and with a 3.6-fold increase in the adjusted relative risk for fetal growth restriction. Women who delivered postterm had significantly lower CRH levels in the early third trimester than those who delivered at term. When outcomes were stratified by gestational length and birth weight, the lowest CRH levels at 33 weeks' gestation were associated with the term non-SGA births, intermediate and approximately equal CRH levels were associated with the preterm non-SGA and term SGA births, and the highest CRH levels were associated with the preterm SGA births. For deliveries occurring after 33 weeks' gestation (the time of CRH sampling in this study), our findings support the notion that in humans placental CRH may play an impending, direct role in not only the physiology of parturition but also in processes related to fetal growth and maturation. Our results also support the notion that the timing of onset of parturition may be determined or influenced by events occurring earlier in gestation rather than those close to the time of actual onset of labor (ie, the notion of a "placental clock").
Highlights
Women who delivered postterm had significantly lower corticotropin-releasing hormone (CRH) levels in the early third trimester than those who delivered at term
Other studies have found that CRH levels are elevated in pregnancies complicated by high-risk conditions for preterm birth and/or fetal growth restriction.[16,17,18]. These findings suggest that CRH levels may relate to the length of gestation and fetal growth either directly by participating in physiologic processes involved in parturition and fetal maturation, or indirectly as a surrogate marker of antepartum conditions that reflect maternal or fetal risk for prematurity
The mean infant birth weight was 3384 G 34.9 g (GSEM) and ranged between 1840 and 4750 g; 13 infants (5.6%) were classified as low-birth weight (!2500 g), 20 (8.6%) and 23 infants (9.9%) were categorized as small-forgestational age birth (SGA) and LGA births, respectively, and the remaining 189 infants (81.5%) were categorized as AGA births. (The unequal distribution of sex-adjusted estimates of SGA and LGA births reflects the unequal distribution of male [n = 109; 47%] and female [n = 123; 53%] newborn infants in the study sample.)
Summary
Prematurity (ie, preterm birth, fetal growth restriction) is presently the most significant problem in maternal-child health in the United State because it results in severe adverse health consequences, it has a relatively high prevalence rate that has remained essentially unchanged over the past four decades, and its causes are poorly understood.[1]. Recent advances have implicated placental corticotropin-releasing hormone (CRH) as one of the primary endocrine mediators of spontaneous labor and possibly fetal development.[2,3,4] CRH is a hypothalamic neuropeptide that plays a central role in regulating the activity of the hypothalamicpituitary-adrenal (HPA) axis and physiologic response to stress.[5] During human pregnancy, the CRH gene is expressed in the placenta and membranes, and results over the course of gestation in exponentially increased production and release of placental CRH into both maternal and fetal compartments.[2,3,4]. The aim of this study was to examine these possibilities to clarify the role(s) of CRH in these outcomes
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