News in pathophysiology and management of preterm labour

2009 
OBJECTIVE: To summarize available data concerning pathophysiology and management of preterm labour and their use in clinical practice. SETTING: Department of Obstetrics and Gynecology od the First Faculty of Medicine, Charles University, and General Teaching Hospital, Prague. DESIGN: Review article. METHODS: Compilation od published data from scientific literature. CONCLUSION: Birth canal infections seem to play a key role in the ethiopathogenesis of premature delivery; the related biochemical changes significantly affect perinatal morbidity and mortality. Other potential causes, particularly hormone metabolism disorders or uteroplacental ischaemia have been intensively studied. The particular pathogenetic process of premature delivery is inflammation. This process is related to both mother and fetus. Fetal inflammatory response (FIRS)--can occur without maternal response--is connected with significant increase in perinatal morbidity. FIRS is characterised by defined laboratory, histological and clinical criteria. Effective primary prevention of premature delivery does not exist at present. The sensitivity and specificity of the laboratory markers having been used so far is low. Thus, the research is focused on finding new inflammation markers to allow early identification of pregnant women at a high risk of premature delivery and fetal inflammation. The screening of women at a high risk by means of new laboratory and ultrasound tests belongs to the most important steps in secondary and tertiary prevention of premature delivery. Intensive research of potential trigger mechanisms has been carried out, including a variety of gene types, which are potentially related to the process of premature delivery. We try to exercise new informations about pathophysiology of preterm labour in prenatal care, firstly about thrombophillias and gestagens. We also use a principles of "evidence based medicine" and revalue importance of steroids, tocolytics and antibiotics.
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