Objectives: The study aimed to evaluate the clinical course, predictors of relapse and long-term outcome of immune thrombocytopenia associated with SLE.
Methods: This retrospective, single-centre, cohort study included 105 SLE patients with thrombocytopenia (platelets <100 × 109/l), who were followed between 1983 and 2025. The 'early', 'initial' and 'durable' response rates in the first week, first and sixth months were analysed. Two multivariable logistic regression models were used to identify predictors of relapse. The first model was adjusted for baseline factors (including antiphospholipid serology, SLEDAI-2K and platelet count), whilst the second evaluated on-treatment variables. The associations between damage accrual and cumulative glucocorticoid dose, thrombocytopenia severity and relapse frequency were evaluated.
Results: Among 90 patients with acute/acute-on-chronic thrombocytopenia, 30 (33%) experienced a relapse. aPL positivity was identified as an independent predictor of relapse (OR: 3.38, 95% CI 1.19-9.58), whereas higher baseline SLEDAI-2K was inversely associated with relapse risk (OR: 0.91, 95% CI 0.85-0.97). Major bleeding events occurred in 13% of patients, with a significantly increased frequency when platelet counts fell below 30 × 109/l (P = 0.003). Damage accrual was observed in 61% of the cohort. Cumulative glucocorticoid dose was the primary independent driver of damage (OR: 1.056/g, P = 0.005). However, neither the severity of thrombocytopenia nor the number of relapses independently predicted damage.
Conclusion: aPL positivity is associated with relapse of thrombocytopenia in SLE. While severe thrombocytopenia can lead to bleeding complications, long-term organ damage is primarily caused by cumulative exposure to glucocorticoids used to treat the relapsing disease.
Keywords: SLE; aPLs; damage; immune thrombocytopenia.
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