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Purinergic Signaling of ATP in COVID-19 Associated Guillain-Barré Syndrome.
新型冠状病毒肺炎相关吉兰-巴雷综合征中ATP的嘌呤能信号传导。
- 影响因子:25.02
- DOI:10.1007/s11481-020-09980-1
- 作者列表:"Simões JLB","Bagatini MD
- 发表时间:2021-03-01
Abstract
:Declared as a global public health emergency, coronavirus disease 2019 (COVID-19) is presented as a disease of the respiratory tract, although severe cases can affect the entire organism. Several studies have shown neurological symptoms, ranging from dizziness and loss of consciousness to cerebrovascular and neurodegenerative diseases. In this context, Guillain-Barré syndrome, an immune-mediated inflammatory neuropathy, has been closely associated with critical cases of infection with "severe acute respiratory syndrome of coronavirus 2" (SARS-CoV-2), the etiological agent of COVID-19. Its pathophysiology is related to a generalized inflammation that affects the nervous system, but neurotropism was also revealed by the new coronavirus, which may increase the risk of neurological sequel, as well as the mortality of the disease. Thus, considering the comorbidities that SARS-CoV-2 infection can promote, the modulation of purinergic signaling can be applied as a potential therapy. In this perspective, given the role of adenosine triphosphate (ATP) in neural intercommunication, the P2X7 receptor (P2X7R) acts on microglia cells and its inhibition may be able to reduce the inflammatory condition of neurodegenerative diseases. Finally, alternative measures to circumvent the reality of the COVID-19 pandemic need to be considered, given the severity of critical cases and the viral involvement of multiple organs.
摘要
: 宣布为全球公共卫生紧急情况,冠状病毒疾病2019 (新型冠状病毒肺炎) 被认为是呼吸道疾病,尽管严重的病例可能会影响整个生物体。几项研究表明神经系统症状,从头晕和意识丧失到脑血管和神经退行性疾病。在这种情况下,吉兰-巴雷综合征是一种免疫介导的炎症性神经病,与新型冠状病毒肺炎的病因 “冠状病毒2严重急性呼吸综合征” (SARS-CoV-2) 感染的严重病例密切相关。其病理生理学与影响神经系统的全身炎症有关,但新冠状病毒也揭示了神经嗜性,这可能增加神经系统后遗症的风险以及疾病的死亡率。因此,考虑到SARS-CoV-2感染可以促进的合并症,嘌呤能信号传导的调节可以用作潜在的疗法。从这个角度来看,鉴于三磷酸腺苷 (ATP) 在神经相互通讯中的作用,P2X7受体 (P2X7R) 作用于小胶质细胞,其抑制作用可能能够减轻神经退行性疾病的炎症状况。最后,鉴于严重病例的严重性和多个器官的病毒参与,需要考虑规避新型冠状病毒肺炎大流行现实的替代措施。
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METHODS::Purpose: To report on ocular Vogt-Koyanagi-Harada (VKH)-like syndrome under vemurafenib treatment for metastatic melanoma.Design: A case report.Method: Description of clinical and imaging manifestations including fundus photography, fluorescein, and indocyanine green angiography.Results: A 46-year-old Thai female was diagnosed with metastatic melanoma of the skin and had been treated with multiple surgical excisions, radiotherapy, and vemurafenib (initial dose 480 mg orally twice daily, subsequently increased to maximum dose of 960 mg twice daily). After 6 months of vemurafenib use, she complained of bilateral redness and photophobia and was diagnosed with bilateral anterior uveitis, which was topically treated. Two weeks later, her visual acuity (VA) sharply deteriorated to 20/80 and counting fingers. Ocular examination at that stage stronly resembled acute VKH disease. She exhibited intraocular inflammation, and her fundus examination revealed bilateral optic disc swelling and serous retinal detachment. Fluorescein angiogram showed disc leakage and multiple pinpoint hyperfluorescence leakage spots and indocyanine green demonstrated multiple hypofluorescent spots. Oral prednisolone 30 mg/day was commenced while vemurafenib medication was ceased. Three weeks later, her vision improved, and serous retinal detachment subsided. However, her cutaneous melanoma recurred.Conclusions: Vemurafenib, a potential adjunct treatment for metastatic melanoma, was complicated by the development of panuveitis, papillitis, and multiple serous detachments. These ocular symptoms were similar to the presentation of acute VKH syndrome.
METHODS::Comprehensive reviews of the clinical characteristics and pathogenesis of Aicardi-Goutières syndrome (AGS), particularly its contextualization within a putative type I interferonopathy framework, already exist. However, recent reports of attempts at treatment suggest that an assessment of the field from a therapeutic perspective is warranted at this time. Here, we briefly summarize the neurological phenotypes associated with mutations in the seven genes so far associated with AGS, rehearse current knowledge of the pathology as it relates to possible treatment approaches, critically appraise the potential utility of therapies, and discuss the challenges in assessing clinical efficacy. WHAT THIS PAPER ADDS: Progress in understanding AGS disease pathogenesis has led to the first attempts at targeted treatment. Further rational therapies are expected to become available in the short- to medium-term.
METHODS::Purpose: To report the efficacy of adalimumab in a case of chronic Vogt-Koyanagi-Harada (VKH) disease refractory to conventional corticosteroids and immunosuppressive therapy and complicated by central serous chorioretinopathy (CSC).Case report: A 66-year-old woman diagnosed with VKH was treated with intravenous corticosteroids followed by oral corticosteroids and cyclosporine. However, systemic corticosteroids could not be tapered because of recurrent ocular inflammation and systemic complications (diabetes mellitus, moon face, bone weakness), while CSC appeared in both eyes. A diagnosis of chronic VKH resistant to medications complicated by corticosteroid-induced CSC was made. Systemic corticosteroids and cyclosporine were tapered and adalimumab initiated. Bilateral ocular inflammation and CSC were gradually reduced and visual acuity improved without any adverse effect. Twelve months after starting adalimumab monotherapy, no signs of active VKH and CSC were present.Conclusions: Adalimumab is one of the effective therapeutic options for refractory VKH disease complicated with corticosteroid-induced adverse effects.
神经系统自身免疫性疾病是以自身免疫细胞、免疫分子等攻击神经系统为主要致病机制的自身免疫性疾病。在免疫反应中,作用于神经系统自身抗原的致病抗体统称为神经系统自身抗体。