Work

Tumor Necrosis Factor Inhibitor Therapy Increases Absolute Lymphocyte Count and Is Associated With Lower Mortality in Patients With Psoriatic Arthritis

Year: 2025

Type: article

Abstract: Objective Pathogenic inflammation in psoriatic arthritis (PsA) includes tumor necrosis factor (TNF) signaling. We observed that lower absolute lymphocyte count (ALC) was associated with greater mortality in persons with rheumatoid arthritis, and the start of TNF inhibitor (TNFi) therapy was associated with increased ALC. The effect of TNFi on ALC and mortality in PsA is not known. Methods Using the VA Corporate Data Warehouse, we identified patients with PsA that initiated TNFi in 2010 through 2015 with laboratory tests before and 3 to 24 months after therapy initiation. Patients with PsA seen in rheumatology clinics were matched by age, sex, race and ethnicity with controls. In a subset of local patients and controls, we evaluated markers of inflammation and other correlates of ALC. Results Among 1923 patients with PsA, ALC increased by a mean of 0.22 × 10 3 cell/μL (95% confidence interval [CI] = 0.20, 0.25) following TNFi initiation, whereas in controls, there was minimal change in ALC (0.01 × 10 3 cell/μL, 95% CI = 0.00, 0.02). Survival curves differed significantly among patients with PsA with baseline ALC above 1.2 × 10 3 cell/μL, below 1.2 × 10 3 cell/μL that remained low after start of TNFi, and below 1.2 × 10 3 cell/μL that increased to above 1.2 × 10 3 cell/μL with therapy. Higher ALC at baseline and increased ALC at follow‐up were associated with higher subsequent survival. Local cohort analysis indicated lower circulating T cell effector and terminal effector memory frequencies in PsA that positively correlated with ALC. Patients with PsA treated with TNFi had lower interleukin‐6 (IL‐6) levels that negatively correlated with ALC. Conclusion TNFi therapy increases the peripheral blood ALC in patients with PsA, and this is associated with lower subsequent mortality. Mechanisms underlying this relationship may include effects of PsA, TNFi, and IL‐6 on T cell subset homeostasis.

Source: ACR Open Rheumatology

DOI: 10.1002/acr2.70135