The emerging role of rituximab in autoimmune blistering diseases

Rituximab is a chimeric monoclonal antibody that selectively binds to the CD20 molecule on B cells, resulting in their lysis. In autoimmune blistering diseases, the auto-antibody-producing B cells are destroyed and auto-antibody levels are reduced or eliminated. In the majority of patients, rituximab produces rapid clinical response and early resolution. In part, this accounts for the increased use of rituximab. Rituximab does not distinguish normal from pathologic B cells. Hence, shortly after its use, B-cell levels are zero and remain so for several months. In most patients, the use of systemic corticosteroids and immunosuppressive agents are continued after rituximab therapy, while their dosages are significantly decreased. In the majority of patients rituximab is used according to the protocol used in treating lymphoma patients or patients with rheumatoid arthritis. Approximately 50% of patients experience a relapse, requiring additional therapy. Serious adverse events and fatal outcomes have been reported, although their incidence is less than that observed with conventional therapy. Nonetheless, the causes, i.e. infections and septicemia, are similar. Several gaps exist in our understanding of how to optimally benefit from the use of this valuable biological agent. Future studies need to be targeted in designing and implanting protocols that maximize the benefit of rituximab and result in producing sustained prolonged remissions with minimal adverse events and a high quality of life.