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空肠弯曲菌感染会引发“脱髓鞘型”吉兰-巴雷综合征吗?

Does Campylobacter jejuni infection elicit "demyelinating" Guillain-Barre syndrome?

作者信息

Kuwabara S, Ogawara K, Misawa S, Koga M, Mori M, Hiraga A, Kanesaka T, Hattori T, Yuki N

机构信息

Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.

出版信息

Neurology. 2004 Aug 10;63(3):529-33. doi: 10.1212/01.wnl.0000133205.05169.04.

DOI:10.1212/01.wnl.0000133205.05169.04
PMID:15304587
Abstract

BACKGROUND

Campylobacter jejuni enteritis is the most common antecedent infection in Guillain-Barré syndrome (GBS). C. jejuni-related GBS is usually acute motor axonal neuropathy (AMAN), but previous reports described many cases of the demyelinating subtype of GBS (acute inflammatory demyelinating polyneuropathy [AIDP]) after C. jejuni infection.

OBJECTIVE

To investigate whether C. jejuni infection elicits AIDP.

METHODS

In 159 consecutive patients with GBS, antibodies against C. jejuni were measured using ELISA. Antecedent C. jejuni infection was determined by the strict criteria of positive C. jejuni serology and a history of a diarrheal illness within the previous 3 weeks. Electrodiagnostic studies were performed weekly for the first 4 weeks, and sequential findings were analyzed.

RESULTS

There was evidence of recent C. jejuni infection in 22 (14%) patients. By electrodiagnostic criteria, these patients were classified with AMAN (n = 16; 73%) or AIDP (n = 5; 23%) or as unclassified (n = 1) in the first studies. The five C. jejuni-positive patients with the AIDP pattern showed prolonged motor distal latencies in two or more nerves and had their rapid normalization within 2 weeks, eventually all showing the AMAN pattern. In contrast, patients with cytomegalovirus- or Epstein-Barr virus-related AIDP (n = 13) showed progressive increases in distal latencies in the 8 weeks after onset.

CONCLUSION

Patients with C. jejuni-related Guillain-Barré syndrome can show transient slowing of nerve conduction, mimicking demyelination, but C. jejuni infection does not appear to elicit acute inflammatory demyelinating polyneuropathy.

摘要

背景

空肠弯曲菌肠炎是吉兰 - 巴雷综合征(GBS)最常见的前驱感染。与空肠弯曲菌相关的GBS通常为急性运动轴索性神经病(AMAN),但既往报告描述了许多空肠弯曲菌感染后出现GBS脱髓鞘亚型(急性炎症性脱髓鞘性多发性神经病[AIDP])的病例。

目的

研究空肠弯曲菌感染是否会引发AIDP。

方法

对159例连续性GBS患者采用酶联免疫吸附测定(ELISA)检测抗空肠弯曲菌抗体。根据空肠弯曲菌血清学阳性及前3周内有腹泻病史的严格标准确定前驱空肠弯曲菌感染。在最初4周每周进行电诊断研究,并分析连续结果。

结果

22例(14%)患者有近期空肠弯曲菌感染的证据。根据电诊断标准,这些患者在首次研究中被分类为AMAN(n = 16;73%)或AIDP(n = 5;23%)或未分类(n = 1)。5例有空肠弯曲菌阳性且呈AIDP模式的患者在两条或更多神经中表现出运动远端潜伏期延长,并在2周内迅速恢复正常,最终均表现为AMAN模式。相比之下,巨细胞病毒或爱泼斯坦 - 巴尔病毒相关AIDP患者(n = 13)在发病后8周内远端潜伏期呈进行性增加。

结论

空肠弯曲菌相关吉兰 - 巴雷综合征患者可出现神经传导的短暂减慢,类似脱髓鞘,但空肠弯曲菌感染似乎不会引发急性炎症性脱髓鞘性多发性神经病。

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