Dear Editor,
We would like to thank the authors for their helpful comments and constructive suggestions regarding our study (1). We agree with the possibility that “SARS-Cov-2 may trigger or even induce SLE and NPSLE”. In fact, a recent case report presented the first case of SLE triggered by COVID-19 infection (2). However, the letter to the Editor mentioned that the authors did not assess whether the patients had other viral infections, so they were not certain that SARS-Cov-2 itself actually triggered SLE (3). Although studies have shown that SLE patients have a higher susceptibility to depression and anxiety during the SARS-Cov-2 pandemic (4), it is questionable whether the neuropsychiatric symptoms of SLE (such as depression and anxiety) are exacerbated by the disease itself, or by the mental health related factors or the SARS-Cov-2 epidemic. It is worth our time and effort to explore these questions in depth.
Moreover, several studies have shown that serum S100B, a marker for brain injury which can also be elevated in cases of COVID-19 infection, is considered to be a potential biomarker of cognitive impairment and SLE (particularly important in distinguishing NPSLE) (5., 6., 7.). In addition to S100B, we also need to add the other specific molecular markers related to NPSLE itself and COVID-19 infection to confirm the possible sequences and interactions between them on neuropsychiatric manifestations. Therefore, additional clinical and laboratory data from multiple cases of SARS-Cov-2 infection in patients with SLE is needed, especially focusing on neuropsychiatric symptoms, in order to determine the practical value or clinical significance of serum S100B in SLE patients during and after the SARS-Cov-2 pandemic.
Conflict of Interest
None.
Footnotes
Supplementary material associated with this article can be found, in the online version, at doi:10.1016/j.arcmed.2022.05.005.
Appendix. Supplementary materials
References
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