Literature DB >> 32584451

COVID-19 infection on IL-23 inhibition.

Catherine J Wang1, Allison K Truong2.   

Abstract

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Year:  2020        PMID: 32584451      PMCID: PMC7361849          DOI: 10.1111/dth.13893

Source DB:  PubMed          Journal:  Dermatol Ther        ISSN: 1396-0296            Impact factor:   3.858


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Dear Editor, The novel 2019 coronavirus disease (COVID‐19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and has infected patients worldwide. In the midst of this global pandemic, physicians have questioned whether to continue patients on biologic therapy. In developed countries, psoriasis affects approximately 1% to 4% of the population, and many patients with moderate‐to‐severe psoriasis require biologics for disease management. We herein report a patient with psoriasis treated with risankizumab, an interleukin‐23 (IL‐23) inhibitor, who was infected with SARS‐CoV‐2 and report his favorable clinical outcome.

CASE REPORT

A 37‐year‐old man with a history of psoriasis, previously treated with narrowband UVB, etanercept, ustekinumab, secukinumab, adalimumab, guselkumab, currently on risankizumab since December 2019, presented to the emergency department (ED) in March 2020 with a fever to 39.1°C, cough, shortness of breath, and chest congestion. The patient had recently traveled to Thailand, Singapore, Hong Kong, and New York 1 week prior to presentation. The patient's influenza test was negative, and his chest x‐ray was normal. Given mild symptoms, the patient was discharged. The next day, the patient returned to the ED with new onset hemoptysis. Computed tomography (CT) chest demonstrated bilateral ground glass opacities and his SARS‐CoV‐2 polymerase chain reaction (PCR) test was positive. The patient's hospital course was mild, and he was treated symptomatically with nebulizers, benzonatate, and guaifenesin. The patient was discharged 1 week later on home quarantine. Two weeks later, he recovered completely. Per the recommended risankizumab dosing schedule (every 12 weeks after initial loading doses at week zero and four), the patient received his next dose in April with no complications. The patient in this manuscript has given informed consent to publication of his case details.

DISCUSSION

Risankizumab is a monoclonal antibody that inhibits the p19 subunit of IL‐23 and is one of the most recent IL‐23 inhibitors approved for the treatment of moderate‐to‐severe psoriasis. IL‐23 induces the proliferation of T helper 17 (Th17) cells, leading to a pro‐inflammatory state. Patients treated with risankizumab had a similar overall safety profile to patients on placebo, with upper respiratory tract infections as the most frequently reported adverse events. Due to the immunosuppressive nature of biologics, a new challenge clinicians face is the question of whether these medications should be continued in patients during the COVID‐19 pandemic and in those with active infection. Studies have shown that patients with COVID‐19 have high amounts of pro‐inflammatory cytokines, and cytokine storm may be associated with severe lung disease requiring ICU admission. Data show that Th1 cells secreting IL‐6, interferon gamma (IFN‐ ), and granulocyte‐macrophage colony stimulating factor (GM‐CSF) are involved in COVID‐19 cytokine storm. Studies have also suggested that Th17 may be involved in severe immune injury in COVID‐19. , IL‐23 inhibitors via its effects on Th17 may play a role in attenuating key cytokines, possibly resulting in a milder manifestation of COVID‐19. It has been reported that a patient on guselkumab, an IL‐23 inhibitor, achieved full recovery from COVID‐19. Our case adds to this growing body of evidence that IL‐23 biologic therapy may not worsen clinical outcomes for COVID‐19 patients. More studies are needed to characterize the immunologic milieu in COVID‐19 cytokine storm. Another question is when biologics with long half‐lives should be restarted. In our case, the patient recovered from COVID‐19 before his next scheduled risankizumab dose. However, more data needs to be obtained about biologics in COVID‐19 patients, in particular whether or not biologic dosage timeline should be adjusted based on resolution of infection. A database to collect information on COVID‐19 patients on biologic therapy and their outcomes would be instrumental to guide clinicians on best practices for now and in future pandemics. In conclusion, this case illustrates that IL‐23 inhibition via biologic therapy in COVID‐19 may not correlate with severe respiratory disease. However, the decision to continue biologic treatment should be a shared process between physician and patient on a case‐by‐case basis.

CONFLICT OF INTEREST

The authors declare no conflicts of interest.
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