Abstract
Background: Respiratory distress syndrome (RDS) incidence is increased in infants of preeclamptic mothers with hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome. RDS and HELLP syndrome have been associated with oxidative stress and inflammatory processes. Objectives: We hypothesize that end-tidal carbon monoxide corrected for inhaled CO (ETCOc), malondialdehyde (MDA) (markers of oxidative stress) and proinflammatory cytokine (IL-6, IL-8) production are higher in infants of preeclamptic mothers with HELLP syndrome than in those of preeclamptic mothers without HELLP syndrome. Methods: Prospective study of 36 infants of preeclamptic mothers (GA <32 weeks) admitted to the Neonatal Intensive Care Unit. ETCOc was measured at 0–12, 48–72 and 168 h postnatally using the CO-Stat™ End-Tidal Breath Analyzer. Simultaneously, blood was sampled for MDA, IL-8 and IL-6. Results: At 0–12 h, ETCOc, MDA and IL-8 values (median[range]) were significantly higher in HELLP infants than in infants from preeclamptic mothers without HELLP (ETCOc 2.2 [1.5–3.9] vs. 1.8 [0.5–2.9] ppm; MDA 2.3 [1.3–4.1] vs. 1.5 [0.4–3.1] µmol/l; IL-8 145 [24–606] vs. 62 [26–397] pg/ml; all p <0.05). MDA remained significantly higher during the first 168 h of life (2.3 [0.8–5.8] vs. 1.1 [0.8–3.7] µmol/l, p = 0.02). Conclusion: Oxidative stress and proinflammatory cytokine levels are increased in infants of preeclamptic mothers with HELLP syndrome. These processes may cause inactivation of surfactant explaining the increased RDS incidence in these infants.
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