Op0315 Unveiling Complexity: Exploring the Correlation of Damage Index for Antiphospholipid Syndrome With the Antibody Profile in Thrombotic Antiphospholipid Syndrome Patients

Background: Antiphospholipid syndrome (APS) is an autoimmune disorder marked by the presence of antiphospholipid antibodies (aPL) and a range of complications that may encompass thrombotic manifestations, pregnancy-related morbidity, and other factors, contributing to significant morbimortality. Evaluating and characterizing damage in APS poses challenges. To address this, the Damage index for APS (DIAPS) was created as a tool to gauge accumulated damage over time. Objectives: Examine potential correlations between the DIAPS and the aPL profile in Thrombotic APS Patients. Methods: Unicentric retrospective study involving the collection of data from all patients currently under follow-up and diagnosed with thrombotic APS (n=141). Patients were divided into 3 subpopulations according to their aPL profile in high, medium and low risk and the DIAPS of each person was calculated. The aPLs are lupus anticoagulant (LA), anticardiolipin (aCL) and antibeta2 glycoprotein I (anti-beta2GPI). High-risk corresponds to a persistently positive LA and presence of double or triple aPL positivity, medium risk to a persistently positive moderate to high-titer aCL or anti-beta2GP and low risk to persistently positive low-titer aCL or anti-beta2GPI. Data analysis was conducted utilizing the R software, with the alpha level established at 0.05. Results: The Kruskal-Wallis analysis (χ2 = 11.56, p = 0.003, ε2 = 0.08, CI 95% [0.03, 0.18]) indicates significant DIAPS variation among immune profiles. The medium-risk immune profile showed a slightly higher average DIAPS compared to the high-risk group, and both were greater than the low-risk group (Figure 1, top graph). Pairwise comparisons using the Dunn test with Holm adjustment confirmed significant differences between medium-risk and high-risk profiles compared to the low-risk profile. Subsequently, binary generalized linear models for specific damage domains were conducted, with the immune profile as an independent variable (Table 1), revealing that the immune profile significantly predicts only peripheral vascular damage, which exhibits a linear relationship, indicating increased risk with a higher immune profile (Figure 1). Other damage dimensions do not show significant variations across different immune profile levels. However, it's essential to interpret these results cautiously, as only the peripheral vascular, cardiovascular, neuropsychiatric, and renal dimensions have enough cases for reliable conclusions. Although not statistically significant, neuropsychiatric and renal damage are more likely in individuals with a medium-risk immune profile. These specific damage types may contribute to the overall DIAPS, resulting in a higher score for medium-risk profiles. Interestingly, the association with peripheral vascular damage remains consistent even when controlling for years since diagnosis, the presence of other autoimmune disease, arterial hypertension, and dyslipidemia (all p-values <0.04). Conversely, the inclusion of these confounding variables did not reveal a significant impact of the immune profile on the likelihood of neuropsychiatric, cardiovascular, or renal damage (all p-values > 0.247). Conclusion: Despite the importance of aPLs in stratifying patients with APS, our current study reveals the potential existence of other pathophysiological mechanisms causing damage across different domains in this population. Therefore, the identification of these factors becomes crucial, extending beyond the classic aPL profile. REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests: None declared.