[Prolonged pregnancy--prostaglandins as the cause of labor onset]

The causes of prolonged pregnancy are still largely unknown and their investigation requires a detailed observation of potential birth-initiating stimuli on the endocrine and biomolecular level. A large number of clinical and biochemical studies point to the central importance of prostaglandins for the beginning of human birth. The main places of origin of the intensified prostaglandin formation and release are the amnion and the decidua which has "macrophage-like" properties and functions. The superordinate regulation and trigger mechanisms for intensified uterine prostaglandin production has not been sufficiently investigated either. Possible factors currently being debated include local changes in estrogen and progesterone biosynthesis in fetal membranes and decidua, subclinical inflammatory reactions with the activation of macrophages and the consecutive release of cytokines, and a loss of maternal immune tolerance with a time-determined rejection reaction. In addition, the substances inhibiting and stimulating prostaglandin synthesis have been detected in the amniotic fluid, fetal membranes and decidua. The fetus itself also plays an important part in the initiation of labor. Prolongation may be due to anatomic functional disturbances of the one hand which prevent the activation of the fetal hypothalamic-hypophyseal-adrenal axis and the release of the birth-initiating stimuli originating in the fetus; on the other hand, an elevated immune tolerance with a delayed rejection reaction or the lack of "bacterial stimulus" may inhibit the activation of the macrophages and hence the formation of cytokines. The consequences would be the development and release of a quantity of prostaglandins from the fetal membranes and decidua insufficient to overcome the pregnancy-maintaining safety systems.(ABSTRACT TRUNCATED AT 250 WORDS)