Antiphospholipid Syndrome Antibodies Linked to TNF Inhibitor Treatment of Psoriasis

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There is evidence of a link between rises in frequency of antiphospholipid syndrome autoantibodies and tumor necrosis factor (TNF)-inhibitor treatment of those with psoriasis, according to recent findings, with the association indicating a possible immunomodulatory relationship between autoimmunity and inflammation.¹

This retrospective analysis, led by Lixin Li from the department of dermatology at the University of Tokyo’s Graduate School of Medicine, was conducted to assess the incidence among psoriasis patients of antinuclear antibodies and antiphospholipid syndrome-associated autoantibodies. Li and colleagues noted that autoantibody development connected to antiphospholipid syndrome, antibodies aimed at antiphospholipid antigens, and others have been found to be present among individuals with rheumatoid arthritis given TNF inhibitors.²

“In this study, a retrospective analysis was conducted to investigate the incidence of (antinuclear antibodies) and (antiphospholipid syndrome)-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 (antiphospholipid syndrome) autoantibodies.”

Background and Design

The investigators used a retrospective trial design, assessing individuals with psoriasis vulgaris, psoriatic arthritis (PsA), or generalized pustular psoriasis who had been diagnosed by dermatologists. These individuals had been given biologic treatment between January 2010 - December 2021 at the University of Tokyo Hospital in Japan.

Those with palmoplantar pustulosis were excluded. The research team implemented an opt-out consent method and participants were given detailed points of information about the study and allowed to reject any participation in the research.

Sex, age, body mass index (BMI), and duration of disease were included in the team's assessment of baseline data prior to initiating treatment with biologic therapies. The study also involved an evaluation of clinical comorbidities present among patients such as hypertension, diabetes, arthritis, and dyslipidemia.

Diagnoses of arthritis were done by rheumatologists using the Classification Criteria for Psoriatic Arthritis (CASPAR) and severity of disease was evaluated by the research team through the use of Psoriasis Area Severity Index (PASI) scores. Hematological laboratory data were gathered by the team using the patient registry.

The team conducted Multivariate Cox regression analyses to examine the link between the likelihood of positive antiphospholipid syndrome autoantibodies and variables deemed to be predictive. They considered a P-value below .05 as statistically significant in all of their analyses.

Conclusions

Overall, the investigators concluded that TNF inhibitor therapy was shown to be linked to a higher antiphospholipid syndrome autoantibody occurrence versus treatment with interleukin (IL)-17 and IL-23 inhibitors. They highlighted that the specific presence of antiphospholipid syndrome autoantibodies among those given TNF inhibition had been shown to be linked with concurrent arthritis as well as increased severity of disease severity at the point of therapy initiation.

High PASI as well as anti-nuclear antibody titers which were shown to be above 320 were found by the research team to be predictive variables of the production of antiphospholipid syndrome autoantibodies. While there had been increases in levels of autoantibodies, the team did note that subjects had not shown clinical symptoms of antiphospholipid syndrome.

This research was also reported by the investigators to be the first of its kind in providing a wide range of evidence of increased antiphospholipid syndrome autoantibody production frequency among individuals with psoriasis who were also treated with TNF inhibitors. This notable correlation between TNFi and APS autoantibody positivity, in addition to the different clinical parameters, was acknowledged by the team as suggesting a possible interaction between autoimmunity among patients 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 (antiphospholipid syndrome)-associated autoantibody production,” they wrote. “The findings indicate that elevated PASI scores and high (antinuclear antibodies) titers serve as predictors for susceptibility to (antiphospholipid syndrome) antibody positivity, underscoring the immunomodulatory interplay between autoimmunity and inflammation in the pathogenesis of psoriasis.”

References

1. ^{Li L, Toyama S, Shibata S, et al. Prevalence of antiphospholipid autoantibodies associated with biologics treatment for psoriasis. Sci Rep. 2024 Jul 10;14(1):15975. doi: 10.1038/s41598-024-65378-6. PMID: 38987260; PMCID: PMC11237117.}
2. ^{Olech E, Merrill JT. The prevalence and clinical significance of antiphospholipid antibodies in rheumatoid arthritis. Curr. Rheumatol. Rep. 2006;8:100–108. doi: 10.1007/s11926-006-0049-8.}