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Implications of SARS-CoV-2 infection for patients with rheumatic disease
  1. Changsong Lin1,
  2. Ziyu Wang1,
  3. Jie Li1,
  4. Xinyi Xia2,3,
  5. Yun Liu4,5,
  6. Qianghu Wang1,6
  1. 1Bioinformatics, Nanjing Medical University, Nanjing, China
  2. 2Institute of Laboratory Medicine, Nanjing University School of Medicine, Nanjing, China
  3. 3Laboratory Medicine and Blood Transfusion, Wuhan Huoshenshan Hospital, Wuhan, China
  4. 4Medical Informatics, Nanjing Medical University, Nanjing, China
  5. 5Geriatrics Endocrinology, The First Affiliated Hospital, Nanjing Medical University, Nanjing, China
  6. 6Center for Global Health, Nanjing Medical University, Nanjing, China
  1. Correspondence to Dr Changsong Lin, Bioinformatics, Nanjing Medical University, Nanjing 211166, China; lcs04bio{at}; Professor Xinyi Xia; xiaxynju{at}; Professor Yun Liu; liuyun{at}; Professor Qianghu Wang; wangqh{at}

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We read with great interest the letter by Mathian et al in the Annals of the Rheumatic Diseases. In the letter, the authors reported that hydroxychloroquine (HCQ) did not protect patients with systemic lupus erythematosus (SLE) from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in the clinical treatment. We report similar results from our study of treatment of patients with SLE on HCQ. We wish to add supplemental evidence to some of the points not adequately addressed in Mathian et al’s1 letter.

Mathian et al did not report the incidence rate of COVID-19 in patients with SLE. We agree with Mathian et al. that it is not practical to assess the actual incidence rate of SARS-CoV-2 in patients with SLE. However, we observed that during the outbreak, 6 (0.2%) cases had SLE in 3057 patients with COVID-19 who were admitted to Wuhan Huoshenshan Hospital (China). Taking that the prevalence of SLE is approximately 0.05%–0.1% in China, this may suggest that patients with SLE are susceptible to SARS-CoV-2 infection.2 3 As HCQ is the first-line drug that will be prescribed to patients with SLE, our result confirmed the observations in Mathian et al’s letter that HCQ cannot prevent patients with SLE from SARS-CoV-2 infection.

The effect of myocardial damage in SARS-CoV-2-infected patients with SLE is another interesting observation represented in the letter by Mathian et al. Cardiac injury is frequent and often silent in patients with SLE.4 However, it may cause cardiac arrest.5 Notably, in our cohort, patient 2 had congenital heart disease and other pre-existing diseases, with a short (12 days) and deteriorating course (figure 1, table 1). Prior to being admitted to the hospital, the patient’s condition had already progressed to stage IV renal failure. The patient’s condition did not improve and finally resulted in renal and heart failure. This case highlights the fact that COVID-19 may accelerate the progression to heart and kidney failure, which also supports the findings by Mathian et al.

Figure 1

Timeline showing general and symptom onset, timing of hospital admission, timing of therapy and discharge of patients with systemic lupus erythematosus and rheumatoid arthritis.

Table 1

Characteristics of 11 COVID-19 patients with systemic lupus erythematosus and rheumatoid arthritis

Our cohort included 11 COVID-19 patients with SLE (patients 1–6) and rheumatoid arthritis (RA) (patients 7–11), respectively. One patient (patient 3) suffered from both SLE and RA. The COVID-19 course duration of patients with SLE was 36 (12–66) days. Patient 6 developed severe hypertension (170/120 mm Hg), lacunar infarction, hyponatraemia, moderate anaemia and hypokalaemia during hospitalisation. Furthermore, the nucleic acid test results for SARS-CoV-2 infection for this patient were repeatedly positive during the treatment period, and SARS-CoV-2 antibody was produced after a convalescent plasma transfusion. Five patients were discharged after antiviral and antibiotic treatment, while patient 2 died. All patients with RA were female, with an overall course of 40.6 (33–55) days, which was not different from that of patients with SLE (table 1). Patients 8 and 9 only suffered from RA and SARS-CoV-2 infection, while the other four patients also had other comorbidities, such as hypertension and diabetes. The biochemical indicators of myocardial injury and liver injury in patients with RA, such as brain natriuretic peptide and creatine kinase, were lower than those in the SLE patient group (online supplementary figures S1–S5). All patients with RA were discharged after symptomatic treatment.

Overall, our clinical data suggest that SARS-CoV-2 infection worsens the outcome of patients with SLE/RA, and the severity of SARS-CoV-2 infection is associated with pre-existing diseases, especially heart disease and kidney disease, which may cause severe failure or even death. Therefore, treatment of COVID-19 patients with RA/SLE needs to consider the use of drugs that can protect the heart and reduce the burden on the kidneys.



  • CL, ZW and JL contributed equally.

  • Contributors CL, JL, ZW and XX contributed to the acquisition and analysis of data. QW and YL were involved in the interpretation of data. All authors contributed to drafting and/or revising the manuscript.

  • Funding Supported by the National Natural Science Foundation of China (grant nos 81572893, 81972358, 81959113), Key Foundation of Wuhan Huoshenshan Hospital (grant no 2020[18]), Key Research and Development Program of Jiangsu Province (grant nos BE2017733, BE2018713), Medical Innovation Project of Logistics Service (grant no 18JS005), Science and Technology Development Fund of Nanjing Medical University (grant no NMUB2019031), and Basic Research Program of Jiangsu Province (grant no BK20180036).

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Ethics approval This study was approved by the Research Ethics Committee of Nanjing Medical University (2020-511).

  • Provenance and peer review Not commissioned; internally peer reviewed.

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