Phagocyte activation in preterm infants following premature rupture of themembranes or chorioamnionitis

Phagocyte activation was studied in 48 preterm infants, gestational age 27. 3 +/- 0.3 wk, birthweight 968 +/- 40 g, during the first postnatal week. Hu man neutrophil lipocalin as a marker of neutrophil activation was measured in plasma and tracheal aspirate fractions; and lysozyme, as a marker of mon ocyte and macrophage activation, in plasma. The concentration of plasma hum an neutrophil lipocalin was 69 (46-126) mug/l (median and quartiles), trach eal aspirate fraction fluid 213 (71-133) 433) mug/l and plasma lysozyme 133 7 (923-1764) mug/l. Infants born to mothers with premature rupture of the m embranes or clinical chorioamnionitis (group A, n = 20) had significantly h igher plasma [73 (58-151) vs 53 (38-108) mug/l; p = 0.027], and tracheal as pirate fraction human neutrophil lipocalin [319 (129-540) vs 190 (57-324) m ug/l; p = 0.019], and plasma lysozyme [1739 (1356-2021) vs 1140 (739-1557) mug/l; p =0.0001] than did infants whose mothers had intact membranes and w ho had no suspicion of infection (Group B, n = 28). In infants born to moth ers receiving corticosteroids ante partum, correlations existed between tim e from treatment to delivery and plasma (r = 0.322, p = 0.0256) and trachea l aspirate fraction human neutrophil lipocalin (r = 0.314, p = 0.0096). Infants born to mothers with at risk of infection are exposed to the potent ially harmful effects of activated neutrophils. Premature rupture of the me mbranes, even without signs of clinical infection of the mother or the fetu s, is associated with phagocyte activation that may begin already in utero. Corticosteroid treatment of the mother may cause transient inhibition of n eutrophil activation in the newborn.