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  • Title: Effect of corticosteroid interval on markers of inflammation in spontaneous preterm birth.
    Author: Subramaniam A, Cliver SP, Andrews WW, Faye-Petersen OM, Goldenberg RL, Biggio JR.
    Journal: Am J Obstet Gynecol; 2013 Oct; 209(4):379.e1-6. PubMed ID: 23764022.
    Abstract:
    OBJECTIVE: The objective of the study was to evaluate whether the time interval from corticosteroid administration to delivery is associated with variations in inflammatory/infectious markers in women with spontaneous preterm birth (SPTB). STUDY DESIGN: We conducted a secondary analysis of a prospectively collected cohort of women experiencing SPTB from 23(0/7) to 31(6/7) weeks. Patients were categorized by corticosteroid receipt and time interval until delivery. Prevalence of markers of inflammation and colonization/infection (cord blood interleukin [IL]-6 levels; Ureaplasma urealyticum [UU], Mycoplasma hominis [MH], and other anaerobic/aerobic cultures; histology of the placental disc, membranes and cord) were compared between groups using χ(2) and Mantel-Haenszel tests. RESULTS: Two hundred seventy-three patients had SPTB. Prevalence of elevated IL-6 (P = .028) and positive UU/MH cultures (P = .019) were highest in women not receiving corticosteroids and those delivering more than 7 days from receipt. The prevalence of both decreased in groups with delivery delayed at least 12 hours but increased as the interval lengthened to more than 48 hours. Overall positive placental cultures also nadired among those delivering at 12-24 hours after corticosteroids (P = .049). As the interval increased, prevalence of acute inflammation at the rupture site increased (P = .017). There were similar, but nonsignificant, increases in chorionic plate inflammation and funisitis. CONCLUSION: The relationship between time interval from corticosteroids and evidence of inflammation in women experiencing SPTB is U shaped, suggesting earlier stages of inflammation in women with delayed delivery or transient decreases of inflammation in response to corticosteroids. This warrants further investigation to elucidate the natural history of SPTB and its modulation by corticosteroids.
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