Abstract
Pyoderma gangrenosum is a rare neutrophilic dermatosis that presents as a tender, rapidly progressive ulcer with violaceous, undermined borders. Pathophysiology is multifactorial and has been suggested to involve neutrophil dysfunction, increased T-cell activation, and inflammatory mediator release, often in settings that are known to have autoimmune or genetic diseases. Some medications that modify the immune response have been described to trigger pyoderma gangrenosum. Vedolizumab is a monoclonal antibody used in the management of inflammatory bowel disease that has been shown to be effective in the treatment of pyoderma gangrenosum but, in some cases, has been shown to paradoxically induce pyoderma gangrenosum. Vedolizumab causes gut-selective inhibition of lymphocyte migration, which may lead to the activation of lymphocytes in other organ systems, such as the skin. In this report, we present a case of pyoderma gangrenosum in a patient treated with vedolizumab for ulcerative colitis and explore the possible mechanism behind vedolizumab-induced pyoderma gangrenosum.