Clinical Research Directory

A Single Cycle of Intravenous Immunoglobulin as Adjuvant to Rituximab in Patients With Pemphigus: A Retrospective Cohort Study at a Tertiary Referral Center

Pemphigus is a critical autoimmune skin condition mediated by pathogenic autoantibodies mainly against desmoglein (Dsg)1 and Dsg3, and is traditionally managed with systemic corticosteroids and immunosuppressants.The revolutionary introduction of rituximab (RTX) has opened up a new era of pemphigus treatment by enabling treatment strategies to specifically target CD20+ B cells.Studies have highlighted the superior efficacy of RTX combined with systemic corticosteroids, making this therapy first-line treatment for pemphigus patients.Currently, the main challenge for pemphigus management is to maximize efficacy while preventing relapses and reducing risks over the course of the disease. RTX achieves maximum effect typically at 4-8 weeks post-treatment, and is associated with an elevated risk of infection.On the other hand, intravenous immunoglobulin (IVIg), historically employed for the management of refractory pemphigus, is appreciated for its rapid action and lack of added immunosuppressive risk.It has also been shown to induce long-term clinical remission, and continues to serve as a rescue therapy for difficult cases. While there have been reports on the successful use of RTX and concomitant IVIg for treating refractory pemphigus, there is a lack of extensive research weighing the pros and cons of adding IVIg to the currently recommended RTX regimen (Rheumatoid arthritis protocol, RAP). To investigate the efficacy and safety of this combined therapy, we conducted an retrospective cohort study to evaluate the impact of incorporating IVIg into the RTX and systemic corticosteroid treatment protocol for pemphigus patients.

Impact of a Lifestyle Program on Quality of Life in Pemphigus Patients

The aim of this study is To evaluate the impact of lifestyle modifications, including dietary changes and regular exercise, on skin-related quality of life in patients with pemphigus by assessing changes in Skindex-16 scores over a three-month period.

A Randomized Study on Pemphigus Treatment With Humanized CD38 Antibody CM313.

Pemphigus is characterized by the presence of IgG antibodies that lead to the loss of keratinocyte adhesion, resulting in blister formation. The etiology of pemphigus antibodies is multifactorial, involving immune dysregulation, genetic predisposition, and potential viral triggers. CD38, a multifunctional transmembrane glycoprotein, plays a crucial role in B-cell maturation and function. CM313, a novel humanized monoclonal antibody targeting CD38, has shown promise in clinical trials for autoimmune diseases, including refractory/relapsed multiple myeloma (RRMM), systemic lupus erythematosus (SLE), and immune thrombocytopenia (ITP). By binding to CD38 on B cells, CM313 modulates B-cell activation, proliferation, and differentiation, potentially reducing the production of autoantibodies, such as those against desmogleins 1/3 in pemphigus. Preclinical studies have demonstrated that CM313 effectively inhibits CD38 enzymatic activity through antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and Fc-mediated apoptosis. The long-term modulation of B-cell-mediated immune responses by CM313, through the depletion of both short-lived and long-lived plasma cells, suggests a novel therapeutic strategy for pemphigus by targeting the production of pathogenic autoantibodies.