Changes in myocardial enzyme spectrum, procalcitonin and C-reactive protein levels in neonates with hyperbilirubinemia / 中国基层医药

ABSTRACT

Objective:To investigate the changes in myocardial enzyme spectrum, procalcitonin, and C-reactive protein levels in neonates with hyperbilirubinemia.Methods:A total of 150 neonates with hyperbilirubinemia who received treatment in the 1 st Affiliated Hospital of Wenzhou Medical University during January-December 2019 were included in this study. They were allocated to mild (total bilirubin level 221-256.5 μmol/L, n = 68) and moderate-to-severe hyperbilirubinemia (total bilirubin level > 256.5 μmol/L, n = 82) groups according to different serum total bilirubin levels. An additional 70 healthy neonates who were born concurrently served as controls. Myocardial enzyme spectrum (creatine kinase, creatine kinase-MB, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase), procalcitonin, and C-reactive protein levels were compared among groups. The correlation between myocardial enzyme spectrum, procalcitonin, and C-reactive protein levels and the severity of hyperbilirubinemia was investigated. The factors related to hyperbilirubinemia in neonates were analyzed using logistic regression analysis. Results:Serum levels of creatine kinase, creatine kinase-MB, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase were (1130.23 ± 385.42) U/L, (194.82 ± 60.33) U/L, (993.45 ± 271.46) U/L, and (493.76 ± 105.65) U/L, respectively in the moderate-to-severe hyperbilirubinemia group, which were significantly higher than those in the mild hyperbilirubinemia and control groups [(682.23 ± 258.53) U/L, (82.67 ± 24.43) U/L, (486.38 ± 112.57) U/L, (252.63 ± 38.73) U/L; (368.13 ± 104.20) U/L, (27.90 ± 8.29) U/L, (402.13 ± 102.20) U/L, (228.53 ± 34.30) U/L; F = 67.12, 56.23, 66.57, 44.34, all P < 0.01]. Serum levels of creatine kinase, creatine kinase-MB, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase were significantly higher in the mild hyperbilirubinemia group than those in the control group (all P < 0.05). Premature infants, intrauterine distress, neonatal asphyxia, amniotic fluid pollution, sepsis, omphalitis, erythrocyte glucose-6-phosphate dehydrogenase defect, and delayed passage of meconium are the risk factors for neonatal hyperbilirubinemia ( OR = 6.13, 5.40, 5.29, 4.26, 7.79, 6.99, 5.79, 5.44, all P < 0.05). Breastfeeding is an independent protective factor for the development of neonatal hyperbilirubinemia ( OR = 5.87, P < 0.05). Conclusion:Myocardial enzyme, procalcitonin, and C-reactive protein levels increase in neonates with hyperbilirubinemia with the aggravation of the disease. Close monitoring of high-risk factors of neonatal hyperbilirubinemia (including preterm infants, intrauterine distress, neonatal asphyxia, amniotic fluid pollution, sepsis, omphalitis, erythrocyte glucose-6-phosphate dehydrogenase defect, and delayed passage of meconium) and strengthening perinatal health care and high-risk pregnancy management can reduce the incidence of pathological jaundice.