The Great Pediatric Debate—Corticosteroids in SLE: Slay or Stay?

Dr. von Scheven explained that 50–60% of damage accrual in SLE is due to corticosteroids, particularly in doses over 6–7 mg.¹⁰ She argued that the EULAR guidelines, which recommend steroid dose reduction and discontinuation when possible were in line with her position. She also highlighted a cohort of adult patients with SLE in Naples, demonstrating that corticosteroid discontinuation was feasible, with flare rates comparable to patients continued on corticosteroids.¹¹

She advocated for the development of research protocols to guide corticosteroid tapering, analogous to the careful attention given to induction regimens. As an example, she shared the experience of the Toronto Lupus Clinic, which gradually discontinued prednisone over three months, and demonstrated reduced flare risk by 70%.¹² However, Dr. Brunner later reviewed the same data, countering that these patients had already been in clinical remission for more than two years.

Dr. von Scheven clearly demonstrated the deleterious effects that corticosteroids have on children, and advocated for a rational approach to prednisone tapering, rather than one rooted in negativity bias and fear of flare.

Against Discontinuing Corticosteroids

Dr. Hermine Brunner

The counterargument was presented by Hermine Brunner, MD, MSc, MBA, professor of pediatrics and director of the Division of Rheumatology at the Cincinnati Children’s Hospital Medical Center. She opened by expressing appreciation for corticosteroids, stating that they save lives. She provided important historical context: before the advent of corticosteroids, children died from complications of SLE within 20 months.¹³ She displayed striking images of patients with various manifestations of severe disease, illustrating the important role that corticosteroids play in limiting patient suffering.

Dr. Brunner cited additional benefits of corticosteroids: They are affordable, fast acting and effective. At an immune level, they are a jack of all trades, affecting numerous inflammatory pathways, such as blocking neutrophil adhesion, preventing cytokine release from monocytes and blocking T cell maturation.

In agreement with Dr. von Scheven, she emphasized that we are lacking data on how to manage low-dose prednisone, perhaps rooted in the complexity of the steroid receptor, and made more challenging by the concepts of steroid resistance and tolerance seen in some patients.

She focused the remainder of her argument on the risk of flare, emphasizing that stopping corticosteroids in DORIS remission offered no protection against flares, and highlighted the association between flare and reductions in quality of life and significant healthcare associated costs for patients and their families.^14-16