Dear Editor,
At the end of April 2020, a 46‐year‐old man with type I Brugada syndrome and arterial hypertension reported his history of COVID‐19 disease. He had been recently switched to ixekizumab 80 mg following secondary inefficacy of ustekinumab 45 mg for moderate–severe chronic plaque psoriasis. One week after the first dose of ixekizumab, the patient developed fever and malaise. A nasopharyngeal swab resulted positive for SARS‐CoV‐2. After 4 days from onset of symptoms, he presented to the Emergency Department with dyspnea and chest pain. Oxygen saturation was 90%, and thoracic ultrasound was consistent with bilateral interstitial pneumonia; chest x‐ray did not show lung opacities or pleural effusion. The patient was hospitalized and treated with hydroxychloroquine 400 mg BID p.o. the first day followed by 200mg BID, ceftriaxone 1g BID IM, and noninvasive continuous positive airway pressure (CPAP) in courses of prone ventilation. Antivirals were not given because of risk of arrhythmia. Fever remitted after 14 days, enabling transition from CPAP to low‐flow oxygen. The patient was discharged after 22 days, with 97% oxygen saturation on walking test. Two repeated SARS‐CoV‐2 nasopharyngeal swabs resulted negative 30 days from diagnosis.
COVID‐19 is caused by the SARS‐CoV‐2 virus, a new variant beta‐coronavirus first isolated from the bronchoalveolar lavage fluid from patients with interstitial pneumonia. On January 30, 2020, the SARS‐CoV‐2 outbreak was declared a public health emergency of international concern. COVID‐19 is characterized most commonly by fever and cough, although the clinical picture may range from completely asymptomatic to bilateral interstitial pneumonia. About 20% of patients develop acute respiratory distress syndrome (ARDS). Risk of severe complications and case fatality rate (CFR) are highest in the elderly, immunosuppressed, and those with chronic diseases.
Uncontrolled immune response and excessive inflammation may play a role in amplifying tissue damage in COVID‐19. Levels of interleukin (IL)‐1, IL‐6, and other proinflammatory cytokines were shown to be significantly higher in patients with severe disease compared to uncomplicated SARS‐Cov‐2 infection. Increased tumor necrosis factor (TNF) and IL‐17 were detected in serum of patients with Middle East Respiratory Syndrome (MERS) caused by coronaviruses and also associated with high morbidity and mortality. 1 It is currently speculated that during the cytokine release syndrome, a frequently fatal clinical sequela of COVID‐19 infection, anti‐inflammatory drugs may be beneficial. 2 Interestingly, immunosuppressive drugs including tocilizumab, an anti‐IL‐6 receptor humanized monoclonal antibody, used in rheumatoid arthritis and in controlling the cytokine release syndrome in CAR‐T cell therapy, are now under investigation in this context. 2 , 3 An ongoing clinical trial is evaluating adalimumab, a human anti‐TNF monoclonal antibody also used for psoriasis, in severe COVID‐19 pneumonia (Chinese Clinical Trial Registry: ChiCTR2000030089). 4 Ixekizumab is a humanized anti‐IL‐17A monoclonal antibody approved for chronic plaque psoriasis and psoriatic arthritis. Among the most common side effects, upper respiratory tract infections are reported. Since our patient interrupted ixekizumab after its first 160 mg injection, we cannot speculate on its role in COVID‐19, although it seems unlikely that it was helpful in preventing a complicated course. Currently, limited data have not yet allowed the implementation of guidelines in predicting the risk of infection and its complications in psoriatic patients treated with biologics. Expert recommendations 5 indicate that their use is relatively safe and that therapeutic decisions should be taken considering the individual patient’s characteristics such as age, gender, comorbidities, compliance with safety measures, work‐related risks, etc. Arterial hypertension is a common comorbidity of moderate–severe psoriasis, and in our relatively young patient, we did not deem this sufficient to interrupt treatment with ixekizumab for the risk of SARS‐CoV‐2 infection. Clinical practice should follow currently available data on overall safety profile and licensed indications of ixekizumab before new evidence‐based guidelines are definitively issued.
Funding source: None.
Conflict of interest: Antonio Costanzo has received speaker honoraria or grants for research from Abbvie, Almirall, Pfizer, Novartis, Lilly, UCB, and Janssen. The other authors have no conflict of interest to disclose.
References
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