Rapid attenuation of anti-SARS-CoV-2 antibodies in patients with musculoskeletal diseases in whom intensive immunosuppressive therapies were reinitiated after COVID-19: comment on the article by Curtis et al
Rapid attenuation of anti-SARS-CoV-2 antibodies in patients with musculoskeletal diseases in whom intensive immunosuppressive therapies were reinitiated after COVID-19: comment on the article by Curtis et al
复制标题
在 COVID-19 后重新开始强化免疫抑制治疗的肌肉骨骼疾病患者中，抗 SARS-CoV-2 抗体迅速减弱：对 Curtis 等人文章的评论
DOI：
10.1002/art.42003
复制
发表时间：
2022
影响因子：
13.3
通讯作者：
Kumanogoh Atsushi
中科院分区：
文献类型：
--
作者：
Okamoto Masashi;Kawada Shoji;Shimagami Hiroshi;Fujii Naoko;Matsukawa Kazuki;Ishikawa Nachi;Kawamoto Keisuke;Higa Shinji;Ishida Yutaka;Ogata Atsushi;Yamaguchi Yuta;Morita Takayoshi;Kato Yasuhiro;Kumanogoh Atsushi
我们怀着极大的兴趣阅读了美国风湿病学会最近发表的关于风湿和肌肉骨骼疾病（RMD）患者接种COVID-19疫苗的最新指南（1）。由于在接受某些全身免疫调节治疗的许多RMD患者中，认为对疫苗接种的预期应答可能减弱（2-4），因此建议中断或以其他方式优化某些免疫调节治疗的时机。然而，SARS-CoV-2（5）的长期免疫记忆受损仍然是感染后需要持续免疫调节治疗的RMD患者的一个问题。我们最近评估了经历自然SARS-CoV-2感染的RMD患者的纵向抗体应答，并在此报告结果。患者在日本大坂警察医院的COVID-19爆发期间感染了SARS-CoV-2。在感染后2-11个月，使用抗SARS-CoV-2刺突S1蛋白和核衣壳蛋白免疫测定法（Elecsys; Roche）对10名RMD患者进行了COVID-19后每月一次的随访血清学调查（表1）。这些患者在SARS-CoV-2感染前接受了强化免疫调节治疗，并在感染恢复后重新开始免疫抑制治疗。COVID-19的严重程度根据世界卫生组织临床进展量表（6）确定。所有患者在感染后2-3个月均表现出对SARS-CoV-2的充分抗体应答。在大多数患者中，对刺突S1蛋白的初始抗体应答维持至9-11个月。这些患者中的抗体保留与先前研究中健康个体中报告的抗体保留相当（7，8）。然而，在COVID-19后重新开始强化免疫抑制治疗的2例患者中，初始有利的尖峰S1蛋白抗体滴度下降（表1）。其中一名患者重新开始环孢菌素A（CSA）治疗（补充图1A，可在关节炎和风湿病学网站https：//onlineliphonology上获得。威利com/doi/10.1002/art.42003），另一名患者患有血小板减少症、全身水肿、发热、网硬蛋白纤维化和器官肿大（TAFRO;多中心Castleman病的一种变体[8]），重新开始每周一次皮下托珠单抗与CSA治疗（补充图1B）。强化免疫抑制治疗，如CSA治疗，可能会改变免疫记忆，有助于长期保护性免疫。相反，在COVID-19感染后暂停强化免疫抑制治疗的患者中，尖峰S1蛋白抗体应答保持稳定（补充图1C）。
We read with great interest the recently published, updated guidance from the American College of Rheumatology on COVID-19 vaccination in patients with rheumatic and musculoskeletal diseases (RMDs)(1). Because the expected response to vaccination was deemed likely to be blunted in many RMD patients receiving treatment with certain systemic immunomodulatory therapies (2–4), interrupting or otherwise optimizing the timing of some immunomodulatory therapies was recommended. However, the impairment of long-term immunologic memory of SARS–CoV-2 (5) remains a concern in RMD patients requiring continuous immunomodulatory therapies after infection. We recently assessed the longitudinal antibody response in patients with RMDs who experienced natural SARS–CoV-2 infection, and we report the results herein. Patients were infected with SARS–CoV-2 during a COVID-19 outbreak in the Daini Osaka Police Hospital in Japan. A post–COVID-19 monthly follow-up serosurvey was conducted using an anti–SARS–CoV-2 spike S1 protein and nucleocapsid protein immunoassay (Elecsys; Roche) 2–11 months postinfection in 10 patients with RMDs (Table 1). The patients were receiving intensive immunomodulatory therapies prior to SARS–CoV-2 infection, and immunosuppressive therapy was reinitiated after recovery from the infection. The severity of COVID-19 was determined based on the World Health Organization Clinical Progression Scale (6). All patients exhibited a sufficient antibody response to SARS–CoV-2 at 2–3 months postinfection. The initial antibody response to the spike S1 protein was maintained until 9–11 months in most patients. Antibody retention in these patients was comparable to that reported in healthy individuals in previous studies (7, 8).However, the initial favorable spike S1 protein antibody titer decreased in 2 patients in whom intensive immunosuppressive therapies were reinitiated after COVID-19 (Table 1). One of the patients resumed cyclosporin A (CSA) therapy (Supplementary Figure 1A, available on the Arthritis & Rheumatology website at https://onlinelibrary. wiley. com/doi/10.1002/art. 42003), and the other patient, who had thrombocytopenia, anasarca, fever, reticulin fibrosis, and organomegaly (TAFRO; a variant of multicentric Castleman’s disease [8]), resumed weekly treatment with subcutaneous tocilizumab with CSA (Supplementary Figure 1B). Intensive immunosuppressive therapy, such as treatment with CSA, may alter immunologic memory that contributes to long-term protective immunity. Conversely, the spike S1 protein antibody response remained stable in a patient in whom intensive immunosuppressive therapy was suspended after COVID-19 infection (Supplementary Figure 1C).