Article Text
Abstract
Background Belimumab is the only biologic agent approved for systemic lupus erythematosus (SLE). In cornerstone clinical trials, belimumab demonstrated SRI-4 response in patients with moderate disease activity, and real-world studies showed consistent findings.1–3 However, most previous studies have been conducted in patients with use of steroids, with mean prednisolone-equivalent dose of approximately 10 mg/day (1¬3). Therefore, the effect of belimumab has been focused on the steroid sparing. Here, we aimed to identify the effect of belimumab in SLE patients treated with minimal or no steroid with mild-to-moderate activity.
Methods We retrospectively reviewed the electronic medical records of patients (age ≥ 18 years) who first received belimumab from May 2021 to June 2022 and maintained use at least 6 months. We only included patients who received prednisolone-equivalent ≤5mg or without steroid (for more than 1 year). The primary endpoint was SRI-4 response at 6 months, and secondary endpoint was improvement in serology at 6 months. Analysis Of Variance (ANOVA) with Bonferroni’s post hoc analysis were performed to compare the continuous variables.
Results In total, 31 patients were included, with 12 minimal steroid users and 19 non-steroid users. The mean age was 39.2 (±11.4) years, and 90.3% were female. Baseline SELENA-SLEDAI was 6.0 (4.0¬9.0). The primary endpoint was seen in 32.3% (10/31). Anemia (p=0.025), C4 level (p<0.001), and SELENA-SLEDAI (p=0.016) showed significant improvement over time during treatment. Univariable analysis showed baseline SELENA-SLEDAI and arthritis were significantly associated with SRI-4 response at 6 months, and SELENA-SLEDAI only remained significant in multivariable logistic regression analysis.
Conclusions In our cohort study, belimumab was shown to be effective in improving SELENA-SLEDAI, anemia and low C4 in patients who did not use or did use minimal dose of steroids. Therefore, the effect of belimumab can be expected even in patients not taking steroids.
References
Lancet 2011 Feb 26;377(9767):721–31
J Autoimmun 2018 Jan;86:1–8
Autoimmun Rev 2017 Apr;16(4):343–351.
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