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Antiphospholipid antibodies in adult IgA vasculitis: observational study

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Abstract

We evaluated the occurrence of antiphospholipid antibodies (aPLs) in acute adult IgA vasculitis (IgAV), and potential correlations with IgAV clinical presentation. We determined lupus anticoagulants (LAs) and IgG, IgM, and IgA isotypes of anticardiolipin antibodies (aCL), antibodies against β2-glycoprotein I (aβ2GPI) and against the phosphatidylserine-prothrombin complex (aPS/PT) in prospectively collected, histologically proven IgAV, diagnosed for the first time between January 2013 and February 2018 at our secondary/tertiary rheumatology center. During the 62 months, we determined aPLs in 125 IgAV patients (56.8% male; median (IQR) age 64.7 (48.6–78.2) years). Sixty-four (51.2%) patients had aPLs. We found LAs, aPS/PT, aβ2GPI, and aCL in 24.8%, 21.6%, 13.6%, and 11.2% of cases, respectively. With 17.6%, the IgA aPS/PT was the most common aPL subtype. aPL-positive and aPL-negative patients did not differ in the clinical presentation of acute IgAV or in the frequency of thrombotic events. aPL-positive IgAV patients had significantly higher erythrocyte sedimentation rate (p < 0.001), and C-reactive protein (p < 0.001). The subset of IgA aPS/PT-positive patients more commonly had renal involvement in acute disease (RR 2.4 (95% CI 1.6–3.7)). aPLs are commonly detected during acute IgAV episodes. Patients with aPLs have similar clinical presentation, but higher markers of inflammation at than those without them. The subset of IgAV patients with IgA aPS/PT more commonly had renal involvement.

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Funding

The study was funded by the Slovenian national research grant P3-0314.

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Correspondence to Alojzija Hočevar.

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The informed consent for this study was not required nor obtained. The study was approved by the Slovenian National medical ethics committee.

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Rheumatology in Slovenia: Clinical practice and translational research

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Hočevar, A., Rotar, Ž., Žigon, P. et al. Antiphospholipid antibodies in adult IgA vasculitis: observational study. Clin Rheumatol 38, 347–351 (2019). https://doi.org/10.1007/s10067-018-4248-2

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  • DOI: https://doi.org/10.1007/s10067-018-4248-2

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