Literature DB >> 32358791

SARS-CoV-2 infection in a psoriatic patient treated with IL-17 inhibitor.

R Balestri1, G Rech1, C R Girardelli1.   

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Year:  2020        PMID: 32358791      PMCID: PMC7267317          DOI: 10.1111/jdv.16571

Source DB:  PubMed          Journal:  J Eur Acad Dermatol Venereol        ISSN: 0926-9959            Impact factor:   9.228


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Editor We read with great interest the article entitled ‘SARS‐CoV‐2 infection in a psoriatic patient treated with IL‐23 inhibitor’ published by Messina F. and Piaserico S. in the JEADV. This is the first report of coronavirus disease 2019 (COVID‐19) in a psoriatic patient treated with a biologic. Whilst the authors reported an infection that occurred during therapy with an IL‐23 inhibitor, we would like to briefly report one that occurred during therapy with an IL‐17 inhibitor. The case here reported is peculiar for two reasons: (i) the patient was infected during the induction regimen; (ii) he was completely asymptomatic. He was a 55‐year‐old general practitioner, with a 4‐year history of psoriasis, previously treated with conventional drugs and the biological drug adalimumab. On January 20, due to a worsening of the psoriasis, he was switched to ixekizumab and started the currently approved induction dosing regimen (160 mg at week 0, followed by 80 mg at weeks 2, 4, 6, 8, 10 and 12). On March 3, following contact with a COVID positive patient, even though he was completely asymptomatic, he was tested for SARS‐CoV‐2, and resulted positive. Although we advise all biological‐treated patients to report any alteration in their health status, he did not inform us and decided to continue biological therapy as formerly prescribed. Since our Psoriasis Outpatient Service suspended all follow‐up visits, in accordance with the directives of the Regional Health Service, we contacted all scheduled patients by phone. We were informed of his history only when we called him on April 2 after his second test had already resulted negative (i.e. the patient could be considered healed). He confirmed never having suffered from cough, dyspnoea, anosmia, ageusia, myalgia or any other symptom of the infection. There are some evidences that IL‐17 is implicated in acute respiratory distress syndrome, which is the major life‐threatening complication of COVID‐19, as well as observations that an aberrant Th17 polarization may correlate with a worse outcome in coronavirus‐related pneumonia. Since the inhibition of IL‐17 pathway may have beneficial effects in treating COVID‐19, ixekizumab associated with antiviral drugs is being investigated for the treatment of COVID‐19 infection. However, all the previous observations and studies concern cases characterized by progression of the disease towards an abnormal and exaggerated inflammatory response, similar to cytokine release syndrome, that can be considered a secondary phase of the SARS‐COV‐2 infection. On the contrary, the case here reported seems to suggest that blockade of IL‐17 does not negatively affect the primary phase of infection that is the virus binding to human cells and its replication, since our patient was on continuous medication with ixekizumab and furthermore was following the induction regimen, taking the drug every other week. In conclusion, our observation strengthens the hypothesis that IL‐23/IL‐17 axis inhibition might not be detrimental in the setting of COVID‐19 infection, even though it remains of upmost importance to collect more evidences and to gather as many cases as possible related to psoriasis patients in biological therapy who have contracted COVID‐19, in order to better quantify the risk of infection under biologic therapy.
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