Molecular aspects of preterm labor.

Preterm birth is a major problem in clinical obstetrics, occurring in approximately 10% of all pregnancies, and leading to 75% of early neonatal mortality and morbidity. Studies in our laboratory have examined the neuroendocrine mechanisms by which the fetus, through activation of the hypothalamic-pituitary adrenal axis, provides the stimulus to the onset of parturition. Maturation of this axis occurs prematurely in response to stimuli such as stress. Stress induced activation of HPA function in human pregnancy, may lead to increased output of corticotropin-releasing hormone (CRH) from placenta and fetal membranes. CRH is one of the agonists that acts in concert with increased prostaglandin biosynthesis to provide the stimulus to myometrial contractility in late gestation. Recent studies have also recognized that approximately 15% of patients in idiopathic preterm labor present, with deficiency of the major prostaglandin metabolizing enzyme in the fetal membranes, particularly chorionic trophoblast. Understanding these processes may lead to new methods of managing the patient presenting in preterm labor.