ABSTRACT
Objective:To study the clinical value of blood neutrophil gelatinase-associated lipocalin (NGAL) in the early diagnosis and prognostic evaluation of late-onset sepsis in very/extremely low birth weight infants (VLBWI/ELBWI).Method:From January 2017 to December 2019, VLBWI/ELBWI older than 3 days admitted to NICU of our hospital were prospectively enrolled in the study. The infants were assigned into suspected-sepsis group and non-infection (control) group according to their clinical symptoms and laboratory indicators. In the suspected-sepsis group, complete blood count, C-reactive protein (CRP), procalcitonin (PCT) and blood culture were examined on the 1st day of disease onset and blood NGAL was examined on the 1st day of disease onset, 3rd day of treatment and 2nd week of treatment. In the control group, blood NGAL was examined at the time of enrollment. The suspected-sepsis group was later assigned into sepsis group and non-sepsis infection group and the sepsis group was further assigned into mild sepsis group and severe sepsis group according to the severity of the disease. Blood NGAL levels between the sepsis group and the non-sepsis infection group on the 1st day of onset and the control group were compared. The dynamic changes of NGAL in the sepsis group and the non-sepsis infection group at different time points were compared and analyzed. ROC curve of NGAL level on the first day of onset predicting sepsis was drawn.Result:(1) On the 1st day of disease, the sepsis group (n=106) had higher level of NGAL compared with non-sepsis infection group (n=121) and the control group (n=84). Non-sepsis infection group had significantly higher level of NGAL compared with the control group ( P<0.05). (2) A gradual decrease of NGAL was found in both sepsis and non-sepsis infection group. Significantly higher level of NGAL in sepsis group was found comparing with non-sepsis infection group at different time points ( P<0.05). (3) For blood culture positive and negative patients in the sepsis group, no statistically significant differences existed in NGAL,CRP, PCT levels on the 1st day of disease onset ( P>0.05).(4) The NGAL level in the severe sepsis group was significantly higher than the mild sepsis group on the 1st day of disease onset ( P<0.05). However,CRP and PCT showed no differences between the two groups. (5) On the 1st day of disease onset, to establish the diagnosis of sepsis, the area under the ROC curve of NGAL level was 0.852. The sensitivity and specificity of cut-off value 205.25 ng/ml were 84.0% and 66.9%, respectively. Conclusion:The serum NGAL level is elevated in VLBWI/ELBWI with late-onset sepsis. The more severe the sepsis,the more elevated the NGAL level. NGAL has certain predictive value for late onset sepsis in VLBWI/ELBWI.
ABSTRACT
Objective To study the clinical significance of globus pallidus signal intensity and the intensity ratio of globus pallidus and putamen (G/P ratio) on magnetic resonance T1WI for the early recognition of neonatal bilirubin encephalopathy.Method From January to December 2017,full-term neonates with hyperbilirubinemia admitted to the neonatology department of our hospital were enrolled in the case group,and full-term neonates without hyperbilirubinemia in the control group.The clinical data,globus pallidus T1WI signal intensity,G/P ratio and the follow-up data were collected.According to the level of hyperbilirubinemia,the neonates in the case group were further assigned into mild hyperbilirubinemia group (serum bilirubin:222 to ＜256 μmol/L),moderate hyperbilirubinemia group (serum bilirubin:256 to ＜342 μmol/L),and severe hyperbilirubinemia group (serum bilirubin:≥ 342 μmol/L).According to the injury score of ABE,the neonates with ABE were assigned into mild ABE group,moderate ABE group and severe ABE group.The correlation of globus pallidus T1WI and T2WI signal values,G/P ratio and the serum bilirubin level and ABE degree were analyzed;receiver operating characteristic (ROC) curve was drawn to explore the predictive value of the T1WI signal value and G/P ratio for the diagnosis of ABE;the changes of globus pallidus T1WI and T2WI signal values during the first 6 months after birth and the results of follow-up to 1 year after discharge were also analyzed.Result A total of 175 neonates were included in the case group (65 in the mild hyperbilirubinemia group,71 in the moderate hyperbilirubinemia group and 39 in the severe hyperbilirubinemia group) and 43 neonates in the control group.39 neonates were diagnosed as ABE (21 mild ABE,12 moderate ABE,and 6 severe ABE).The first T1WI signal value and G/P ratio of neonates in the severe hyperbilirubinemia group was higher than the moderate hyperbilirubinemia group,the mild hyperbilirubinemia group and the control group;the T1WI signal value and G/P ratio in the moderate hyperbilirubinemia group was higher than the mild hyperbilirubinemia group and the control group (P ＜ 0.05).No significant difference existed between the mild group and the control group(P ＞ 0.05).T2WI values showed no differences among neonates with different bilirubin levels (P ＞ 0.05).The first T1WI signal value and G/P ratio in the severe ABE group were significantly higher than the moderate and mild ABE group,and the moderate ABE group higher than the mild ABE group (P ＜ 0.05).The ROC curve indicated the optimal cut-off value of T1WI signal and G/P ratio were 628 and 1.38,respectively.Among all the 175 neonates,9 had a decrease in T1WI signal value and an increase in T2WI signal value at 6 months after birth.After 1 year of follow-up visits,7 children were finally diagnosed as chronic bilirubin encephalopathy.All these children had increased signal intensity on T1WI in the acute phase,plus a decreased T1WI signal and an increased T2WI signal in 1 ～ 6 months after birth.Conclusion The globus pallidus T1WI signal and G/P ratio are closely related to the serum bilirubin level and ABE severity.If T1WI signal value ＞ 628 or G/P value ＞ 1.38,ABE should be considered.The T1WI signal value and G/P ratio play important roles as indicators for the early recognition of neonatal bilirubin encephalopathy.