RGD Reference Report - Early prediction of sepsis-induced disseminated intravascular coagulation with interleukin-10, interleukin-6, and RANTES in preterm infants. - Rat Genome Database
BACKGROUND: The progression to disseminated intravascular coagulation (DIC) in infected very low birth weight (VLBW; <1500 g) infants is difficult to predict with precision at the onset of sepsis. We investigated the immunologic profiles of preterm infants with sepsis, using chemokine and cytokine measurements to predict the development of sepsis-induced DIC at the onset of infection. METHODS: We measured a panel of chemokines and cytokines at 0 and 24 h after clinical presentation in VLBW infants with suspected infection requiring full sepsis screening. The chemokines measured were interleukin (IL)-8, interferon-gamma-inducible protein-10 (IP-10), monokine induced by interferon-gamma, monocyte chemoattractant protein-1, and regulated upon activation normal T-cell expressed and secreted (RANTES), and the cytokines were IL-6, IL-10, and tumor necrosis factor-alpha. RESULTS: Of 195 episodes of suspected clinical sepsis investigated, 62 were culture-confirmed septicemia or necrotizing enterocolitis (28 of these infants developed DIC), 22 were culture-negative clinical infections, and 111 involved noninfected episodes. All studied inflammatory mediators except RANTES showed significantly greater up-regulation in culture-positive infected infants than in noninfected infants at 0 and 24 h, whereas RANTES showed significant down-regulation. The model that used plasma IL-10 (>208 ng/L), IL-6 (>168 ng/L), and RANTES (<3110 ng/L) at 0 h had sensitivity, specificity, and positive and negative predictive values of 100%, 97%, 85%, and 100%, respectively, for identifying infected patients who subsequently developed DIC. CONCLUSIONS: IL-10, IL-6, and RANTES measured at clinical presentation sensitively and accurately predicted the development of DIC in severely infected infants. This information could be vital for early and effective treatment of neonatal sepsis.