Discussion
Viral infection has been shown to be strongly associated with the onset
or exacerbation of psoriasis. The possible mechanism of COVID-19
infection leading to psoriasis flare-ups is the stimulation of toll-like
receptor 3 by viral RNA, leading to dysregulation of the innate immune
response and production of IL-36-γ and CXCL8. In addition, psoriasis may
be exacerbated due to the hyperinflammatory state of COVID-19
patients[2]. Our patient’s recurrent rash was
atypical, possibly related to the use of secukinumab therapy. Combined
with the patient’s past history and pathology, the diagnosis was
psoriasis. Although the causality between the COVID-19 infection and
psoriasis flare-up cannot be definitively established in this single
case, previous study has reported associations between COVID-19
infections and the exacerbation of psoriasis[3].
Currently, there is no consensus on whether biological agents increase
the risk of coronavirus infection[4]. Several
studies have shown that the levels of circulating IL-17 are elevated in
the peripheral blood of COVID-19 patients, therefore the use of IL-17
inhibitors may become a new treatment option for COVID-19, which
directly block the IL-17 pathway[5]. That may also
account for the mild symptoms of COVID-19 infection in our patient when
using the treatment of secukinumab.
Despite the patient’s previous positive response to secukinumab, the
increasing psoriatic activity suggested possible resistance or tolerance
to this IL-17A inhibitor. Blood tests of our patient revealed an
increased level of TNF, a key cytokine in the process of psoriatic
inflammation[6]. The elevation of TNF may suggest
a compensatory mechanism or an alternative pathway of psoriasis
inflammation, warranting a change in the therapeutic approach.
In light of the lack of response to secukinumab and the increased TNF
levels, a decision was made to switch the patient’s treatment to
adalimumab. The transition to adalimumab therapy led to a significant
improvement, suggesting a relevant role of TNF in driving the psoriasis
flare-up and reaffirming the importance of individualizing treatment
choices based on patient characteristics and disease manifestations. The
patient continues to be under follow-up to monitor the response to
adalimumab and assess the long-term treatment outcomes.
It is essential to acknowledge the limitations of this case report. As a
single-patient observation, it does not establish a causative
relationship between COVID-19 infection and psoriasis flare-up or the
efficacy of adalimumab. Further larger-scale studies, including
controlled trials or observational studies, are needed to elucidate the
complex interactions between viral infections and psoriasis, as well as
to assess the comparative effectiveness of different biologic agents in
similar scenarios.
In conclusion, this case highlights the potential impact of COVID-19
infection on psoriasis course and the importance of adapting treatment
strategies to address individual patient responses. The patient’s
experience with secukinumab followed by adalimumab demonstrates the need
for continuous evaluation and optimization of therapeutic approaches in
psoriasis management, particularly in the context of viral infections or
other triggering factors. Further research and clinical observations are
warranted to develop a comprehensive understanding of the underlying
mechanisms and to guide evidence-based treatment decisions in similar
cases.