Trials of anti-tumour necrosis factor therapy for COVID-19 are urgently needed

[...]after anti-TNF infusion tissue TNF is reduced as it passes into the blood bound to the anti-TNF antibody. Experimental studies suggest that if the duration of inflammation is limited, with its associated collateral lung damage, then bacterial superinfection is reduced.23 There is concern that anti-TNF therapy might increase the risk of bacterial infection.24 Yet two randomised studies in critically unwell patients with septic shock25,26 showed that monoclonal anti-TNF therapy had good safety data with no evidence of increased secondary bacterial infections in the anti-TNF treated group. In an observational trial in rheumatoid arthritis patients with serious infections, the risk of sepsis and death was reduced in patients on TNF inhibitors compared with those on synthetic disease-modifying anti-rheumatic drugs (DMARDS).27 46 (11%) of 399 patients on TNF inhibitors developed sepsis after serious infection, of whom 20 (43%) died, compared with 74 (17%) of 444 patients on DMARDS who developed sepsis, of whom 54 (74%) died.27 Paradoxically, another class of TNF inhibitor, a TNF-R2 Ig-Fc fusion protein, etanercept, was associated with moderately increased mortality in a randomised trial of this treatment for sepsis,28 possibly due to its faster off-rate for TNF potentially resulting in some redistribution and bioavailability of pathogenic TNF rather than its clearance. By contrast, about half of 71 patients on sulfasalazine/mesalamine recovered without hospital admission and six patients died. [...]IBD patients with COVID-19 on anti-TNF therapy do not fare worse than those treated with other drugs, but there are insufficient data to make conclusions about a better outcome.