Background/Purpose: Glucocorticoids (GC) are used to treat various inflammatory and autoimmune diseases, though despite widespread use, real-world data on skin-specific GC toxicity are limited. To better characterize the burden of GC-related skin adverse effects, we prospectively evaluated GC-related skin toxicity over 6 months in a rheumatology clinic setting.

Methods: We obtained data from the Longitudinal Glucocorticoid Toxicity (LONG-TOX) prospective cohort, which enrolls adults with rheumatic diseases receiving or initiating GC therapy (≥3 month expected duration) at a large academic hospital. The domains of the Glucocorticoid Toxicity Index (GTI) were used to assess the GT-SNAPSHOT, a comprehensive baseline assessment of GC toxicity, at baseline, and the GTI at 6 months. GC exposure was tracked using patient diaries and electronic health records. GTI-defined skin toxicities (acneiform rash, easy bruising, hirsutism, atrophy/striae, and erosions/tears/ulcerations) were assessed by a study team member at both visits. We used the GTI Skin Toxicity domain to evaluate changes in GC-related skin toxicity and examined factors associated with baseline skin toxicity and worsening in skin toxicity (i.e., new and/or worsened skin manifestation) over 6 months using univariable logistic regression.

Results: Of 90 enrolled individuals, 74 completed 6-month follow-up. The mean (SD) age was 60.0 (16.6) years, 62.2% were female, median prednisone-equivalent GC dose was 30.0 mg daily, and most (64.4%) were receiving concomitant immunomodulatory therapy (Table 1). Those with skin toxicity at baseline had higher median GT-SNAPSHOT scores (195 vs. 141, p< 0.01) and significantly more neuropsychiatric (90.7% vs. 61.1%, p< 0.01) and infection-related toxicity (20.4% vs. 0.0%, p< 0.01) than those without baseline skin toxicity. At baseline, 61.1% had at least one GTI skin toxicity manifestation, with the most common including easy bruising (34.5%), followed by atrophy/striae (22.2%) and acneiform rash (15.5%) (Table 2). At 6 months, 62.2% had at least one GTI skin toxicity manifestation, with the most common including easy bruising (37.9%), followed by acneiform rash (21.7%) and atrophy/striae (16.3%). Over 6 months, those with worsening skin toxicity (56.8%) had higher overall GTI Cumulative Worsening Scores (median 58.5 vs. 30.5, p< 0.01), higher baseline disease activity (42.9% in remission vs 62.5%, p=0.048), and numerically higher cumulative GC exposure (2167 vs. 2014 prednisone-equivalent mg, p=0.27) compared to those without worsening skin toxicity (Table 3). There were no differences in sex, body mass index, race, or baseline immunomodulatory therapy between groups. Those with worsening skin toxicity had more worsening in the Neuropsychiatric (42.9% vs. 18.8%, p=0.03) and Myopathy (23.8% vs. 6.3%, p=0.04) domains.

Conclusion: Skin-related adverse effects are common with GC use and highlight the need for routine assessment in long-term GC users. Neuropsychiatric GC toxicity was more common in individuals with skin toxicity. Routine assessment of the skin manifestations of the GTI may enhance detection and guide interventions to mitigate morbidity associated with GC treatment.

Table 1. Baseline Demographics and Clinical Characteristics of Individuals With and Without Glucocorticoid-Related Skin Toxicity

Table 2. Glucocorticoid Toxicity Index Skin Toxicity Manifestations at Baseline (Enrollment) and 6 Months

Table 3. Factors Associated with Worsening in Glucocorticoid-Related Skin Toxicity over 6 Months

ACR Meeting Abstracts - https://acrabstracts.org/abstract/real-world-assessment-of-glucocorticoid-induced-skin-toxicity-in-individuals-with-rheumatic-diseases/