Tag Archives: pathophysiology

We read with interest the study by Koga H et al1 and we believe that in light of recent observations including our data (Table 1) the “desmoglein compensation theory” as a explanation for localization of blisters should be revisited 2,3,4. Although the disruption of desmoglein-dependent cell adhesion by autoantibodies is the basic pathophysiology underlying blister formation in pemphigus 2−4, the clinical spectrum does not always mirror this pathogenic process. Three clinical types of pemphigus have been described, the mucosal dominant, cutaneous and mucocutaneous type 2,,3,4 .

By Sergei A. Grando, M.D., Ph.D., D.Sci.
Professor of Dermatology
University of California Davis
NPF Advisory Board Member

The goal of my research is to develop a safer and more rational treatment for pemphigus. I am deeply concerned that we, as physicians caring for patients with pemphigus, have to accept the risk of severe side effects related to the use of long term, high dose corticosteroid therapy.

Despite recent progress in developing nonhormonal therapy for other autoimmune conditions, the treatment of pemphigus remains largely dependent on corticosteroid hormones. The lack of progress in developing new therapies for pemphigus is ironic because we thought we understood the basic mechanisms responsible for the development of this disease. But, perhaps our understanding was wrong and possibly this misunderstanding has hampered advancement in treatment.