A detailed discussion of the hormonal, molecular, and genetic factors associated with preterm parturition is beyond the scope of this article, and has been reviewed in detail elsewhere.19–21 Accumulating evidence suggests that the myometrial activity associated with preterm labor results primarily from a release of the inhibitory effects of pregnancy on the myometrium rather than an active process mediated through the release of uterine stimulants, and progesterone appears to play a central role in this regard. In the first trimester, progesterone produced by the corpus luteum is critical to the maintenance of early pregnancy until the placenta takes over this function at 7 to 9 weeks of gestation, hence its name (pro-gestational steroidal ketone). Indeed, removal of the source of progesterone (the corpus luteum)22 or administration of a progesterone receptor antagonist23 readily induces abortion before 7 weeks (49 days) of gestation. The role of progesterone in later pregnancy, however, is less clear.
Recent data suggest that progesterone may be important in maintaining uterine quiescence in the latter half of pregnancy by limiting the production of stimulatory prostaglandins and inhibiting the expression of contraction- associated protein genes (ion channels, oxytocin and prostaglandin receptors, and gap junctions) within the myometrium.19–21 It is now clear that, although levels of progesterone in the maternal circulation do not change significantly in the weeks preceding labor, the onset of labor both at term and preterm is associated with a functional withdrawal of progesterone activity at the level of the uterus.19–21,24–27 It is data such as these that provide the rationale behind the use of progesterone supplementation to prevent preterm labor and birth.