medwireNews: Glucocorticoid use is associated with an increased risk for organ damage in people with systemic lupus erythematosus (SLE) regardless of the level of disease activity, study findings indicate.
Writing in The Lancet Rheumatology, Diane Apostolopoulos (Monash University, Melbourne, Victoria, Australia) and co-authors say: “Disentangling the potential contribution of glucocorticoid use to organ damage in SLE is confounded, in most studies, by the fact that glucocorticoid use is usually associated with active disease.
“Our study showed that organ damage accrual occurred in a similar proportion of patients without disease activity as in the overall cohort, and that glucocorticoid use was a significant risk factor for damage.”
The study included 1707 patients (93% women) from the Asia-Pacific Lupus collaboration cohort who were observed for a median of 2.2 years. During this period, the majority (82.3%) of patients were exposed to prednisolone, with a median time-adjusted mean prednisolone dose of 5.0 mg/day.
Overall, 14.9% of participants experienced damage accrual events, defined as an increase of at least 1 point on the Systemic Lupus International Collaborating Clinics Damage Index (SDI), whilst under observation.
After adjustment for age, smoking status, baseline damage, timeadjusted mean prednisolone dose, and disease activity defined by time-adjusted mean SLEDAI-2K (AMS) score, the researchers found that having SDI damage (SDI >0) at baseline was significantly associated with a 32% increased risk for damage accrual.
A second multivariate model, in which Physician’s Global Assessment (PGA) score replaced AMS score, showed that time-adjusted mean PGA score was also significantly associated with damage accrual, with each 0.1-unit increase associated with a 5% increase in risk.
In both models, each additional year in age at baseline was associated with a significant 1% increased risk for damage accrual, while time-adjusted mean prednisolone dose was associated with a 5–6% increased risk per 1-mg/day increase. Conversely, Asian ethnicity was associated with a significant 37–39% lower risk for damage accrual relative to non-Asian ethnicity.
The researchers also analyzed data for a subgroup of 157 patients who had no clinical or serological disease activity for the entire study period (AMS score=0). Of these, 65.6% had glucocorticoid exposure and the median time-adjusted mean prednisolone dose was 2.0 mg/day.
Despite the absence of disease activity, 13.4% of these patients experienced a damage accrual event during the follow-up period. Multivariate analysis revealed that the risk for damage among these patients was significantly and independently associated with time-adjusted mean prednisolone dose (hazard ratio [HR]=1.14 per 1-mg/day increase), time-adjusted mean PGA score (HR=1.13 per 0.1-unit increase), and age at enrolment (HR=1.04 per year), but not baseline SDI damage.
“These findings support the contention that glucocorticoid use is indeed an independent contributor to the risk of organ damage in SLE overall, and suggest that damage accrual continues even when active disease is not measurable on SLEDAI2K,” Apostolopoulos et al remark.
They stress, however, that “[in the absence of more effective and safer treatments for SLE, glucocorticoid use remains essential in patients with significant disease activity.”
Nonetheless, the authors conclude that their data “suggest that unnecessary use of glucocorticoids should be avoided in the management of the disease where possible.”
By Laura Cowen
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