Maternal intravascular inflammation in preterm premature rupture of membranes

Objective: Intrauterine inflammation has been implicated in the mechanisms responsible for preterm premature rupture of membranes (PROM). However, it is unclear whether this inflammatory process remains localized to the uterus, at the site of membrane rupture, or extends to the maternal compartment. Flow cytometric analysis is a sensitive method to assess the presence and magnitude of in vivo inflammation. This study was conducted to determine whether preterm PROM is associated with changes in the phenotypic and metabolic characteristics of maternal granulocytes and monocytes consistent with the presence of maternal intravascular inflammation. Study design: A prospective cross-sectional study was performed including patients with preterm PROM (n = 43) and with a normal pregnancy (n = 51). Maternal inflammation was assessed by flow cytometric analysis of maternal plasma. Intravascular inflammation was studied using flow cytometry. Maternal blood was assayed to determine granulocyte and monocyte phenotypes using monoclonal antibodies, which included cluster differentiation (CD) markers CD11b, CD14, CD15, CD16, CD18, CD49d, CD62L, CD64, CD66b and human leukocyte antigen (HLA)-DR. The presence of basal intracellular oxygen radical species (iROS) and oxidative burst was assessed. Statistical analysis was conducted with the use of non-parametric methods. A p value < 0.01 was considered significant. Results: Preterm PROM was associated with a significant increase in the median mean channel brightness (MCB) of CD11b, CD14, CD64 and CD66b on granulocytes and median MCB of CD11b on monocytes. The ratio of oxidative burst over basal iROS in both granulocytes and monocytes was higher in preterm PROM than in normal pregnancy (p < 0.01). Conclusion: Preterm PROM is associated with a maternal intravascular inflammatory response.