Bullous pemphigoid is an autoimmune skin disease caused by the influence of IgG antibodies on antigens in subepidermal cells, which cause inflammation and the formation of bumps in the subepidermal tissue that are prone to rupture and the development of suprainfection.
All of this leads to a significant reduction in the quality of life in these patients, but also to a threefold increase in mortality. The cause of this increase in mortality is an increased susceptibility to infections, but also an increase in cardiovascular risk due to the increased concentration of IgG antibodies in the blood and the enhanced effect of IgG on vascular endothelium.
The only therapeutic option in these patients is topical or systemic administration of glucocorticoids. Although glucocorticoids can bring the disease into remission in the short term, their long-term use is associated with a number of side effects and an increase in cardiovascular risk, which is still increased in this group of patients. Other endogenous and immunosuppressive therapies are only partially effective and have several potential side effects.
A drug, which is administered subcutaneously, that blocks the production of IgG antibodies has so far been shown to be effective in treating myasthenia gravis, a disease that is also mediated by IgG antibodies. In more detail the drug is a receptor antagonist for circulating IgG that results in decreased IgG activity to the major antigens BP180 and BP 230 involved in disease development.
So far it has proven to be very effective with an excellent safety profile and is currently in a randomized double-blind phase II / III study. The inclusion of patients with bullous pemphigoid in this study offers the possibility of more targeted treatment of the disease under strictly controlled conditions.
We are pleased to be working part of this clinical trial and to be the second clinical research site in the world to successfully screen a patient with bullous pemphigoid into this new clinical trial.
