中国现代神经疾病杂志 ›› 2022, Vol. 22 ›› Issue (9): 770-776. doi: 10.3969/j.issn.1672-6731.2022.09.005

• 神经系统免疫性疾病 • 上一篇    下一篇

2 视神经炎合并慢性乙型肝炎病毒感染临床分析

刘雪菲, 王佳伟   

  1. 100730 首都医科大学附属北京同仁医院神经内科
  • 收稿日期:2022-09-05 出版日期:2022-09-25 发布日期:2022-10-10
  • 通讯作者: 王佳伟,Email:wangjwcq@163.com

Clinical analysis of optic neuritis with chronic hepatitis B virus infection

LIU Xue-fei, WANG Jia-wei   

  1. Department of Neurology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China
  • Received:2022-09-05 Online:2022-09-25 Published:2022-10-10

摘要: 目的 总结视神经炎合并慢性乙型肝炎病毒(HBV)感染临床特征,评估不同治疗方案有效性,以及视神经炎复发、视力预后及HBV再激活、肝功能、肝脏结构变化。方法与结果 纳入2015年1月至2021年6月首都医科大学附属北京同仁医院收治的19例(23眼)呈急性病程的视神经炎合并慢性HBV感染患者,女性13例、男性6例,单眼发病15例,呈单向病程17例,仅6例发生视盘水肿,发病后进展至视力最差时间(达峰时间)为3(2,7) d,重度视功能损害16/23眼。MRI增强扫描显示视神经眶内段、管内段或颅内段异常信号,甚至累及鞘膜和视交叉。自身免疫抗体检测抗核抗体阳性5例、抗干燥综合征A型抗体弱阳性1例;脑脊液压力降低1/7例、白细胞计数增加2/7例。HBV DNA阳性组(HBV DNA ≥ 100 IU/ml,10例11眼)甲泼尼龙冲击并序贯治疗前后重度视功能损害比例均高于HBV DNA阴性组(HBV DNA < 100 IU/ml,9例12眼;Fisher确切概率法:P=0.005,0.003);HBV DNA阳性组激素治疗同时加用恩替卡韦,随访期间无视神经炎复发病例;HBV DNA阴性组未行抗病毒治疗,1例进展为肝硬化、3例肝功能异常、2例HBV再激活。结论 视神经炎合并慢性HBV感染患者视功能损害严重,且对激素冲击治疗反应欠佳,HBV DNA阳性患者视功能损害较阴性者更严重,建议视神经炎合并慢性HBV感染患者激素治疗同时预防性应用抗病毒药物。

关键词: 视神经炎, 乙型肝炎,慢性, 糖皮质激素类, 免疫抑制法, 药物疗法, 预后

Abstract: Objective To summarize the clinical features of optic neuritis (ON) complicated with chronic hepatitis B virus (HBV) infection, and evaluate the effectiveness of different treatment regimens, recurrence of ON, visual prognosis, HBV reactivation, liver function and liver structure changes. Methods and Results Total 19 patients (23 eyes) with acute ON complicated with chronic HBV infection admitted to Beijing Tongren Hospital, Capital Medical University from January 2015 to June 2021 were included. There were 13 females and 6 males, 15 cases with monocular onset, 17 cases with unidirectional course of disease, and 6 cases with optic disc edema. The time to the worst visual acuity (peak time) was 3 (2, 7) d after onset, and 16/23 eyes had severe visual impairment. Enhanced MRI showed abnormal intensity in orbital, intraductal or intracranial segments of optic nerve, even involving optic nerve sheath and optic chiasm. Anti-nuclear antibody (ANA) was positive in 5 cases and A type Sjögren's syndrome antibody (SSA) was weakly positive in one case. Cerebrospinal fluid (CBF) pressure decreased in 1/7 cases and white blood cell count increased in 2/7 cases. HBV DNA positive group (HBV DNA ≥ 100 IU/ml, 10 cases and 11 eyes) had more severe visual impairment than negative group (HBV DNA < 100 IU/ml, 9 cases and 12 eyes), the difference was statistically significant (Fisher's exact probability:P=0.005, 0.003). HBV DNA positive group was treated with entecavir, and the recurrence of ON was ignored during follow-up. HBV DNA negative group didn't receive antiviral therapy, one case progressed to cirrhosis, 3 cases had abnormal liver function, and 2 cases had HBV reactivation. Conclusions The visual function of patients with ON complicated with chronic HBV infection was seriously impaired, and the response to glucocorticoid therapy was not good. The visual impairment of patients with positive HBV DNA was more serious than patients with negative HBV DNA. Patients with ON complicated with chronic HBV infection should be treated with antiviral drugs in combination with glucocorticoid therapy.

Key words: Optic neuritis, Hepatitis B, chronic, Glucocorticoids, Immunosuppression, Drug therapy, Prognosis