Value of homocysteine levels, troponin I, and score for neonatal acute physiology and perinatal extension II as early predictors of morbidity (original) (raw)
Related papers
Cord Blood Cardiac Troponin I and Creatine Kinase MB Levels in Poor Neonatal Outcomes
2006
Objective: To compare cord blood cardiac-troponin I and creatine kinase-MB levels in fetuses with poor neonatal outcome to completely healthy newborns. Materials and Methods: Cord blood cardiac-troponin I and creatine-kinase-MB (CK-MB) levels of 398 completely healthy newborns were measured via microparticle enzyme immunoassay. These were compared to the levels of fetuses with acidosis defined as pH <7.1 and/or base excess <-12 mmol/L (n=21), hypoxic ischemic encephalopathy (n=12), fetal anomaly (n=13) and early neonatal mortality (n=8). The median levels were compared using Mann-Whitney U test. Receiver operator characteristics were analyzed to find a cut-off value with best sensitivity and lowest false positive rate. Results: The median level of troponin I in healthy newborns was 0.2 ng/ml (Range=0-4.4) and CK-MB was 6.0 U/L (Range=0.3-32). These values were 0.8 ng/ml (Range=0-8, p=0.001) and 6.4 U/L (Range=1.4-14.5, p=0.5) for newborns with fetal acidosis. Fetuses that died...
The effect of blood gas and Apgar score on cord blood cardiac Troponin I
Journal of Maternal-Fetal and Neonatal Medicine, 2004
Objectives: The aims of this study were to (a) establish a reference range for cardiac troponin I (cTnI) in the cord blood of healthy infants, and (b) investigate the effect of Apgar score, cord blood gas, gestational age, and creatine kinase (CK) and creatine kinase MB (CK-MB) fraction levels on cord blood cTnI levels. Methods: 112 perinatal hypoxic and 84 control newborns without perinatal hypoxia were enrolled in this study. Cord blood samples were collected from the babies for arterial blood gas analysis, cTnI, CK and CK-MB measurements. Gestational age, birth weight, sex, Apgar score and history of fetal distress were recorded. Hypoxic ischemic encephalopathy (HIE) group, hypoxic but without HIE group and control groups were identified according to clinical observations during the first 72 h in the newborn unit. Results: HIE and perinatal hypoxic without HIE groups had a significantly higher cord blood cTnI level according to the control group (1.8 ng/mL (0-13), 0 ng/ml (0-1.1) and 0 ng/ml (0-0.3) respectively). Cord blood cTnI level did not have a correlation with birth weight and gestational age (r = 70.02, p 4 0.05 and r = 0.08, p 4 0.05 respectively). Cord blood cTnI level also had a negative correlation with pH, bicarbonate, base deficit, and Apgar score (r = 70.40, p 5 0.001; r = 70.39 p 5 0.001; r = 70.45 p 5 0.001; r = 70.41, p 5 0.001) respectively). Cord blood cTnI level showed a positive correlation with CK and CK-MB levels (r = 0.45, p 5 0.001 and r = 0.37, p 5 0.001 respectively). Receiver operator curve analysis revealed that the most sensitive factor for prediction of perinatal hypoxia is cord cTnI value [area under curve = 0.929]. The optimal cut-off value of cord cTnI was 0.35 ng/ml for hypoxia. Conclusion: cTnI levels in the cord blood are not affected by gestational age and birth weight. cTnI together with CK and CK-MB has been found to be elevated in hypoxic infants compared to normal infants. Therefore cTnI may be an indicator for perinatal hypoxia in neonates.
Journal of Perinatal Medicine, 2000
To determine the value of cord blood cardiac troponin I levels (cTnI) as an early prognostic factor in critically ill newborns, and to compare cord cTnI levels with the prognostic value of the score for neonatal acute physiology (SNAP). Methods: Cord arterial samples were collected routinely for blood gas analysis, and cord venous samples for cTnI and cardiac-specific creatine kinase assay. The study group (ns109) comprised critically ill newborns who required mechanical ventilation. The control group (ns96) comprised newborns who were either completely healthy (ns48) or were followed in a level I neonatal care unit due to moderate-severity problems. Results: The critically ill newborns had significantly higher cTnI levels than control babies (median wmin-maxx 1.4 w0-13x vs. 0 w0-1.8x ng/mL, respectively; P-0.001). In critically ill newborns, non-survivors had significantly higher cTnI levels than survivors (median wmin-maxx 6.6 w1.3-13.0x vs. 1.3 w0-8.0x ng/mL, respectively; P-0.001). Receiver-operator curve analysis revealed that, compared with SNAP, cTnI was a more sensitive predictor of mortality in critically ill newborns (area under curves0.96; 95% CIs0.90-1.02). Conclusion: Significantly elevated cord cTnI may be a valuable predictor of mortality in critically ill newborns.
Homocysteine, Cysteine, and Related Metabolites in Maternal and Fetal Plasma in Preeclampsia
Pediatric Research, 2007
Homocysteine is associated with endothelial dysfunction and cardiovascular disease, and elevated concentrations of homocysteine have been found in preeclampsia. The purpose of this study was to investigate maternal and fetal concentrations of total homocysteine and related metabolites (including cysteine, choline, and betaine), and possible associations with infant birth weight. Women with preeclampsia (n ϭ 47) and controls (n ϭ 51), who underwent cesarean section, were included. Maternal plasma, umbilical vein, and artery plasma were analyzed. Median concentrations of homocysteine, cysteine, choline, and betaine were significantly higher in women with preeclampsia than controls, both in maternal and fetal plasma. There were no differences in folate and vitamin B 12 concentrations between the groups, neither for maternal nor fetal samples. Maternal homocysteine concentration was a negative predictor for birth weight only in the preeclampsia group. Elevated homocysteine and cysteine concentration in maternal circulation in preeclampsia is reflected in the fetal circulation. The clinical significance of elevated homocysteine and cysteine concentrations in maternal and fetal compartments in preeclampsia remain to be explored, both regarding fetal growth and development of disease later in life.
