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Response to: ‘Monitoring of patients with systemic lupus erythematosus during the COVID-19 outbreak’ by Holubar 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, 75013 Paris, France; alexis.mathian{at}aphp.fr

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We thank Holubar 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.1 2 Their results showing a low incidence of symptoms of viral infections in a population of patients with SLE corroborates those from Favalli et al,3 suggesting that the impact of COVID-19 in patients with SLE is rather low. However, as acknowledged by Holubar et al, the prevalence of COVID-19 in the general population is very low as well, and even lower in regions, such as Occitanie in Southern France where the study of Holubar et al was carried out between 1 February and 24 April.1 2 By 11 May, Salje et al estimated that only 4.4% (range 2.8–7.2) of the general French population had been infected and that this proportion was likely to be even lower, that is, 1.9% (range 1.2–3.3) in Occitanie, as compared with 9.9% (range 6.6–15.7) in Ile-de France, including Paris, and 9.1% (range 6–14.6) in Grand Est, the two most affected regions of the country.4 A recent study also shows that even in one of the epicentres of the outbreak, the prevalence of anti-SARS-CoV-2 antibodies was very heterogeneous.5 In the latter study, the infection attack rate (IAR) based on specific antibody detection ranged from 25.9% (95% CI 22.6 to 29.4) in a sample of 661 participants, including pupils, their parents and siblings as well teachers and non-teaching staff involved in a cluster of COVID-19 that took place in a high school in the Oise department to 3.0% (95% CI 1.1 to 6.4) in samples from two nearby blood donors centres.5 Therefore, given the low IAR of SARS-CoV-2 in general, it is currently impossible to draw any meaningful conclusions on the incidence and severity of COVID-19 in patients with SLE.

It is also seems important to mention that the reporting of symptoms suggestive of an infection cannot by any means replace the use of reliable markers of infection, particularly in regions with a low IAR. Whereas anosmia and ageusia may have a high positive predictive value for SARS-CoV-2 infection in epicentres of the outbreaks, this is certainly not the case outside these regions. This consideration is also applicable to all other symptoms suggestive of infection such as dry cough, fever, diarrhoea, and so on, and only the systematic use of reliable tests such as viral detection by real-time reverse transcription-PCR analysis and/or the detection of anti-SARS-CoV-2 antibodies should be used to confirm COVID-19 positive cases. In addition, a chest CT scan suggestive of SARS-CoV-2 pneumonia will also allow, in the context of a COVID-19 outbreak, to confirm the diagnosis of SARS-CoV-2 infection.

We agree with Holubar et al that only studies of a large cohort of patients with SLE, infected with SARS-CoV-19, will permit to better understand the impact of COVID-19 on this population, although they will undoubtedly be difficult to conduct. Meanwhile, the relatively low IAR observed during the pandemic in France indicates that establishing protective herd immunity will be a lengthy process.4 5 Therefore, in the absence of a reliable preventive and curative treatment, it is likely that patients with SLE will have to experience continued uncertainty as to whether or not they are at risk to develop a severe form of COVID-19.

References

Footnotes

  • Handling editor Josef S Smolen

  • Contributors Both authors wrote the response letter.

  • 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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