Early end-tidal carbon monoxide levels and neurodevelopmental outcome at 3 years 6 months of age in preterm infants.

AIM: Increased end-tidal carbon monoxide (ETCOc) and cytokines in preterm infants are related to bronchopulmonary dysplasia and intraventricular haemorrhages. The aim was to study the predictive value of ETCOc and cytokine levels for long-term outcome. METHODS: This study comprised 105 very preterm infants (57 males, 48 females; gestational age range 25 wks 5d-31 wks 4d; birthweight 610-2100 g) who were admitted to a neonatal intensive care unit between 1 February and 31 December 2002. ETCOc, plasma tumour necrosis factor alpha (TNF-α) and interleukins (IL) 6 and 8, and malondialdehyde (MDA, a marker of lipid peroxidation), were measured at days 1, 3, and 5 of life and related to outcome at 3 years 6 months of age (Griffiths Mental Developmental Scales). RESULTS: Of the 105 infants, 69 were eligible for follow-up (37 males; 32 females; bronchopulmonary dysplasia, n = 12). ETCOc at 0 to 24 hours was higher in infants with adverse outcome (Griffiths developmental quotient <85, n = 15) compared with favourable outcome (2.7SD 0.7 vs 2.0SD 0.5; p < 0.05). MDA and cytokines did not differ between groups. Regression analysis with bootstrapping of independent variables (gestational age, birthweight, ETCOc, TNF-α, IL-6, IL-8, and bronchopulmonary dysplasia) showed that ETCOc was the only parameter that correlated with outcome. The sensitivity and negative predictive value of ETCOc for adverse outcome were 93% and 85% respectively. INTERPRETATION: Adverse neurodevelopmental outcome is associated with increased endogenous carbon monoxide. ETCOc less than 2.0 ppm during the first day indicates a favourable outcome.

HELLP syndrome is associated with an increased inflammatory response, which may be inhibited by administration of prednisolone.

OBJECTIVE: To investigate the effect of prednisolone on HELLP syndrome by assessing several markers of the inflammatory response and hepatic damage associated with HELLP syndrome. DESIGN: Prospective study. SETTING: Single-center, tertiary obstetric care facility at the University Medical Centre Utrecht, The Netherlands. POPULATION: Study subjects included normal controls, patients with non-HELLP preeclampsia, and patients with preeclampsia and HELLP syndrome. METHODS: HELLP syndrome was defined by hemolysis (serum lactate dehydrogenase [LDH] >600 IU/L and/or haptoglobin 70 U/L and/or serum alanine aminotransferase [ALT] >70 U/L), and a low platelet count (<100 x 10(9)/L). Blood samples from patients with HELLP syndrome who were receiving either prednisolone or placebo were obtained before, during, and after a HELLP exacerbation in the antepartum period. Plasma levels of CRP, IL-1RA, IL-6, sIL-6R, IL-8, IL-10, TNF-alpha, and GSTA1-1 were determined. Samples from women with preeclampsia but without HELLP syndrome and from healthy pregnant women were included as controls. MAIN OUTCOME MEASURES: Plasma levels of CRP, IL-1RA, IL-6, sIL-6R, IL-8, IL-10, TNF-alpha, and GSTA1-1. RESULTS: During a HELLP exacerbation CRP, IL-6, IL-1Ra, and GSTA1-1 levels are significantly increased (p < 0.01). In the group of patients treated with prednisolone, significantly lower IL-6 levels were observed during a HELLP exacerbation, compared with patients who did not receive prednisolone (p < 0.01). CONCLUSION: HELLP syndrome is associated with an increased inflammatory response. Circulating IL-6 levels in HELLP syndrome are reduced during prednisolone administration, suggesting a stabilizing effect on the inflammatory endothelial process.