Advances in refractory ulcerative colitis treatment: A new therapeutic target, Annexin A2

摘要

Medical treatment has progressed significantly over the past decade towards achieving and maintaining clinical remission in patients with refractory ulcerative colitis (UC). Proposed mediators of inflammation in UC include pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-2, and the cell-surface adhesive molecule integrin alpha 4 beta 7. Conventional therapeutics for active UC include 5-aminosalicylic acid, corticosteroids and purine analogues (azathioprine and 6-mercaptopurine). Patients who fail to respond to conventional therapy are treated with agents such as the calicineurin inhibitors cyclosporine and tacrolimus, the TNF-alpha inhibitors infliximab or adalimumab, or a neutralizing antibody (vedolizumab) directed against integrin alpha 4 beta 7. These therapeutic agents are of benefit for patients with refractory UC, but are not universally effective. Our recent research on TNF-alpha shedding demonstrated that inhibition of annexin (ANX) A2 may be a new therapeutic strategy for the prevention of TNF-alpha shedding during inflammatory bowel disease (IBD) inflammation. In this review, we provide an overview of therapeutic treatments that are effective and currently available for UC patients, as well as some that are likely to be available in the near future. We also propose the potential of ANX A2 as a new molecular target for IBD treatment.