Progesterone supplement in pregnancy: an immunologic therapy?

One of the most interesting functions of the placenta is the regulation of the maternal immune response such that the fetal semi-allograft is tolerated during pregnancy. Trophoblasts are presumed to be essential to this phenomenon because they lie at the maternal-fetal interface, where they are in direct contact with cells of the maternal immune system. Trophoblasts do not express classic major histocompatibility complex (MHC) class II molecules. Surprisingly, cytotrophoblasts express more HLA-G, a MHC class Ib molecule, as they invade the uterus. Progesterone plays an important role in postovulatory regulation of the menstrual cycle. If fertilization occurs, progesterone supports implantation of the ovum and maintains the pregnancy. Progesterone has been named the 'hormone of pregnancy', because in preparing the endometrium for embryo implantation and facilitating endometrial development, it is critical to the very survival of a pregnancy. In addition, this key hormone inhibits the rejection of T cell-mediated tissue and also decreases myometrial activity and sensitivity throughout pregnancy. The cellular actions of progesterone are mediated through intracellular progesterone receptors (PRs), which are well studied gene regulators, not express classic major histocompatibility complex. The more used paradigm is relative to the alteration of relationship TH1/TH2, but the complexity of the respective distributions of cytokines at the materno-fetal interface, strongly suggest that, as useful as it certainly was for a while, the Th1/Th2 paradigm must now be considered as an oversimplification. Rather, the existing data point to sequential windows and are suggestive of a system where an extreme complexity is allied to very precise timing and tuning. They also suggest that the materno-fetal relationship is not simply maternal tolerance of a foreign tissue, but a series of intricate mutual cytokine interactions governing selective immune regulation and also control of the adhesion and vascularization processes during this dialogue. However, as shifting the immune response toward the Th2 pattern (IL-4, IL-5, IL-6) may benefit the fetus, whereas development of proinflammatory Th1 cells (secreting IL-2, IFN g, TNF a) may be harmful. Now we are working to open comprise the precise behaviour of NK populations, with the hope of obtaining a diagnostic test of the condition of abortion from 'immunological causes'.

Induction of labor with intravaginal prostaglandin E2 gel.

OBJECTIVE: The aim of our study was to evaluate the optimum dose of intravaginal prostaglandin E2 gel for induction for labor in nulliparous women with a relatively ripe cervix (modified Bishop score 4 or 5). METHOD: One hundred and sixty-seven nulliparous women at term with indications for the induction of labor were treated randomly with two doses of intravaginal 2.0 (group A) or 3.0 mg (group B) of prostaglandin PGE2 gel every 12 h. Data were analyzed by chi 2-test and Student's t-test. RESULTS: Of 87 patients 64 went into labor after gel application in group A, compared with 68/80 in group B (73.5% vs. 85.0%) (P = NS). A second gel administration was needed for 9 women in group A and 6 women in group B. More side effects (both local and systemic) were noted in group B than in group A (28.7% vs. 14.9%) (P = 0.03). In particular, more local (hyperstimulation or hypertonus) side effects were noted in group B (13.7% vs. 2.3%) (P = 0.01). CONCLUSION: The vaginal administration of 2.0 mg of PGE2 gel seems to be equally effective as 3.0 mg in terms of labor success rate with a significant lower incidence of side effects.