TY - JOUR
T1 - Infection risk in atopic dermatitis patients treated with biologics and JAK inhibitors
T2 - BioDay results
AU - van der Gang, Lian F
AU - Atash, Keneshka
AU - Zuithoff, Nicolaas P A
AU - Haeck, Inge
AU - Boesjes, Celeste M
AU - Bacoş-Cosma, Octavian I
AU - Loman, Laura
AU - Kamsteeg, Marijke
AU - Stadhouders-Keet, Simone
AU - Oosting, Albert J
AU - van Lynden-van Nes, Anneke M T
AU - Politiek, Klaziena
AU - Gostynksi, Antoni
AU - Berntsen-Zandbergen, Lisette
AU - Christoffers, Wianda A
AU - Flinterman, Annebeth
AU - Touwslager, Wouter R H
AU - Velstra, Berit
AU - Stewart, Shiarra M
AU - van Erp, Francine C
AU - de Graaf, Marlies
AU - Schuttelaar, Marie-Louise A
AU - de Bruin-Weller, Marjolein S
N1 - Publisher Copyright:
© 2025 The Author(s). Journal of the European Academy of Dermatology and Venereology published by John Wiley & Sons Ltd on behalf of European Academy of Dermatology and Venereology.
PY - 2025/12
Y1 - 2025/12
N2 - Background: Limited data exist on the comparative risk of infections during biologic and Janus kinase inhibitor (JAKi) treatment for atopic dermatitis (AD) in daily practice. Objectives: To assess the differential infection risk of biologic and JAKi treatment in patients with moderate-to-severe AD in a real-world setting. Methods: This prospective, multicentre study evaluated treatment-emergent infections in patients (age ≥ 12 years) using biologics or JAKi from the BioDay registry from October 2017 to July 2024. Crude incidence rates were calculated per 100 patient-years (PY) per treatment. Cox regression for recurrent events, adjusted for potential confounders, was used to estimate hazard ratios (HR) for the rate of infections, with subgroup and sensitivity analyses in bio-/JAKi-naïve patients. Results: In total 1793 patients were included (4044.1 PY; 1886 biologic treatment episodes (TEs); 480 JAKi), with 794 infections. JAKi showed higher infection rates (58.4–65.5/100 PY) compared to biologics (13.6–22.0), especially for herpes infections (n = 195, 24.6%; JAKi 13.6–19.8 vs. biologicals 3.0–3.6). Cox regression indicated increased rates with JAKi (abrocitinib HR 4.1, 95% CI: 3.1–5.5; baricitinib HR 4.2, 95% CI: 2.9–6.2; upadacitinib HR 4.0, 95% CI: 3.2–5.0; all p < 0.0001) and a slight increase with tralokinumab (HR 1.4, 95% CI: 1.0–2.0, p = 0.039) compared to dupilumab. Sensitivity analyses confirmed these results, except for tralokinumab. Rates of severe infections were higher with JAKi compared to dupilumab, although absolute numbers were low and associations were not consistently significant. History of infection, predominantly viral or fungal skin infections (HR 1.9, 95% CI: 1.4–2.6, p < 0.0001; 2.4, 1.3–4.4, p = 0.003, resp.), was identified as an independent factor associated with infection. Conclusions: This cohort study demonstrated an increased risk of infection during JAKi treatment compared to dupilumab for moderate-to-severe AD. These findings enhance understanding of the differential infection risk with targeted therapies in AD, aiding tailored treatment choices that consider patient-specific risks such as prior skin infections.
AB - Background: Limited data exist on the comparative risk of infections during biologic and Janus kinase inhibitor (JAKi) treatment for atopic dermatitis (AD) in daily practice. Objectives: To assess the differential infection risk of biologic and JAKi treatment in patients with moderate-to-severe AD in a real-world setting. Methods: This prospective, multicentre study evaluated treatment-emergent infections in patients (age ≥ 12 years) using biologics or JAKi from the BioDay registry from October 2017 to July 2024. Crude incidence rates were calculated per 100 patient-years (PY) per treatment. Cox regression for recurrent events, adjusted for potential confounders, was used to estimate hazard ratios (HR) for the rate of infections, with subgroup and sensitivity analyses in bio-/JAKi-naïve patients. Results: In total 1793 patients were included (4044.1 PY; 1886 biologic treatment episodes (TEs); 480 JAKi), with 794 infections. JAKi showed higher infection rates (58.4–65.5/100 PY) compared to biologics (13.6–22.0), especially for herpes infections (n = 195, 24.6%; JAKi 13.6–19.8 vs. biologicals 3.0–3.6). Cox regression indicated increased rates with JAKi (abrocitinib HR 4.1, 95% CI: 3.1–5.5; baricitinib HR 4.2, 95% CI: 2.9–6.2; upadacitinib HR 4.0, 95% CI: 3.2–5.0; all p < 0.0001) and a slight increase with tralokinumab (HR 1.4, 95% CI: 1.0–2.0, p = 0.039) compared to dupilumab. Sensitivity analyses confirmed these results, except for tralokinumab. Rates of severe infections were higher with JAKi compared to dupilumab, although absolute numbers were low and associations were not consistently significant. History of infection, predominantly viral or fungal skin infections (HR 1.9, 95% CI: 1.4–2.6, p < 0.0001; 2.4, 1.3–4.4, p = 0.003, resp.), was identified as an independent factor associated with infection. Conclusions: This cohort study demonstrated an increased risk of infection during JAKi treatment compared to dupilumab for moderate-to-severe AD. These findings enhance understanding of the differential infection risk with targeted therapies in AD, aiding tailored treatment choices that consider patient-specific risks such as prior skin infections.
UR - https://www.scopus.com/pages/publications/105002392919
U2 - 10.1111/jdv.20674
DO - 10.1111/jdv.20674
M3 - Article
C2 - 40176741
SN - 0926-9959
VL - 39
SP - 2056
EP - 2068
JO - JEADV : journal of the European Academy of Dermatology and Venereology
JF - JEADV : journal of the European Academy of Dermatology and Venereology
IS - 12
ER -