Labor at term is regarded as a release of the myometrium from the inhibitory effects of pregnancy (phase 0) which are mediated by a variety of suppressors that maintain uterine quiescence.
Dr. Hayashi is Director of Maternal-Fetal Medicine and Professor of Obstetrics at the University of Michigan Medical Center. He is a renowned perinatologist and past president of the Society for Maternal-Fetal Medicine.
Dr. Hayashi reviewed the article in the August 26, 1999 issue of The New England Journal of Medicine entitled "Current Concepts: The Control of Labor" (Norwitz, et al.). He found the article presented compelling evidence supporting the timing and initiation of human parturition. Of particular interest was the role of salivary estriol in the hormonal mechanism associated with the initiation of human parturition.
Parturition has four phases that are tightly controlled by endocrine and paracrine hormones.
Labor at term is regarded as a release of the myometrium from the inhibitory effects of pregnancy (phase 0) which are mediated by a variety of suppressors that maintain uterine quiescence. As term approaches, the uterus becomes activated (phase 1) by uterotrophins, including estrogen, increasing the number of myometrial gap junctions and receptors for prostaglandins and oxytocin. Labor is defined as a switch in the pattern of myometrial contractility from irregular contractures to regular contractions, which results in effacement and dilatation of the cervix. The increased number of gap junctions facilitates the electrical synchrony required for coordinated contractions, allowing the primed uterus to be stimulated (phase 2) to contract by oxytocin and prostaglandins E2 and F2a. The last phase of parturition (phase 3) is the involution of the uterus after delivery.
The cascade of uterine changes that precedes delivery can last up to a few weeks. When the myometrium and cervix are duly prepared, activation of the fetal hypothalamic-pituitary-adrenal (HPA) axis induces the release of endocrine, paracrine, and autocrine factors from the fetoplacental unit that trigger the switch in myometrial activity.
Preterm labor before 37 weeks of gestation accounts for more than 85% of perinatal mortality and morbidity, although it only occurs in 7-10% of births.
Seen as a breakdown in the mechanisms responsible for maintaining uterine quiescence, preterm labor may be triggered by a spectrum of physiologic conditions including a deficiency in the enzymes that normally degrade stimulatory prostaglandins, or an intraamniotic infection that creates a hostile intrauterine environment for the fetus.
Until recently, risk factors for preterm labor only identified approximately 50% of women who ultimately delivered preterm.
Aside from cervical ultrasound, which can identify a subpopulation of women more likely to deliver preterm, biochemical markers hold the greatest promise for identifying women at risk for preterm delivery. While elevated levels of fetal fibronectin indicate a separation of the fetal membranes from the decidua, the usefulness of this test lies mainly in its high negative predictive value.
In contrast, maternal serum estriol levels accurately reflect activation of the fetal HPA axis, which occurs before the onset of term and preterm labor. Elevations in salivary estriol, which mirror elevated levels of biologically active serum estriol, are predictive of delivery before 37 weeks with a sensitivity of 68-87% in high-risk women.
Management protocols for preterm labor must distinguish between uterine conditions, such as infection, that should not be prolonged because they are hostile to the fetus, and instances in which aggressive interventions to stop labor may be beneficial.
Although bed rest and hydration are commonly recommended, drug therapy remains the cornerstone of management. The two most commonly used agents due to their safety and efficacy are magnesium sulfate and -adrenergic agonists, both of which lower intracellular calcium.