Search in the Abstract Database

* = Presenting author

P370. Formation of antiphospholipid antibodies (APLA) is associated to the presence of anti-Saccharomyces cerevisiae antibodies (ASCA) in inflammatory bowel disease

P370. Formation of antiphospholipid antibodies (APLA) is associated to the presence of anti-Saccharomyces cerevisiae antibodies (ASCA) in inflammatory bowel disease

M. Papp1, Z. Koromi1, L. Davida1, I. Altorjay1, K. Palatka1, M. Udvardy1, G.L. Norman2, Z. Shums2, G. Veres3, L.S. Kiss4, P.L. Lakatos4, J. Harsfalvi5

12nd Department of Medicine, University of Debrecen, Debrecen, Hungary; 2INOVA Diagnostics Inc., San Diego, CA, United States; 31st Department of Pediatrics, Semmelweis University, Budapest, Hungary; 41st Department of Medicine, Semmelweis University, Budapest, Hungary; 5Clinical Research Center, University of Debrecen, Debrecen, Hungary

Antiphospholipid antibodies (APLA) are a prothrombotic group of antibodies acquired in inflammatory bowel disease states. Formation, prevalence and clinical significance of APLA in inflammatory bowel diseases (IBD) remain unclear. Cross-reactive epitopes on beta2 glycoprotein I (beta2-GPI) and Saccharomyces cerevisiae has been reported in antiphospholipid syndrome patients.

Aims: To assess the prevalence of APLA in IBD and their possible association with the disease activity, clinical phenotype, thromboembolic events, and presence of anti-microbial or autoantibodies.

Materials and Methods: Sera of 161 patients (CD: 96 [age: 32.4±12.1 yrs, m/f: 38/58, duration: 6.7±6.0 yrs] and UC: 65 [age: 39.0±14.1 yrs, m/f: 30/35, duration: 13.3±11.0 yrs]) and 267 healthy controls (HC) were tested on individual anti-beta2-GPI (IgG, IgA, IgM), anti-cardiolipin (ACA IgG, IgA, IgM), anti-Saccharomyces cerevisiae antibodies (ASCA IgG, IgA), anti-OMP Plus TM IgA (INOVA Diagnostics) and high-sensitivity C-reactive protein (hs-CRP) by ELISA assays. NOD2/CARD15 genotypes were tested PCR-RFLP. Detailed clinical phenotypes were determined by reviewing the patients' medical charts. Disease activity in CD was evaluated by use of the CDAI score and in UC by the Truelove-Witts grading system.

Results: Patients with CD (30.2%) and UC (24.6%) had significantly higher prevalence of APLA than HC (1.9% p < 0.0001, for both). APLA was dominantly IgM isotype (42.9% for anti-B2GPI and 73.5% for ACA). No correlation was found between disease activity or hs-CRP and the presence of APLA. In the short-term, the APLA status did not show significant variation. 5.2% of patients had thromboembolic events during the disease course and the presence of APLA was not associated to these events. Presence of APLA appeared to play no role in these complications. In CD, APLA were associated with non-inflammatory disease and risk for surgery but not with the disease location. Moreover, significantly higher proportion of APLA positivity was more common in ASCA positive patients (39.0%) as compared to those with ASCA negativity (16.2%, p = 0.022). There was no significant correlation between the presences of ALPA and anti-OMP Plus TM or NOD2/CARD15 genotype.

Conclusion: The present study demonstrated enhanced formation of APLA in IBD patients which was significantly associated with the presence of ASCA, suggesting a possible contributory role of bacterial translocation to antibody development. The excessive causative role of microbes may also be advocated by the significant proportion of IgM type antibodies. The impact of APLA on the disease course should be evaluated longitudinally in a large series of IBD patients.