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Abstract：
UNASSIGNED: Echovirus type 11(E-11) can cause fatal haemorrhage-hepatitis syndrome in neonates. This study aims to investigate clinical risk factors and early markers of E-11 associated neonatal haemorrhage-hepatitis syndrome.
UNASSIGNED: This is a multicentre retrospective cohort study of 105 neonates with E-11 infection in China. Patients with haemorrhage-hepatitis syndrome (the severe group) were compared with those with mild disease. Clinical risk factors and early markers of haemorrhage-hepatitis syndrome were analysed. In addition, cytokine analysis were performed in selective patients to explore the immune responses.
UNASSIGNED: In addition to prematurity, low birth weight, premature rupture of fetal membrane, total parenteral nutrition (PN) (OR, 28.7; 95% CI, 2.8-295.1) and partial PN (OR, 12.9; 95% CI, 2.2-77.5) prior to the onset of disease were identified as risk factors of developing haemorrhage-hepatitis syndrome. Progressive decrease in haemoglobin levels (per 10 g/L; OR, 1.5; 95% CI, 1.1-2.0) and platelet (PLT) < 140 × 10⁹/L at early stage of illness (OR, 17.7; 95% CI, 1.4-221.5) were associated with the development of haemorrhage-hepatitis syndrome. Immunological workup revealed significantly increased interferon-inducible protein-10(IP-10) (P < 0.0005) but decreased IFN-α (P < 0.05) in peripheral blood in severe patients compared with the mild cases.
UNASSIGNED: PN may potentiate the development of E-11 associated haemorrhage-hepatitis syndrome. Early onset of thrombocytopenia and decreased haemoglobin could be helpful in early identification of neonates with the disease. The low level of IFN-α and elevated expression of IP-10 may promote the progression of haemorrhage-hepatitis syndrome.
UNASSIGNED: This is a multicentre retrospective cohort study of 105 neonates with E-11 infection in China. Patients with haemorrhage-hepatitis syndrome (the severe group) were compared with those with mild disease. Clinical risk factors and early markers of haemorrhage-hepatitis syndrome were analysed. In addition, cytokine analysis were performed in selective patients to explore the immune responses.
UNASSIGNED: In addition to prematurity, low birth weight, premature rupture of fetal membrane, total parenteral nutrition (PN) (OR, 28.7; 95% CI, 2.8-295.1) and partial PN (OR, 12.9; 95% CI, 2.2-77.5) prior to the onset of disease were identified as risk factors of developing haemorrhage-hepatitis syndrome. Progressive decrease in haemoglobin levels (per 10 g/L; OR, 1.5; 95% CI, 1.1-2.0) and platelet (PLT) < 140 × 10⁹/L at early stage of illness (OR, 17.7; 95% CI, 1.4-221.5) were associated with the development of haemorrhage-hepatitis syndrome. Immunological workup revealed significantly increased interferon-inducible protein-10(IP-10) (P < 0.0005) but decreased IFN-α (P < 0.05) in peripheral blood in severe patients compared with the mild cases.
UNASSIGNED: PN may potentiate the development of E-11 associated haemorrhage-hepatitis syndrome. Early onset of thrombocytopenia and decreased haemoglobin could be helpful in early identification of neonates with the disease. The low level of IFN-α and elevated expression of IP-10 may promote the progression of haemorrhage-hepatitis syndrome.
摘要：
■Echovirus11型（E-11）可导致新生儿致命的出血-肝炎综合征。本研究旨在探讨E-11相关新生儿出血-肝炎综合征的临床危险因素和早期标志物。
■这是一项对中国105例E-11感染新生儿的多中心回顾性队列研究。将出血-肝炎综合征患者（严重组）与轻度疾病患者进行比较。分析了出血-肝炎综合征的临床危险因素和早期标志物。此外,在选择性患者中进行细胞因子分析以探索免疫反应。
■除了早产，低出生体重,胎膜早破,全胃肠外营养（PN）（OR，28.7；95%CI，2.8-295.1）和部分PN（OR，12.9;95％CI，2.2-77.5）在发病前被确定为发生出血-肝炎综合征的危险因素。血红蛋白水平逐渐降低(每10克/升；OR，1.5；95％CI，1.1-2.0）和血小板（PLT）<140×10²/L（OR，17.7；95％CI，1.4-221.5）与出血肝炎综合征的发展有关。免疫检查显示，与轻度病例相比，重症患者外周血中干扰素诱导蛋白10（IP-10）显着增加（P<0.0005），但IFN-α降低（P<0.05）。
■PN可能促进E-11相关出血-肝炎综合征的发展。血小板减少症的早期发作和血红蛋白下降可能有助于早期识别患有该疾病的新生儿。IFN-α的低水平和IP-10的表达升高可能促进出血-肝炎综合征的进展。
■这是一项对中国105例E-11感染新生儿的多中心回顾性队列研究。将出血-肝炎综合征患者（严重组）与轻度疾病患者进行比较。分析了出血-肝炎综合征的临床危险因素和早期标志物。此外,在选择性患者中进行细胞因子分析以探索免疫反应。
■除了早产，低出生体重,胎膜早破,全胃肠外营养（PN）（OR，28.7；95%CI，2.8-295.1）和部分PN（OR，12.9;95％CI，2.2-77.5）在发病前被确定为发生出血-肝炎综合征的危险因素。血红蛋白水平逐渐降低(每10克/升；OR，1.5；95％CI，1.1-2.0）和血小板（PLT）<140×10²/L（OR，17.7；95％CI，1.4-221.5）与出血肝炎综合征的发展有关。免疫检查显示，与轻度病例相比，重症患者外周血中干扰素诱导蛋白10（IP-10）显着增加（P<0.0005），但IFN-α降低（P<0.05）。
■PN可能促进E-11相关出血-肝炎综合征的发展。血小板减少症的早期发作和血红蛋白下降可能有助于早期识别患有该疾病的新生儿。IFN-α的低水平和IP-10的表达升高可能促进出血-肝炎综合征的进展。
