A recent retrospective cohort analysis explored the association between risk of serious infection and initiation of interleukin (IL)-17, IL-12/23, and tumor necrosis factor (TNF) inhibitor among real-world patients with psoriasis or psoriatic arthritis (PsA).
Commercially insured patients diagnosed with psoriasis or PsA between 2015 and 2018 were included in the study. The exposure was defined as dispensation for IL-17 (ixekizumab or secukinumab), IL-12/23 (ustekinumab) or TNF (adalimumab, certolizumab pegol, etanercept, golimumab and infliximab). The primary outcome was infection requiring hospitalization after biologic initiation. The researchers calculated incidence rates (IRs) per 100 person-years. Cox proportional hazards regression models were adjusted for inverse probability of treatment-weighted propensity scores.
Final analysis included 11,560 new treatment episodes; during 9,264 person-years of follow-up, 190 serious infections (2% of treatment episodes) were reported. Between IL-17 and TNF, class-specific IRs did not significantly differ, but were significantly lower for IL-12/23. In adjusted analyses, infection risk with IL-17 was not significantly greater compared to TNF (hazard ratio [HR]=0.89; 95% CI, 0.48 to 1.66) or IL-12/23 (HR=1.12; 95% CI, 0.62 to 2.03). Compared to TNF, IL-12/23 was associated with a reduced risk of infection (HR=0.59; 95% CI, 0.39 to 0.90).
“Relative to TNF and IL-17, IL-12/23 inhibitors were associated with a reduced risk of serious infection in biologic-naïve patients with [psoriasis] or PsA,” the researchers concluded. “In biologic-experienced individuals, there was no difference in infection risk across TNF, IL-17 or IL-12/23 inhibitors.”