Bowles N E, Bayston T A, Zhang H Y, Doyle D, Lane R J, Cunningham L, Archard L C
Department of Biochemistry, Charing Cross and Westminster Medical School, London, England.
J Med. 1993;24(2-3):145-60.
Molecular hybridization using an enterovirus group specific probe detected virus RNA in muscle biopsy samples from 25 of 96 cases of inflammatory muscle disease and similarly from 41 of 158 cases of postviral fatigue syndrome (PFS). Enterovirus RNA was detected in only two of 152 samples of control muscle. The inflammatory myopathy group comprised patients with polymyositis (PM), juvenile dermatomyositis (JDM) or adult dermatomyositis (DM), and all showed the presence of an inflammatory infiltrate and fiber necrosis on histological examination of a muscle biopsy sample. In contrast, muscle samples from the PFS group were histologically normal except for non-specific changes such as occasional single fiber atrophy. By analogy with enteroviral myocarditis, which can progress to a post-inflammatory disease with persistence of virus in myocardium and disposes to the rapid development of dilated cardiomyopathy, we propose that PFS syndrome may be a sequela of a previous inflammatory viral myopathy.
使用肠道病毒属特异性探针进行的分子杂交在96例炎性肌病患者中的25例肌肉活检样本以及158例病毒感染后疲劳综合征(PFS)患者中的41例肌肉活检样本中检测到了病毒RNA。在152份对照肌肉样本中,仅在两份样本中检测到肠道病毒RNA。炎性肌病组包括多发性肌炎(PM)、青少年皮肌炎(JDM)或成人皮肌炎(DM)患者,所有患者的肌肉活检样本组织学检查均显示存在炎性浸润和纤维坏死。相比之下,PFS组的肌肉样本除了偶尔出现单纤维萎缩等非特异性变化外,组织学上正常。类比肠道病毒性心肌炎,其可进展为炎症后疾病,病毒持续存在于心肌中,并易于快速发展为扩张型心肌病,我们提出PFS综合征可能是先前炎性病毒性肌病的后遗症。