Recent research has identified a link between the use of tumor necrosis factor (TNF) inhibitors in treating psoriasis and a rise in the frequency of antiphospholipid syndrome (APS) autoantibodies. This association suggests a possible immunomodulatory relationship between autoimmunity and inflammation.
A retrospective analysis led by Dr. Lixin Li from the University of Tokyo’s Graduate School of Medicine assessed the incidence of antinuclear antibodies and APS-associated autoantibodies among psoriasis patients. Dr. Li and colleagues highlighted that autoantibody development, particularly antiphospholipid antibodies, has been observed in individuals with rheumatoid arthritis undergoing TNF inhibitor therapy.
“In this study, a retrospective analysis was conducted to investigate the incidence of antinuclear antibodies and APS-associated autoantibodies in psoriasis patients following treatment with TNF, IL-17, and IL-23 inhibitors,” Li et al. wrote. “Furthermore, the present study investigated the factors predisposing patients to developing APS autoantibodies.”
Study Background and Design
The research team conducted a retrospective trial, examining patients with psoriasis vulgaris, psoriatic arthritis (PsA), or generalized pustular psoriasis diagnosed by dermatologists and treated with biologics at the University of Tokyo Hospital between January 2010 and December 2021. Patients with palmoplantar pustulosis were excluded. The study employed an opt-out consent method, providing participants with detailed information about the study and allowing them to decline participation.
The baseline data assessment included sex, age, body mass index (BMI), and disease duration before initiating biologic therapies. Clinical comorbidities such as hypertension, diabetes, arthritis, and dyslipidemia were also evaluated. Arthritis diagnoses were confirmed by rheumatologists using the Classification Criteria for Psoriatic Arthritis (CASPAR), and disease severity was measured using the Psoriasis Area Severity Index (PASI) scores. Hematological laboratory data were collected from patient registries.
Multivariate Cox regression analyses were used to examine the link between positive APS autoantibodies and predictive variables. A P-value below .05 was considered statistically significant.
Key Findings and Conclusions
The study concluded that TNF inhibitor therapy was associated with a higher occurrence of APS autoantibodies compared to treatment with interleukin (IL)-17 and IL-23 inhibitors. The presence of APS autoantibodies in patients treated with TNF inhibitors was linked to concurrent arthritis and increased disease severity at therapy initiation.
High PASI scores and antinuclear antibody titers above 320 were predictive variables for the production of APS autoantibodies. Despite the increased levels of autoantibodies, patients did not exhibit clinical symptoms of APS.
This study is the first to provide extensive evidence of increased APS autoantibody production frequency in psoriasis patients treated with TNF inhibitors. The correlation between TNF inhibitors and APS autoantibody positivity, along with various clinical parameters, suggests an interaction between autoimmunity and inflammation in psoriasis development.
“In summary, to our knowledge, this is the first study to investigate the association between TNFi and increased frequency of APS-associated autoantibody production,” the researchers wrote. “The findings indicate that elevated PASI scores and high antinuclear antibodies titers serve as predictors for susceptibility to APS antibody positivity, underscoring the immunomodulatory interplay between autoimmunity and inflammation in the pathogenesis of psoriasis.”
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