Serum troponin in neonates of pre-eclamptic mothers

Cardiac troponin I, the biochemical marker of myocardial injury is characterized by high sensitivity and specificity in comparison with other markers used in the past. The aim of this study was to evaluate serum levels of troponin in neonates of pre-eclamptic mothers compared with levels in age and sex matched controls, and to correlate the levels of troponin I with Cardiac Creatine Kinase [CK-MB] and other markers of myocardial injury. Forty neonates of pre-eclamptic mothers were included in the study [group A]. Also, 30 age and sex matched healthy neonates were included as controls [group B]. All neonates were subjected to full clinical assessment and routine laboratory investigations. Echocardiographic study was done stressing on myocardial contractility, and calculating the E/A ratio where E= Mitral peak velocity of early diastole in centimeters per second, and A Peak velocity of the atrial contraction in centimeters per second. Cardiac troponin [was measured in serum by ELIZA. CK-MB was measured in serum by chemical analysis. The results showed that troponin I, CK-MB, and E/A levels were significantly higher in group A compared with group B [p=0.003, p=0.03, and p=0.01 respectively]. There were significant positive correlations between troponin I with CK-MB, C-reactive protein and the mean E/A value in group A [r=0.86; p=0.02, r=0.50; p=0.01, and r=0.75; p=0.05 respectively]. Troponin I had a sensitivity of 83.3% and a sensitivity of 86.6% in diagnosing myocardial injury while CK-MB had a sensitivity of 75% and a specificity of 76% in diagnosing myocardial injury. From the present study we conclude that cardiac Troponin I is a more specific and more sensitive marker for myocardial injury than the standard biochemical markers such as CK-MB and it can detect minor myocardial damage not diagnosed early by echo cardio graphic study. Also we conclude that preterm neonates of preeclamptic mothers are more susceptible to myocardial injury than full-term neonates. Troponin I may have prognostic significance because, if present, it identifies the neonates of pre-eclamptic mothers who are at risk of cardiac injury

Cord blood activin A level as index of fetal hypoxia

Perinatal hypoxic-ischemic cerebral injury is a major determinant of neurologic morbidity and mortality in the neonatal period and later in childhood. Activin-A is a growth factor involved in cell growth and differentiation, neuronal survival, early embryonic development and erythropoiesis. Hypoxemia is a specific trigger for increasing activin-A in fetal lamb circulation. We evaluated the effects of asphyxia on cord blood activin-A levels. The study was carried out on 30 newborns who suffered from perinatal asphyxia and who selected from El-Minia university hospital from January 2005 through June 2005 in addition to 30 newborns of the same age and sex matched as a control group. Blood samples were obtained from the umbilical artery and vein for blood gas analysis, complete blood count with determination of nucleated red blood cells [nRBCs] and measurement of free activin-A. In this study, the arterial cord blood mean values of PH, PaO[2] and base deficit were lower and PaCO2 was higher in asphyxiated group than the control group. Newborns with clinical signs of perinatal asphyxia had higher activin-A levels, which were correlated with indices of hypoxia such as lower pH suggesting that hypoxia is a trigger to stimulate activin-A secretion. It was found that the mean value of activin-A was higher in arterial than in the venous cord blood in both asphyxiated and control groups suggesting that the fetus is the main source of activin-A. Nucleated RBCs were increased in asphyxiated group. The level of nRBCs per 100 WBCs correlated with asphyxia. The correlation found suggests that hypoxia is one of the common stimulus for increased erythropoiesis and activin-A release. intrauterine hypoxia is one of the common factors responsible for increasing activin-A levels in fetal circulation. The strong correlation between activin-A and clinical and biochemical signs of fetal and neonatal hypoxia lead us to suggest that activin-A is a possible indicator of intrauterine hypoxia