Commentary: COVID-19: risk for cytokine targeting in chronic inflammatory diseases?

COMMENTARY

Soon after COVID-19 was declared a pandemic, the question if particular patient groups – those with immune-mediated inflammatory disease (IMID) and/or those on an immunosuppressant treatment – are at higher risk to become infected and/or are at risk for developing a more severe course of the disease. Patients with IMIDs including psoriasis are frequently treated by cytokine inhibitors, and this type of treatment often is referred to as immunosuppressive.

In the beginning of the outbreak, data about COVID-19 in IMID patients were sparse and mostly from China, which made it difficult to extrapolate if patients of other races may show similar signs and symptoms.

Experts from rheumatology, dermatology and gastroenterology at the German Center for Immunotherapy in Erlangen summarized published research on the potential effects of cytokines, being a target for biologic therapy, on the susceptibility for viral infections and anti-viral responses. They concluded that cytokines known as pathogenic in IMID do not affect anti-viral host responses. There is no signal yet that biologic therapies balancing overexpression of these cytokine targets have a negative effect on anti-viral responses. As influenza vaccination is possible during biologic treatment and results in a normal vaccination response there is no scientific rational why SARS-CoV 2 infection (and future vaccination) may behave differently.
Schett, et al., mention that only with anti-TNF and anti-IL6 therapies is there an increased risk for bacterial infections (a complication in patients with severe COVID-19). On the other hand, uncontrolled hyperactivation of primarily innate immune responses in severe COVID-19 known as a “cytokine storm” can be treated with biologics against IL-6.

There is debate whether the new class of Janus kinase inhibitors (JAKi) used to treat rheumatoid arthritis, psoriatic arthritis and ulcerative colitis, may be harmful or beneficial against COVID-19 infection. JAKi decrease IL-6 effectively but also interferons depending on JAK-specificity. Tofacitinib increases the risk of venous thromboembolism a known complication in COVID-19. However, there is evidence that JAK2-inhibition also inhibits viral entry of SARS-CoV-2 and at least two JAKi (baricitinib and ruxolitinib) will be tested in severe COVID-19 patients.

For physicians treating IMID patients including psoriasis, the message given by Schett and colleagues is clear and reassuring: treatment should be continued or initiated in patients newly presenting with severe IMID to control systemic inflammation.

The authors also mention that one common therapy in rheumatology and gastroenterology increases the risk of infections and may lead to COVID-19 complications: systemic steroids. As many psoriasis and/or psoriatic arthritis patients are still being treated with systemic steroids despite negative recommendations, a thorough medical history is necessary and measures to stop systemic steroids needs to be initiated.

Of course, with increasing knowledge from registries and published literature current recommendations will be amended. Physicians need to stay informed.

Disclaimer: Views expressed in this commentary are those of the author and do not necessarily represent the position of the International Psoriasis Council or its Board of Directors.