Rheumatologists' perspective on coronavirus disease 19 (COVID-19) and potential therapeutic targets
Rheumatologists' perspective on coronavirus disease 19 (COVID-19) and potential therapeutic targets
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DOI：
10.1007/s10067-020-05073-9
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发表时间：
2020-04-10
影响因子：
3.4
通讯作者：
Zimba, Olena
中科院分区：
文献类型：
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作者：
Misra, Durga Prasanna;Agarwal, Vikas;Zimba, Olena
由严重急性呼吸系统综合征冠状病毒2型（SARS-CoV-2）引起的持续大流行性冠状病毒病19（COVID-19）是全球关注的问题。空气污染和吸烟等环境因素以及合并症（高血压、糖尿病和潜在的心肺疾病）可能会增加COVID-19的严重程度。风湿病的表现，如关节痛和关节炎可能是普遍的约七分之一的个人。COVID-19可导致急性间质性肺炎、心肌炎、白细胞减少症（伴淋巴细胞减少症）和血小板减少症，也见于狼疮和干燥综合征等风湿性疾病。一部分患者的严重疾病可能是由细胞因子风暴引起的，可能是由于继发性噬血细胞性淋巴组织细胞增多症（HLH），类似于全身性发作的幼年特发性关节炎或成人发作的斯蒂尔病。在这种新兴疾病缺乏高质量证据的情况下，了解发病机制可能有助于假设潜在的治疗方法。血管紧张素转换酶2（ACE 2）似乎对病毒进入肺细胞很重要; ACE抑制剂或布洛芬引起的ACE 2失衡可能易患严重疾病。初步证据表明氯喹或羟氯喹具有潜在益处。抗病毒药物，如洛匹那韦/利托那韦，法匹拉韦和remdesivir也正在探索中。细胞因子风暴和继发性HLH可能需要加强免疫抑制方案。目前的国际社会建议，接受免疫抑制治疗的风湿性疾病患者在COVID-19感染期间不应停止糖皮质激素，尽管可能使用最小剂量。应继续使用改善疾病的药物;根据标准实践，在感染发作期间可以考虑停止。疫苗的开发可能是唯一有效的长期保护这种疾病。
The ongoing pandemic coronavirus disease 19 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a matter of global concern. Environmental factors such as air pollution and smoking and comorbid conditions (hypertension, diabetes mellitus and underlying cardio-respiratory illness) likely increase the severity of COVID-19. Rheumatic manifestations such as arthralgias and arthritis may be prevalent in about a seventh of individuals. COVID-19 can result in acute interstitial pneumonia, myocarditis, leucopenia (with lymphopenia) and thrombocytopenia, also seen in rheumatic diseases like lupus and Sjogren's syndrome. Severe disease in a subset of patients may be driven by cytokine storm, possibly due to secondary hemophagocytic lymphohistiocytosis (HLH), akin to that in systemic onset juvenile idiopathic arthritis or adult-onset Still's disease. In the absence of high-quality evidence in this emerging disease, understanding of pathogenesis may help postulate potential therapies. Angiotensin converting enzyme 2 (ACE2) appears important for viral entry into pneumocytes; dysbalance in ACE2 as caused by ACE inhibitors or ibuprofen may predispose to severe disease. Preliminary evidence suggests potential benefit with chloroquine or hydroxychloroquine. Antiviral drugs like lopinavir/ritonavir, favipiravir and remdesivir are also being explored. Cytokine storm and secondary HLH might require heightened immunosuppressive regimens. Current international society recommendations suggest that patients with rheumatic diseases on immunosuppressive therapy should not stop glucocorticoids during COVID-19 infection, although minimum possible doses may be used. Disease-modifying drugs should be continued; cessation may be considered during infection episodes as per standard practices. Development of a vaccine may be the only effective long-term protection against this disease.