COVID-19 vaccine affects neither prothrombotic antibody profile nor thrombosis in primary anti-phospholipid syndrome: a prospective study.
COVID-19 vaccine affects neither prothrombotic antibody profile nor thrombosis in primary anti-phospholipid syndrome: a prospective study.
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COVID-19 疫苗既不影响促血栓抗体谱，也不影响原发性抗磷脂综合征中的血栓形成：一项前瞻性研究
DOI：
10.1093/rheumatology/keac400
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发表时间：
2023-02-01
期刊：
影响因子：
5.5
通讯作者：
Liu, Tingting
中科院分区：
文献类型：
--
作者：
Pan, Haoyu;Tang, Zihan;Teng, Jialin;Sun, Yue;Liu, Honglei;Cheng, Xiaobing;Su, Yutong;Ye, Junna;Hu, Qiongyi;Chi, Huihui;Zhou, Zhuochao;Jia, Jinchao;Meng, Jianfen;Wang, Mengyan;Wang, Fan;Chen, Xia;Ma, Yuning;Zhang, Hao;You, Yijun;Zhu, Dehao;Chen, Longfang;Yang, Chengde;Shi, Hui;Liu, Tingting
探讨灭活 2019 冠状病毒病疫苗是否会影响原发性 APS 患者的促血栓自身抗体谱并诱导血栓事件。我们在这个前瞻性队列中招募了 39 名原发性 APS 患者，他们自愿接受了两剂灭活的严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 疫苗（BBIBPCorV，国药集团，北京，中国）。在疫苗接种前和第二剂疫苗接种后4周测定促血栓自身抗体。通过医院现场访问和评估来评估血栓性疾病。接种前和接种后4周检测到的所有11种自身抗体的存在没有显着差异：对于aCL，IgG（14 vs 16，P = = 0.64），IgM（13 vs 19，P = 0.34），IgA（2 vs 3，P = 0.64）；抗-β2GP1、IgG（12 vs 12，P = 1.00）、IgM（5 vs 8，P = 0.36）、IgA（4 vs 3，P = 0.69）；抗PS/PT IgG（13 vs 16，P = 0.48），IgM（17 vs 22，P = 0.26）； LAC（22 vs 28，P = 0.16）； aPF4-肝素（0 vs 0，P = 1.00）和 ANA（23 vs 26，P = 0.48）。值得注意的是，接种前和接种后队列中aPL谱的分布不受SARS-CoV-2疫苗接种的影响：分别为低风险aPL谱的患者（11 vs 10，P = 0.799）和高风险aPL谱的患者（28 vs 29，P = 0.799）。此外，在最短 12 周的随访期内，没有病例表现出血栓性疾病的症状。 SARS-CoV-2 疫苗接种后正在进行的治疗方案没有调整。灭活 SARS-CoV-2 疫苗不会影响原发性 APS 患者的抗磷脂抗体和抗 PF4 肝素抗体的特征，也不会诱发血栓事件。
To explore whether inactivated coronavirus disease 2019 vaccine influences the profile of prothrombotic autoantibodies and induces thrombotic events in primary APS patients. We enrolled 39 primary APS patients who received two doses of inactivated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine (BBIBPCorV, Sinopharm, Beijing, China) voluntarily in this prospective cohort. Prothrombotic autoantibodies were determined before vaccination and 4 weeks after the second dose of vaccination. Thrombotic disorders were evaluated via hospital site visits and assessments. There was no significant difference in the presence of all 11 autoantibodies detected before and 4 weeks after vaccination: for aCL, IgG (14 vs 16, P = 0.64), IgM (13 vs 19, P = 0.34), IgA (2 vs 3, P = 0.64); anti-β2GP1, IgG (12 vs 12, P = 1.00), IgM (5 vs 8, P = 0.36), IgA (4 vs 3, P = 0.69); anti-PS/PT IgG (13 vs 16, P = 0.48), IgM (17 vs 22, P = 0.26); LAC (22 vs 28, P = 0.16); aPF4-heparin (0 vs 0, P = 1.00) and ANA (23 vs 26, P = 0.48). Notably, the distribution of the aPL profile in the pre- and post-vaccination cohorts was not affected by SARS-CoV-2 vaccination: for patients with a low-risk aPL profile (11 vs 10, P = 0.799) and patients with a high-risk aPL profile (28 vs 29, P = 0.799), respectively. Furthermore, no case exhibited symptoms of the thrombotic disorder during a minimum follow-up period of 12 weeks. There was no adjustment to the ongoing treatment regimens following SARS-CoV-2 vaccination. Inactivated SARS-CoV-2 vaccine does not influence the profile of anti-phospholipid antibodies and anti-PF4-heparin antibodies nor induces thrombotic events in primary APS patients.
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