Department of Clinical Immunology and Rheumatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
Departments of Rheumatology and Research and Development, Dudley Group NHS Foundation Trust (Teaching Trust of the University of Birmingham, UK), Russells Hall Hospital, Dudley, West Midlands, UK.
Clin Rheumatol. 2020 Jul;39(7):2055-2062. doi: 10.1007/s10067-020-05073-9. Epub 2020 Apr 10.
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.Key Points• Patients with coronavirus disease 19 (COVID-19) may have features mimicking rheumatic diseases, such as arthralgias, acute interstitial pneumonia, myocarditis, leucopenia, lymphopenia, thrombocytopenia and cytokine storm with features akin to secondary hemophagocytic lymphohistiocytosis.• Although preliminary results may be encouraging, high-quality clinical trials are needed to better understand the role of drugs commonly used in rheumatology like hydroxychloroquine and tocilizumab in COVID-19.• Until further evidence emerges, it may be cautiously recommended to continue glucocorticoids and other disease-modifying antirheumatic drugs (DMARDs) in patients receiving these therapies, with discontinuation of DMARDs during infections as per standard practice.
正在流行的新型冠状病毒肺炎(COVID-19)是由严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的,这是一个全球性关注的问题。环境因素,如空气污染和吸烟以及合并症(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。大约有七分之一的人会出现关节痛和关节炎等风湿表现。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,这些在狼疮和干燥综合征等风湿性疾病中也可见到。在一部分患者中,严重疾病可能是由细胞因子风暴引起的,可能是由于继发噬血细胞性淋巴组织细胞增生症(HLH)所致,类似于全身型幼年特发性关节炎或成人Still 病。在这种新发疾病中缺乏高质量证据的情况下,对发病机制的理解可能有助于推测潜在的治疗方法。血管紧张素转换酶 2(ACE2)似乎对病毒进入肺细胞很重要;ACE 抑制剂或布洛芬引起的 ACE2 失衡可能使疾病恶化。氯喹或羟氯喹可能有潜在益处的初步证据。洛匹那韦/利托那韦、法维拉韦和瑞德西韦等抗病毒药物也在探索中。细胞因子风暴和继发 HLH可能需要增强免疫抑制方案。目前国际社会的建议是,COVID-19 感染期间,正在接受免疫抑制治疗的风湿性疾病患者不应停用糖皮质激素,尽管可能使用最低剂量。应继续使用疾病修饰药物;根据标准实践,在感染期间可以考虑停药。疫苗的开发可能是预防这种疾病的唯一有效长期保护措施。
关键点
• COVID-19 患者可能有类似于风湿性疾病的表现,如关节痛、急性间质性肺炎、心肌炎、白细胞减少症、淋巴细胞减少症、血小板减少症和细胞因子风暴,其特征类似于继发噬血细胞性淋巴组织细胞增生症。
• 尽管初步结果令人鼓舞,但仍需要高质量的临床试验来更好地了解羟氯喹和托珠单抗等风湿科常用药物在 COVID-19 中的作用。
• 在进一步的证据出现之前,对于正在接受这些治疗的患者,可能谨慎建议继续使用糖皮质激素和其他疾病修饰抗风湿药物(DMARDs),并根据标准实践在感染期间停用 DMARDs。