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Response to: ‘Implications of SARS-CoV-2 infection for patients with rheumatic disease’ by Lin et al
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  1. Alexis Mathian,
  2. Zahir Amoura
  1. Sorbonne Université, Assistance Publique–Hôpitaux de Paris, Groupement Hospitalier Pitié–Salpêtrière, French National Referral Center for Systemic Lupus Erythematosus, Antiphospholipid Antibody Syndrome and Other Autoimmune Disorders, Service de Médecine Interne 2, Institut E3M, Inserm UMRS, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris, France
  1. Correspondence to Dr Alexis Mathian, Internal Medicine, University Hospital Pitié Salpêtrière, Paris 75651, France; alexis.mathian{at}aphp.fr

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We thank Lin et al for their interest in our study reporting on the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease 2019 (COVID-19) in a case series of patients with systemic lupus erythematosus (SLE) under long-term treatment with hydroxychloroquine (HCQ).1 2 Our work intended to report the failure of HCQ to prevent COVID-19 in a series of patients with SLE. Since our publication, several other studies have also shown the lack of efficacy of HCQ in the treatment of SARS-Cov-2 infection. Lin et al discuss whether patients with SLE are more susceptible to infection with SARS-CoV-2, and, when they are infected, whether they progress to more severe disease and a poorer outcome. Our study however was not designed to address these questions. Hence, both studies cannot really be compared.

First, Lin et al observed that 6 (0.2%) of 3057 patients with COVID-19 admitted to Wuhan Huoshenshan Hospital had been diagnosed with SLE. Based on the fact that the prevalence of SLE was reported to be approximately 0.05%–0.1% in other regions of China, the authors suggest that patients with SLE are more susceptible to SARS-CoV-2 infection than the general population. However, we consider that it is not possible to assess the prevalence of COVID-19 in patients with SLE based on these data. Indeed, as the risk of development of SLE varies according to occupational and environmental exposure3 and because major differences in regional age-standardised prevalence rates are observed within the same country,4 Lin et al had better taken the prevalence of SLE in the region of Wuhan instead of those of Hong Kong and the rural areas of Anhui Province. Furthermore, the number of patients with SLE admitted to hospital care for COVID-19 cannot be used as the sole estimate of the prevalence of COVID-19 in SLE. Indeed, due to the supposed susceptibility of patients with SLE to infections, physicians are likely more inclined to admit a patient with SLE with signs of COVID-19 to the emergency room. The real number of patients with SLE infected with SARS-CoV-2 is difficult to assess as well considering the high number of individuals with symptomatic or asymptomatic COVID-19 who have not been tested for the presence of the SARS-Cov-2, in addition to the considerable false-negative rate of the various testing approaches.5

Second, Lin et al suggest in their study, as we and others have reported previously in limited case series, that patients with SLE and associated comorbidities such as arterial hypertension, diabetes, chronic kidney disease and obesity are at risk of developing a severe form of COVID-19.1 2 6 7 This hypothesis was recently confirmed in a study including a larger number of patients with SLE. Fernandez-Ruiz et al identified in a series of 41 patients with SLE in the New York area that the body mass index and the presence of one or more comorbidities, including malignancy, organ transplantation, hypertension, diabetes, chronic obstructive pulmonary disease, congestive heart failure and asthma, were independent predictors of hospitalisation in case of a confirmed COVID-19.8 Whether patients with SLE treated with glucocorticoids and/or immunosuppressants are at risk for hospital admission during the course of SARS-CoV-2 infection, as has been suggested in immune-mediated inflammatory disease in general,9–11 is as yet unclear and further studies are needed to understand the additional specific risk factors for poor COVID-19 outcome in patients with SLE.

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors AM and ZA wrote the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • 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.

  • Provenance and peer review Commissioned; internally peer reviewed.

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