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Updated: Jul 31, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Baseline neutrophil-to-lymphocyte ratio combined with SLEDAI predicts lupus low disease activity state at 1 year: a
Yadan Zou1, Ruohan Yu1, Kun Yang2
1Department of Rheumatology and Immunology, Peking University International Hospital, Beijing, China.
Background:
Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease in which treat-to-target management increasingly emphasizes attainment of Lupus Low Disease Activity State (LLDAS). Complete blood count (CBC)-derived inflammatory indices are inexpensive and readily available markers, but their value for predicting subsequent LLDAS remains unclear.
Methods:
This retrospective cohort study included 165 hospitalized patients with SLE at Peking University International Hospital between 2022 and 2024 who had baseline CBC data and completed 1-year follow-up. Baseline neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI) were calculated from routine hematologic parameters. The primary outcome was LLDAS achievement at 1 year according to Asia Pacific Lupus Collaboration criteria. Univariable and multivariable logistic regression analyses were performed. Multivariable models adjusted for baseline SLEDAI-2K, age, sex, immunosuppressant use, and prednisone dose. Receiver operating characteristic (ROC) analysis, bootstrap internal validation, calibration, and decision curve analysis (DCA) were also conducted.
Results:
Compared with non-LLDAS patients, those who achieved LLDAS had lower baseline SLEDAI-2K, lower prevalence of renal involvement, lower neutrophil counts, higher hemoglobin levels, and lower baseline NLR, PLR, SII, and SIRI. In univariable analysis, higher baseline NLR (OR 0.69, 95% CI 0.57-0.83, P < 0.001), PLR (OR 0.96 per 10-unit increase, 95% CI 0.93-0.99, P = 0.008), and SII (OR 0.86 per 100-unit increase, 95% CI 0.79-0.94, P < 0.001) were associated with lower odds of LLDAS. In the adjusted model, baseline NLR remained independently associated with LLDAS attainment (aOR 0.690, 95% CI 0.561-0.848, P < 0.001). The NLR+SLEDAI-2K model achieved an AUC of 0.746, with limited optimism on bootstrap validation.
Conclusion:
Baseline CBC-derived inflammatory indices, particularly NLR, were associated with 1-year LLDAS attainment in SLE. NLR, combined with SLEDAI-2K, may provide a practical, low-cost adjunct for early risk stratification in treat-to-target-oriented SLE management.

