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Background Glucocorticoids are the mainstay of treatment for autoimmune blistering diseases (AIBDs). The Glucocorticoid Toxicity Index (GTI) is a novel, outcome-based glucocorticoid-induced adverse effects monitoring instrument. Objective To investigate whether the GTI score was able to accurately quantify the glucocorticoid-induced toxicity in patients with AIBDs. Methods The prospective cohort study included patients with confirmed diagnoses of AIBDs (group1, currently receiving glucocorticoids; and group 2, had glucocorticoids ceased earlier). Data were collected minimally at baseline (V1) and 3 months (V2). Further data from patients who were able to complete the follow-up visits at 6 months (V3) and 12 months (V4) amid the COVID-19 pandemic were also included. GTI scores were calculated after data collection. Results Analysis of data from V1 and V2 found a linear correlation between GTI score and prednisone doses ( P < .05) and a significant difference in GTI scores between group1 and group 2 ( P < .05). Data from V3 and V4 suggested that GTI scores continued to rise progressively alongside increasing cumulative prednisone dose. Limitations Small sample size, further exacerbated by the COVID-19 pandemic. Single-center study. Conclusion The GTI sensitively and specifically captured the changes in glucocorticoids toxicity over time among patients with AIBDs. The GTI could be a feasible tool that can be used in future clinical trials as a glucocorticoid-induced toxicity outcome measure.

IntroductionBullous pemphigoid (BP) is the most common subtype of autoimmune blistering diseases that primarily affects the elderly and is classically defined by the presence of IgG and/or complement C3 against the BP180 and BP230 hemidesmosome proteins. However, most recent studies have introduced the role of specific eosinophil receptors and chemokine mediators in the pathogenesis of BP which are helpful in identifying new targets for future treatments.Areas coveredThis review will focus on the involvement of eosinophils in BP, including the processes that lead to their recruitment, activation, and regulation. Subsequently, covering new therapeutic options in relation to the role of eosinophils. Eotaxin enhances the recruitment of eosinophils in BP, with CCR3 chemoreceptor that is expressed on eosinophils being identified as a key binding site for eotaxin-1. The pathogenic role of IgE and IL-4 in BP is corroborated by successful treatments with Omalizumab and Dupilumab, respectively. IL-5, IL-17 and IL-23 inhibitors may be effective given their roles in promoting eosinophilia.Expert opinionFurther research into inhibitors of eotaxin, IL-4, IL-5, IL-17, IL-23, CCR3, and specific complement factors are warranted as preliminary studies have largely identified success in treating BP with these agents. Learning from novel treatments for other IgG-mediated autoimmune diseases may be beneficial.

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