新型冠状病毒相关性吉兰-巴雷综合征的临床特征分析
摘要
摘要：目的：探究新型冠状病毒（SARS-CoV-2）相关性GBS的相关临床特征。方法：回顾性收集2022年1月至2023年3月期间在青岛大学附属医院确诊为GBS的患者资料43例，根据发病前6周内有无新冠感染将其分为SARS-COV-2组（n=21）和对照组（n=22），收集患者临床病史、检验检查结果、治疗及短期预后等资料进行统计学分析，比较组间差异。结果：SARS-COV-2组患者神经电生理检查结果显示脱髓鞘损害明显高于对照组（p=0.001），并且病情进展严重（p=0.015）、短期预后较差（p=0.046），血液和脑脊液化验指标无差异，特异性神经节苷脂抗体阳性率未见明显差异。 结论：GBS是SARS-CoV-2相关严重并发症之一，且多呈现为AIDP型，病情进展严重和不良预后发生率相对较高，可能与SARS-CoV-2感染引起的相关免疫机制有关。
关键词
镜像
|参考
van Doorn P A. Diagnosis, treatment and prognosis of Guillain-Barré syndrome (GBS)[J]. Presse Medicale (Paris, France: 1983), 2013, 42(6 Pt 2): e193-201.
Laman J D, Huizinga R, Boons G J, et al. Guillain-Barré syndrome: expanding the concept of molecular mimicry[J]. Trends in Immunology, 2022, 43(4): 296-308.
Wiersinga W J, Rhodes A, Cheng A C, et al. Pathophysiology, Transmission, Diagnosis, and Treatment of Coronavirus Disease 2019 (COVID-19): A Review[J]. JAMA, 2020, 324(8): 782-793.
Baig A M, Khaleeq A, Ali U, et al. Evidence of the COVID-19 Virus Targeting the CNS: Tissue Distribution, Host-Virus Interaction, and Proposed Neurotropic Mechanisms[J]. ACS chemical neuroscience, 2020, 11(7): 995-998.
Al-Ramadan A, Rabab’h O, Shah J, et al. Acute and Post-Acute Neurological Complications of COVID-19[J]. Neurology International, 2021, 13(1): 102-119.
Gogia B, Pujara D, Thottempudi N, et al. Impact of Acute Confusional State in Patients With COVID-19 and a Predictive Score[J]. Cureus, 2021, 13(9): e18360.
Zhao H, Shen D, Zhou H, et al. Guillain-Barré syndrome associated with SARS-CoV-2 infection: causality or coincidence?[J]. The Lancet. Neurology, 2020, 19(5): 383-384.
Kajumba M M, Kolls B J, Koltai D C, et al. COVID-19-Associated Guillain-Barre Syndrome: Atypical Para-infectious Profile, Symptom Overlap, and Increased Risk of Severe Neurological Complications[J]. SN comprehensive clinical medicine, 2020, 2(12): 2702-2714.
Desforges M, Le Coupanec A, Dubeau P, et al. Human Coronaviruses and Other Respiratory Viruses: Underestimated Opportunistic Pathogens of the Central Nervous System?[J]. Viruses, 2019, 12(1): 14.
Godschalk P C R, Heikema A P, Gilbert M, et al. The crucial role of Campylobacter jejuni genes in anti-ganglioside antibody induction in Guillain-Barre syndrome[J]. The Journal of Clinical Investigation, 2004, 114(11): 1659-1665.
Zheng X, Fang Y, Song Y, et al. Is there a causal nexus between COVID-19 infection, COVID-19 vaccination, and Guillain-Barré syndrome?[J]. European Journal of Medical Research, 2023, 28(1): 98.
Dalakas M C. Pathogenesis of immune-mediated neuropathies[J]. Biochimica Et Biophysica Acta, 2015, 1852(4): 658-666.
Zhou Z, Kang H, Li S, et al. Understanding the neurotropic characteristics of SARS-CoV-2: from neurological manifestations of COVID-19 to potential neurotropic mechanisms[J]. Journal of Neurology, 2020, 267(8): 2179-2184.
Lucchese G, Flöel A. SARS-CoV-2 and Guillain-Barré syndrome: molecular mimicry with human heat shock proteins as potential pathogenic mechanism[J]. Cell Stress & Chaperones, 2020, 25(5): 731-735.
Wang Y, Zhang J, Luo P, et al. Tumor necrosis factor-α in Guillain-Barré syndrome, friend or foe?[J]. Expert Opinion on Therapeutic Targets, 2017, 21(1): 103-112.
Zanin L, Saraceno G, Panciani P P, et al. SARS-CoV-2 can induce brain and spine demyelinating lesions[J]. Acta Neurochirurgica, 2020, 162(7): 1491-1494.
Li Z, Huang Z, Li X, et al. Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID-19-associated Guillain-Barré syndrome[J]. Cell Proliferation, 2021, 54(5): e13024.
Li X L, Dou Y C, Liu Y, et al. Atorvastatin ameliorates experimental autoimmune neuritis by decreased Th1/Th17 cytokines and up-regulated T regulatory cells[J]. Cellular Immunology, 2011, 271(2): 455-461.
Shi P, Qu H, Nian D, et al. Treatment of Guillain-Barré syndrome with Bifidobacterium infantis through regulation of T helper cells subsets[J]. International Immunopharmacology, 2018, 61: 290-296.
Chen X, Guo Y, Han R, et al. Class I PI3K inhibitor ZSTK474 attenuates experimental autoimmune neuritis by decreasing the frequency of Th1/Th17 cells and reducing the production of proinflammatory cytokines[J]. Cellular Immunology, 2018, 329: 41-49.
Liu S, Liu Y, Xiao Z, et al. Th17 cells and their cytokines serve as potential therapeutic target in experimental autoimmune neuritis[J]. Brain and Behavior, 2019, 9(12): e01478.