Initiation of preterm labor

Abstract

Preterm births are still a major problem in obstetrics. It is estimated that preterm births occur in about 12% of all pregnancies. Due to advances in medical technology and better care of fetuses and premature babies, the preterm mortality rate has been falling (as recently as 1995 the survival rate in the US for premature infants born at 34 weeks amounted to only a fraction of the corresponding rate for those born after 37 weeks). In the US in 2005, preterm births cost society approximately $26 billion, and medical care for premature babies cost more than $51 billion. Only the richest countries can afford such costly medical care. That is why it is not only the individual aspects but also the social aspects that are important when studying preterm birth mechanisms and ways of preventing them. The existing research indicates that both spontaneous mature birth and preterm birth begin and proceed in a similar manner. This is confirmed by the similar involvement in both processes of corticotropin-releasing hormone, urocortin, extracellular stress protein HSP70 (amniotic fluid heat shock protein), prostaglandins, proinflammatory cytokines or glucocorticosteroids. Apparently, at the beginning of either a preterm birth or a term birth, there is a stimulus that ends the development of the fetus or initiates birth. This stimulus works via feedback through placental hormones and through substances present in the fetal membranes, ultimately leading to functional progesterone withdrawal (FPW), thus leaving the uterus sensitive to contractive factors.