Clinical Research Directory

Periodontal Status and Disease Severity in Pemphigus Vulgaris Patients

The aim of this study is to evaluate the relationship between the severity of Pemphigus Vulgaris (a chronic autoimmune skin disease) and periodontal (gum) health. Researchers will assess disease activity using the Oral Disease Severity Score (ODSS) for mouth lesions and measure serum Desmoglein 1 and 3 levels through blood tests. These findings will be compared with clinical gum measurements, such as pocket depth and attachment levels. The study intends to determine how the clinical and biochemical severity of Pemphigus Vulgaris impacts periodontal tissues and overall oral health.

Trichoscopy as a Monitoring Tool for Activity and Remission in Pemphigus Vulgaris: A Clinical Study Supported by Immunological Evaluation.

Pemphigus vulgaris (PV) is a potential life-threatening autoimmune bullous disorder presenting with multiple erosions and flaccid blisters that can involve both mucous membrane and skin. The microscopic findings include intraepithelial blisters caused by acantholysis of keratinocytes as the consequence of autoantibody formation. The antibodies are mainly IgG autoantibodies mostly directed against desmoglein 1 and 3 (Dsg 1, 3), which are adhesion molecules expressed on the surface of keratinocytes.

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.