Prospective study on the relationship between infections and multiple sclerosis exacerbations
Prospective study on the relationship between infections and multiple sclerosis exacerbations
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DOI：
10.1093/brain/awf098
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发表时间：
2002-05-01
期刊：
影响因子：
14.5
通讯作者：
Hintzen, RQ
中科院分区：
文献类型：
--
作者：
Buljevac, D;Flack, HZ;Hintzen, RQ
多发性硬化症的特征之一是不可预测的发作和缓解。这些疾病活动的波动与（自身）免疫活动的改变有关。病情恶化导致短期发病，但也可能影响长期残疾。这项对73例复发缓解型多发性硬化症患者的纵向研究评估了全身性感染对病情恶化自然过程的影响。此外，我们分析了感染是否会导致钆增强病变数量的增加。在6466患者周内共观察到167例感染和145例恶化。在临床感染（主要是上呼吸道感染）发病前2周至发病后5周的预先确定的高危期（ARP）内，加重的风险增加（率比2.1），这与以往的研究一致。与ARP之外发作的加重相比，ARP期间发作的加重更频繁地导致持续的缺陷[增加大于或等于1个扩展残疾状态量表（EDSS）点或大于或等于0.5个EDSS 5.5以上，持续3个月]，比率比为3.8。轻微和严重加重在ARP和非ARP发作组之间分布均匀。ARP加重与炎症标志物可溶性细胞内粘附分子1的血浆水平显著高于非ARP加重相关，表明ARP复发期间免疫激活相对增强。在感染发作后6周内进行三次连续MRI扫描。在三个时间点之间钆增强病变的数量没有差异。总之，在全身性感染情况下的恶化比其他恶化导致更持久的损害。没有迹象表明这种作用是通过加强血脑屏障的开放而发生的。
One of the characteristics of multiple sclerosis is the unpredictable occurrence of exacerbations and remissions. These fluctuations in disease activity are related to alterations in (auto-)immune activity. Exacerbations lead to short-term morbidity, but may also influence long-term disability. This longitudinal study in 73 patients with relapsing-remitting multiple sclerosis assessed the contribution of systemic infections to the natural course of exacerbations. In addition, we analysed whether infections lead to an increase in the number of gadolinium-enhancing lesions. A total of 167 infections and 145 exacerbations were observed during 6466 patient weeks. During a predefined at-risk period (ARP) of 2 weeks before until 5 weeks after the onset of a clinical infection (predominantly upper airway infections), there was an increased risk of exacerbations (rate ratio 2.1), which is in accordance with previous studies. Exacerbations with onset during the ARP led more frequently to sustained deficit [increase of greater than or equal to1 Expanded Disability Status Scale (EDSS) point or greater than or equal to0.5 above EDSS 5.5 for >3 months] than exacerbations with onset outside the ARP, with a rate ratio of 3.8. Minor and major exacerbations were equally distributed between the ARP and non-ARP onset groups. ARP exacerbations were associated with significantly higher plasma levels of the inflammatory marker soluble intracellular adhesion molecule 1 than non-ARP exacerbations, indicating relatively enhanced immune activation during ARP relapses. Three serial MRI scans were performed after the onset of an infection over a 6-week period. There was no difference in the number of gadolinium-enhancing lesions between the three time points. In conclusion, exacerbations in the context of a systemic infection lead to more sustained damage than other exacerbations. There is no indication that this effect occurs through enhanced opening of the bloodbrain barrier.