Australian & New Zealand Journal of Obstetrics & Gynaecology, 2008
Aim: To determine whether homocysteine concentrations in umbilical cord plasma of neonates born to mothers with pre-eclampsia are elevated compared to concentrations in neonates born to normotensive women. Method: Maternal blood from eight women with pre-eclampsia and ten women without pre-eclampsia was collected on admission for labour. Cord blood was collected from these same pregnancies at delivery. Plasma was extracted and stored at −70°C. Samples were batch-analysed for homocysteine. Result: Maternal plasma homocysteine levels were observed to be significantly higher in the pregnancies complicated by pre-eclampsia compared to the control pregnancies (P = 0.043) with median levels of 5.4 μmol/L (interquartile range (IQR) 4.6-7.9; range 3.6-16.7) versus 4.1 μmol/L (IQR 3.4-5.1, range 3.1-6.7). Homocysteine concentrations in umbilical cord plasma in pregnancies complicated by pre-eclampsia were also significantly higher compared to those in normotensive pregnancies (P = 0.016) with median concentration levels of 5.3 μmol/L (IQR 4.8-7.2, range 2.5-16.6) versus 3.8 μmol/L (IQR 2.8-4.4, range 0.8-1.6). Conclusion: Both maternal and umbilical cord plasma homocysteine concentrations were elevated in pregnancies complicated by pre-eclampsia compared to normotensive controls.
Cord blood cardiac troponin I, fetal Doppler velocimetry, and acid base status at birth
International Journal of Gynecology & Obstetrics, 2008
Objective: To analyze the association between umbilical cord cardiac troponin I (cTnI), obstetric Doppler, and birth acidemia. Method: This prospective observational study was conducted on 58 singleton pregnancies at 3 Brazilian hospitals. Umbilical and middle cerebral artery Doppler velocimetry were performed 24 h prior to birth. At delivery, cord blood was collected for pH, blood gas analysis, and cTnI measurement. Results: Cardiac troponin I ≥ 0.20 ng/mL was detected in 5 neonates (8.6%). Centralization was recorded in 12 fetuses; 4 of these (33.3%) had detectable cTnI compared with 1/46 (2.2%) fetuses with normal Doppler (P = 0.005). Acidemia was present in 60% of the neonates with detectable cTnI, compared with 15% of the neonates with undetectable cTnI (P = 0.042). Conclusion: Centralization and birth acidemia are associated with detectable cTnI in cord blood supporting the possibility of myocardial ischemia in these fetuses.
Maternal and umbilical homocysteine in preeclampsia
Periodicum Biologorum, 2016
Background and purpose: Were to assess the association between homocysteine levels and development of preeclampsia, to determine homocysteine levels in fetal circulation, to differentiate homocysteine levels in mild and severe preeclampsia and to compare homocysteine levels in pregnant women with preeclampsia with homocysteine levels measured in the same group of women six months after delivery. Material and methods: The study included 55 pregnant women with mild or severe preeclampsia (hypertensia with proteinuria), while control group of 50 healthy pregnant women. Maternal and umbilical blood homocysteine levels were determined by the fluorescence polarization immunoassay. Shapiro-Wilks, Mann-Whitney and Wilcoxon statistical tests performed for statistical analysis. Results: In women with preeclampsia, the mean homocysteine level was by 0.744 µmol/L higher than in control women; with mild preeclampsia, the level was by 2.752 µmol/L lower as compared to the women with severe preeclampsia (p < 0.0001). In women with preeclampsia, the mean umbilical blood homocysteine level was by 0.268 µmol/L lower than the respective level measured in control group (p < 0.0001). In women with preeclampsia, the mean homocysteine level was by 0.878 µmol/L lower in the same group of women six months after delivery (p < 0.0001). Conclusion: Homocysteine are lower in preeclamptic women six months after delivery. The neonates born to mothers with preeclampsia are not at a higher exposure to homocysteine. IntroductIon S ince the 1990s, homocysteine has been associated with disorders of the fetomaternal unit (1). Studies on recurrent abortions also found clear association between elevated homocysteine levels and the risk of abortion (2,3). Later on, Vollset et al. (4) found the levels of homocysteine to be associated with the prevalence of preeclampsia, preterm delivery, low birth weight, intrauterine growth restriction (IUGR), stillbirth, congenital malformations and abruptio placentae. The association of mild hyperhomocysteinemia with cardiovascular disease and related mortality was demonstrated in a number of studies (5-11). Hyperhomocysteinemia alters vascular morphology, stimulates inflammation, activates endothelium and blood clotting cascade, and inhibits fibrinolysis. Hyperhomocysteinemia results in the loss of endothelial antithrombin function and induction of a procoagulant setting (9,12). The pathogenetic action of homocysteine also includes interference with the nitric oxide (NO) system (homocysteine reduces NO bioavailability by interfering with its synthesis), activation of transcrip