VEDOLIZUMAB FOR REFRACTORY MICROSCOPIC COLITIS: A CASE SERIES

Abstract

Microscopic colitis (MC) is a chronic inflammatory disease of the colon that causes non-bloody, watery diarrhea occurs up to 15 times daily in the presence of normal-appearing mucosa in the colon. There are two main subtypes of MC based on histopathologic features, collagenous colitis (CC) and lymphocytic colitis (LC)1. Treatment of each subtype is similar and should be determined by the severity of symptoms. Some patients suffer severe symptoms despite maximum dosage of budesonide, in these cases biologic therapies should be considered. Vedolizumab, a monoclonal antibody that targets α4β7-integrin, is a gut-specific biologic with an exceptional safety profile. Here, we report our experience with vedolizumab for severe, refractory MC. Eleven patients presenting to the University of Kentucky with severe microscopic colitis refractory to maximum budesonide and Imodium therapy were treated with vedolizumab. Vedolizumab was given at standard induction dosing (300mg IV at week 0, 2 and 6, and then every 8 weeks). Of the eleven patients included in this study, seven reported subjective symptomatic improvement on vedolizumab monotherapy, with four patients attaining less than 3 stools per day. Of the remaining four patients, one continues to do well on vedolizumab and budesonide combination therapy while another developed a rash after vedolizumab induction and treatment was stopped. The third patient was transitioned from vedolizumab to adalimumab and is now well controlled symptomatically and the final patient has not reached symptomatic remission of her disease. Interestingly, of the seven patients who displayed symptomatic improvement with vedolizumab monotherapy, 5/7 patients also showed improvement in albumin levels. Vedolizumab use in refractory microscopic colitis is increasingly recognized as a conceivable therapy for symptomatic improvement and disease remission. Our case series corroborates these findings, as the majority of our patients reported overall improved quality of life. Vedolizumab binds to the α4β7-integrin and prevent adhesion to its ligand, MAdCAM-1, which causes downstream prevention of T-cell adhesion. Although the exact pathophysiology of microscopic colitis remains largely unidentified, it has been postulated that exposure to a luminal antigen may trigger an inflammatory cascade, leading to activation of CD8 T suppressor cells that attack and cause luminal damage to enterocytes2. This hypothesis is supported by vedolizumab’s mechanism of action and proposed efficacy in MC. Due to low volume studies, the data supporting vedolizumab use in refractory microscopic colitis remains limited, and further studies are needed to elucidate the its potential as a first-line therapy. However, based on our experience, we recommend considering vedolizumab for patients suffering from refractory MC.