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婴儿登革出血热:临床与细胞因子谱研究

Dengue hemorrhagic fever in infants: a study of clinical and cytokine profiles.

作者信息

Nguyen Thanh Hung, Lei Huan-Yao, Nguyen Trong Lan, Lin Yee-Shin, Huang Kao-Jean, Le Bich Lien, Lin Chiou-Feng, Yeh Trai-Ming, Do Quang Ha, Vu Thi Que Huong, Chen Lien-Cheng, Huang Jyh-Hsiung, Lam Thi My, Liu Ching-Chuan, Halstead Scott B

机构信息

Department of Dengue Hemorrhagic Fever, Children's Hospital No. 1-Ho Chi Minh City, Vietnam.

出版信息

J Infect Dis. 2004 Jan 15;189(2):221-32. doi: 10.1086/380762. Epub 2004 Jan 9.

DOI:10.1086/380762
PMID:14722886
Abstract

A prospective study of clinical and cytokine profiles of 107 infants with dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS) was conducted. Fever, petechiae on the skin, and hepatomegaly were the most common clinical findings associated with DHF/DSS in infants. DSS occurred in 20.5% of the patients. Hemoconcentration and thrombocytopenia were observed in 91.5% and 92.5% of the patients, respectively. Serologic testing revealed that almost all of the patients (95.3%) had primary dengue virus infections. These data demonstrate that clinical and laboratory findings of DHF/DSS in infants are compatible with the World Health Organization's clinical diagnostic criteria for pediatric DHF. The present study is the first to report evidence of production of cytokines in infants with DHF/DSS and to describe the difference between the cytokine profile of infants with primary dengue virus infections and children with secondary infections. Overproduction of both proinflammatory cytokines (interferon-gamma and tumor necrosis factor-alpha) and anti-inflammatory cytokines (interleukin-10 and -6) may play a role in the pathogenesis of DHF/DSS in infants.

摘要

对107例登革出血热(DHF)/登革休克综合征(DSS)婴儿的临床和细胞因子谱进行了一项前瞻性研究。发热、皮肤瘀点和肝肿大是婴儿DHF/DSS最常见的临床发现。20.5%的患者发生了DSS。分别有91.5%和92.5%的患者出现血液浓缩和血小板减少。血清学检测显示,几乎所有患者(95.3%)为原发性登革病毒感染。这些数据表明,婴儿DHF/DSS的临床和实验室检查结果符合世界卫生组织小儿DHF的临床诊断标准。本研究首次报告了DHF/DSS婴儿产生细胞因子的证据,并描述了原发性登革病毒感染婴儿与继发性感染儿童细胞因子谱的差异。促炎细胞因子(干扰素-γ和肿瘤坏死因子-α)和抗炎细胞因子(白细胞介素-10和-6)的过度产生可能在婴儿DHF/DSS的发病机制中起作用。

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