INTRODUCTION
Epidermolysis bullosa acquisita (EBA) is a rare autoimmune blistering disorder caused by autoantibodies targeting type VII collagen, which is a critical component of anchoring fibrils responsible for maintaining the integrity of the skin's dermo-epidermal junction. Clinically, EBA presents with tense blisters and erosions, primarily on trauma-prone areas such as the hands, feet, knees, and elbows. Diagnosis typically involves a combination of clinical examination, histopathological analysis, and immunofluorescence studies demonstrating linear deposition of immunoglobulin G and complement along the basement membrane zone.
Treatment of EBA involves a multi-faceted approach aimed at controlling the extent of blistering, reducing inflammation, and preventing complications. Due to its rarity, with a prevalence ranging from 0.08 to 0.5 per million individuals, and the variable efficacy of treatments among patients, there is currently no universally endorsed therapeutic regimen. Various modalities have been explored in addressing this condition, select ones are delineated in Table 1 along with their respective mechanisms of action.
EBA presents significant challenges in management due to its chronic and debilitating nature, which impacts patients' quality of life and often requires long-term immunosuppressive therapy. Over the years, various treatment modalities have been explored in an effort to control disease activity and mitigate symptoms associated with EBA. Among these is rituximab (RTX), a monoclonal antibody targeting CD20-positive B cells, which has emerged as a promising therapeutic option. RTX works by depleting B cells and disrupting the production of pathogenic autoantibodies, thereby attenuating the autoimmune response underlying EBA.13, 14, 25
When considering RTX for the treatment of EBA it is important to weigh the potential benefits against the associated risks. While rituximab has shown promise in managing EBA, particularly due
