Detection of enteroviral RNA in end‐stage dilated cardiomyopathy in children and adolescents

Detection of enteroviral RNA in end‐stage dilated cardiomyopathy in children and adolescents
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DOI:
10.1002/(sici)1096-9071(199812)56:4
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发表时间:
1998-12
影响因子:
12.7
通讯作者:
A. Arola;M. Kallajoki;O. Ruuskanen;T. Hyypia
A. Arola;M. Kallajoki;O. Ruuskanen;T. Hyypia
中科院分区:
医学3区
文献类型:
--
作者:
A. Arola;M. Kallajoki;O. Ruuskanen;T. Hyypia

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收集33例终末期特发性扩张型心肌病(IDCM)患儿的病历和档案心肌标本,回顾分析肠道病毒持续感染在IDCM发病机制中的作用。仔细审查每个患者的临床病史和实验室评估,以获得有关过去和诊断心肌病时感染的性质和病因的信息。64例甲醛固定、石蜡包埋的心肌标本,分别来自心内膜心肌活检(n=5)、心脏移植(n=10)或尸检(n=49),采用聚合酶链式反应(PCR)和原位杂交法检测标本中的肠道病毒RNA。对照标本包括34个甲醛固定、石蜡包埋的心肌标本,这些标本来自患有其他心肌疾病、代谢性疾病、结构性心脏缺陷或各种非心脏恶性肿瘤的儿童。以3-磷酸甘油醛脱氢酶(GAPDHm RNA)或β-肌动蛋白(Actin)m RNA扩增为阳性对照,证实细胞内存在核糖核酸。在32例有合适心肌标本的IDCM患者中,只有一例标本经聚合酶链式反应检测出肠道病毒RNA阳性。对扩增的病毒片段的序列分析表明,病毒序列与Echo病毒1有显著的同源性。来自对照患者的一份标本经聚合酶链式反应也呈阳性,但扩增的病毒片段的序列分析表明它是鼻病毒16。这些结果没有表明肠道病毒在儿童IDCM终末期中有任何显著的作用,尽管需要用新鲜冰冻标本进行前瞻性研究来证实。然而,在该年龄段IDCM发展为终末期心力衰竭的过程中,病毒持续存在以外的机制可能更重要。J.Med.维罗尔。56:364-371,1998。©1998 Wiley-Liss,Inc.
Medical records and archival myocardial specimens of 33 children and adolescents with end%stage idiopathic dilated cardiomyopathy (IDCM) were collected to evaluate retrospectively the potential role of enteroviral persistence in the pathogenesis of IDCM. The clinical history and laboratory assessment of each patient were reviewed carefully in order to obtain information on the nature and etiology of infections in the past and at the time of diagnosis of cardiomyopathy. Sixty‐four formaldehyde‐fixed, paraffin‐embedded myocardial specimens, obtained from endomyocardial biopsies (n = 5), explanted hearts (n = 10), or autopsies (n = 49), were studied by the polymerase chain reaction (PCR) and by in situ hybridization to detect enteroviral RNA in the specimens. Control specimens included 34 formaldehyde‐fixed, paraffin‐embedded myocardial specimens from children with other cardiomyopathies, metabolic diseases, structural heart defects, or various noncardiac malignancies. The presence of cellular RNA in the specimens was confirmed by amplification of glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) mRNA or β‐actin mRNA as positive controls. Only one specimen from the 32 IDCM patients with appropriate myocardial specimens was positive for enteroviral RNA by PCR. Sequence analysis of the amplified viral segment showed a significant degree of homology between the viral sequence and echovirus 1. One specimen from the control patients also appeared positive by PCR, but sequence analysis of the amplified viral segment revealed it as rhinovirus 16. The results do not indicate any significant role for enteroviral persistence in end‐stage childhood IDCM, although they need to be confirmed using a prospective study with fresh frozen specimens. However, mechanisms other than viral persistence may be more important in the progression of IDCM to end‐stage heart failure in this age group. J. Med. Virol. 56:364–371, 1998. © 1998 Wiley‐Liss, Inc.