Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD.

Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD.
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MOG 自身抗体提示 NMOSD 两种不同的临床亚型

DOI:
10.1007/s11427-015-4997-y
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发表时间:
2016-12
影响因子:
9.1
通讯作者:
Shi, Fu-Dong
Shi, Fu-Dong
中科院分区:
生物学1区
文献类型:
--
作者:
Yan, Yaping;Li, Yujing;Fu, Ying;Yang, Li;Su, Lei;Shi, Kaibin;Li, Minshu;Liu, Qiang;Borazanci, Aimee;Liu, Yaou;He, Yong;Bennett, Jeffrey L.;Vollmer, Timothy L.;Shi, Fu-Dong

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我们研究了一组独特的视神经脊髓炎谱系障碍(NMOSD)患者,他们携带水通道蛋白-4 (AQP4)和髓鞘-少突胶质细胞糖蛋白(MOG)自身抗体。125例NMOSD患者中,AQP4-和MOG-ab双阳性10例(8.0%),MOG-ab单阳性14例(11.2%)。双阳性患者病程多期,年复发率高(P=0.0431),残障严重(P<0.0001)。双阳性患者中70%出现ms样脑病变,水肿加重,脊髓磁共振多灶区,视网膜神经纤维层厚度明显减少,视神经萎缩。相比之下,仅使用MOG-ab的患者单相病程和轻度残留残疾的比例更高。脊髓MRI显示多灶性脊髓病变伴轻度水肿,脑MRI显示侧脑室周围病变较多。同时携带AQP4和MOG自身抗体的NMOSD患者存在并表现出原型型NMO和复发缓解型MS的综合特征,而携带MOG抗体的NMOSD仅表现出介于NMOSD和MS之间的“中间”表型。我们的研究提示,MOG抗体可能在NMOSD患者中具有致病性,抗MOG抗体的测定对NMOSD患者的管理具有指导意义。
We characterized a unique group of patients with neuromyelitis optica spectrum disorder (NMOSD) who carried autoantibodies of aquaporin-4 (AQP4) and myelin-oligodendrocyte glycoprotein (MOG). Among the 125 NMOSD patients, 10 (8.0%) were AQP4- and MOG-ab double positive, and 14 (11.2%) were MOG-ab single positive. The double-positive patients had a multiphase disease course with a high annual relapse rate (P=0.0431), and severe residual disability (P<0.0001). Of the double-positive patients, 70% had MS-like brain lesions, more severe edematous, multifocal regions on spinal magnetic resonance imaging (MRI), pronounced decreases of retinal nerve fiber layer thickness and atrophy of optic nerves. In contrast, patients with only MOG-ab had a higher ratio of monophasic disease course and mild residual disability. Spinal cord MRI illustrated multifocal cord lesions with mild edema, and brain MRIs showed more lesions around lateral ventricles. NMOSD patients carrying both autoantibodies to AQP4 and MOG existed and exhibited combined features of prototypic NMO and relapsing-remitting form of MS, whereas NMOSD with antibodies to MOG only exhibited an “intermediate” phenotype between NMOSD and MS. Our study suggests that antibodies against MOG might be pathogenic in NMOSD patients and that determination of anti-MOG antibodies maybe instructive for management of NMOSD patients.
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