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Abstract
obstetrics and remains a leading cause of neonatal mortality and morbidity. The clinical diagnosis of PTL that precedes preterm delivery is inaccurate, and almost half of the patients with pre-term uterine contractions and intact fetal membranes delivered at term (Dizon and Townson: 2001).
Increasing Pathophysiologic evidence is emerging that links lower and upper genital tract infection with early spontaneous preterm delivery. Patients who develop warning signs of PTL have reached a critical stage because progression of the symptoms will lead to establishment of PTL and decreased opportunity for effective treatment. Although treatment of lower genital tract infection (ie, BV) has been shown to reduce the occurrence of spontaneous preterm delivery in some high risk populations, it is unclear whether such infections are causal or merely associated with a concurrent occult chronic upper genital tract infection (Goldenberg: 2000b).
It is becoming clear that bacterial infection of the chorionic decidual interface incites an intense inflammatory response that leads to disruption of the interface and the eventual onset of PTL. Bacterial invasion of the chorionic decidual interface leads to activation of mononuclear leukocytes with the production of numerous pro inflammatory cytokines, including IL-6, G-CSF, IL-1?, IL-1?, IL-8, and TNF- ?, which promote a cascade of events that culminates in pre-mature ripening of the cervix and the onset of uterine contractions (Goldenberg: 2000 c). These inflammatory proteins represent potential markers for use in identifying patients with occult upper genital tract infections who are at risk for subsequent spontaneous preterm delivery (Patrick-et al: 2002).