الفهرس | Only 14 pages are availabe for public view |
Abstract Spontaneous preterm labor and intact membranes (PTL) accounts for approximately 70 to 80% of all preterm births, and preterm birth, owing to these causes in particular, is strongly associated with significant neonatal morbidity, mortality, and long-term disability. Vitamin D-binding protein (VDBP) is a 58-kDa protein of the albumin superfamily that is mainly synthesized by hepatocytes. The established functions of VDBP include acting as a major carrier protein for vitamin D and its metabolites in serum, sequestering actin, and potentially modulating the inflammatory and immune response, and it is associated with the clinical progression of many diseases. In particular, previous studies that used the proteomic and cohort approaches have shown significantly increased expression of CVF VDBP in association with the occurrence of impending PPROM in asymptomatic women and of SPTD and intra-amniotic infection in women presenting with symptoms of PTL. However, these findings have not been confirmed by other studies. Moreover, whether the change in VDBP level in the CVF is associated with intra-amniotic infection and impending SPTD in women with PPROM remains unclear. Hence, the aim of this study was to determine whether the level of VDBP in CVF samples is independently predictive of SPTD within 48 hours in women with PTL. In the multivariable analysis, elevated VDBP levels in CVF samples of PTL women were significantly associated with imminent preterm delivery, even after adjusting for potential confounders (e.g., gestational age at sampling, parity, and serum CRP). In women with PTL, the areas under receiver operating characteristic curves of CVF VDBP level for predicting imminent preterm delivery were 0.781, with cut-off values of 2.3 μg/mL (sensitivity of 63.16% and specificity of 96.0%). respectively. The CVF VDBP levels were significantly high in women with PTL. Conclusions: VDBP in the CVF independently predicts imminent preterm delivery in women with PTL. |