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Published on: June 8, 2022
Contributors to organ damage in childhood lupus: corticosteroid use and disease activity
Maria Hanif1, Chandni Sarker1,2, Eslam Al-Abadi3
1Department of Women's & Children's Health, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool, UK.
Insights
Childhood lupus patients with higher disease activity, methylprednisolone use, or baseline damage face increased risk of long-term damage. Early intervention and treat-to-target strategies are crucial for mitigating damage in pediatric lupus.
Area of Science:
- Pediatric Rheumatology
- Systemic Lupus Erythematosus Research
- Clinical Epidemiology
Background:
- Childhood-onset lupus (JSLE) can lead to significant long-term damage.
- Identifying predictors of damage accrual is essential for effective management.
- Paediatric-specific factors influencing damage require further investigation.
Purpose of the Study:
- To identify clinical and demographic predictors of damage in children with lupus.
- To correlate disease activity and treatment variables with damage accrual.
- To inform mitigation strategies for preventing long-term damage in JSLE.
Main Methods:
- Analysis of data from the UK JSLE Cohort Study.
- Application of univariable and multivariable Prentice-Williams-Peterson models.
- Stratified analyses based on disease activity (AMS ≤2, ≤4, >4) and corticosteroid use.
Main Results:
- Higher disease activity (AMS/PGA) and methylprednisolone use predicted damage across the cohort.
- Baseline damage predicted future damage in minimal disease activity and no CS subgroups.
- Predictive factors varied slightly across different disease activity levels.
Conclusions:
- Disease activity (AMS/PGA) and proxy indicators (methylprednisolone, baseline damage) are key predictors of damage.
- Treat-to-target strategies are vital for reducing disease activity and toxicity.
- Proactive management is essential to minimize long-term damage in pediatric lupus.
Objectives:
Awareness of paediatric-specific predictors of damage in childhood lupus is needed to inform mitigation measures. The objective of this study was to ascertain how clinical and demographic variables correlate with damage accrual and identify predictors of damage.
Methods:
This analysis included UK JSLE Cohort Study participants. Univariable and multivariable Prentice-Williams-Peterson models investigated how demographic and clinical factors influenced the hazards of new damage. Analyses were performed across the entire cohort, in patients with minimal disease activity marked by a time-adjusted average SLEDAI-2K score (AMS) of ≤2, in patients with low activity (AMS of ≤4), patients with moderate-to-high activity (AMS of >4) and patients with no CS use.
Results:
Within the entire cohort (n = 430), factors associated with damage included: any methylprednisolone [hazard ratio, HR 2.20 (CI 1.33-3.62)], time-adjusted mean Physician's Global Assessment (PGA) [HR 2.87 (CI 1.48-5.56)] and AMS score [HR 1.13 (CI 1.03-1.24), all P < 0.05]. Within the low activity subgroup, any methylprednisolone [HR 2.61 (CI 1.04-6.53)] and time-adjusted mean PGA [HR 3.41 (CI 1.52-7.76)] were associated with damage (both P < 0.05). Within the moderate-to-high activity subgroup, any methylprednisolone [HR 2.29 (CI 1.31-4.00)], time-adjusted mean PGA [HR 2.66, (CI 1.20-5.87)] and AMS score [HR 1.15 (CI 1.03-1.29)] were predictive of damage (all P < 0.05). Baseline organ damage was predictive of subsequent damage accrual in the minimal disease activity subgroup [HR 1.33 (CI 1.78-8.08)] and the no CSs subgroup [HR 3.64 (CI 1.83-7.24), both P < 0.005].
Conclusion:
Disease activity levels (AMS/PGA) and proxy indicators (methylprednisolone exposure, baseline damage) were found to be key predictors of damage accrual. This highlights the importance of practical strategies, such as treat-to-target, for reducing disease activity and long-term treatment toxicity.
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