| Abstract | Clinical approaches to the diagnosis of PTL and the prediction of PTD are complicated by the absence of a gold standard for the pathogenic process leading to PTD. There is also substantial overlap between the signs and symptoms of PTL and impending PTD, and the normal processes of pregnancies destined to remain uncomplicated (e.g., our inability to convincingly differentiate PTL from Braxton-Hicks contractions). Our emphasis on the diagnosis of PTL rather than the pathogenic process preceding PTD also results in failure to detect the 50% of spontaneous PTDs in which uterine contractions follow PPROM. Thus, clinical predictors of incipient PTD including cervical change, uterine contractions, vaginal bleeding, risk scoring schemes, and fetal breathing activity, either have poor sensitivity or specificity, or are accurate only at late stages in the pathogenic process. The most promising approaches to the detection of impending PTD are laboratory indices of the putative pathogenic processes including: maternal serum or plasma CRH, salivary E3, serum collagenase and cervicovaginal cytokines, granulocyte elastase, and FFN levels. However, even if these indices prove sensitive, specific, and early predictors of PTD, they will be useful only if more appropriate therapies are found to treat patients. The latter will depend on addressing the primary causes of chorionic-decidual cell activation (e.g., infection, stress, utero-placental ischemia, hemorrhage, endocrinopathies). |
