Infection risk in patients undergoing treatment for inflammatory arthritis: non-biologics versus biologics

The anti-viral facet of anti-rheumatic drugs: Lessons from COVID-19

“…Depending on conditions, TNFR induces cell survival/apoptosis, and programmed necrosis which may play a role in controlling viral infection [232]. The risks of bacterial and mycobacterial infection are increased in patients receiving biological DMARDs therapy, particularly TNFi [233]. These drugs are relevant immunosuppressants leading to reactivation of latent infections such as hepatitis B and tuberculosis [233].…”

“…The risks of bacterial and mycobacterial infection are increased in patients receiving biological DMARDs therapy, particularly TNFi [233]. These drugs are relevant immunosuppressants leading to reactivation of latent infections such as hepatitis B and tuberculosis [233]. For instance, hepatitis B and C assessment is required prior to start a TNFi and in patients with a positive HBsAg, infliximab has the most reported cases associated with HBV reactivation [234].…”

“…Baricitinib, at therapeutic dosing (either as 2 mg or 4 mg once daily) is sufficient to inhibit AAK1, thus it has been suggested to be trialed in an appropriated COVID population [6,292]. On the other hand, therapies targeting JAK complexes may interfere with normal anti-viral response including inhibition of IFN-γ activity and may potentially increase the risk of infection and/or reactivation of several viral infectious diseases [293][294][295], including a dose dependent risk for VZV observed for tofacitinib and baricitinib [296]. Thus, their usage should be carefully evaluated.…”

Recognition and management of respiratory co-infection and secondary bacterial pneumonia in patients with COVID-19

“…The risk of serious bacterial infections has been consistently reported to be higher with tocilizumab use for rheumatological diseases. [33][34][35][36] C-reactive protein (CRP) and other acute phase reactants including white blood cell count may be unreliable acute phase reactants and may not rise in response to a secondary bacterial infection after tocilizumab use. 34,37,38 Exactly how long this effect lasts with 1 or 2 doses is unclear.…”

“…[33][34][35][36] C-reactive protein (CRP) and other acute phase reactants including white blood cell count may be unreliable acute phase reactants and may not rise in response to a secondary bacterial infection after tocilizumab use. 34,37,38 Exactly how long this effect lasts with 1 or 2 doses is unclear. Procalcitonin may be less affected by IL-6 inhibitors, [21][22][23] but the data to differentiate bacteria from viral pneumonia in this context is limited and should be further evaluated.…”