Ulcerative colitis: Treatment updates

Dysbiosis has been observed to increase pathogenic and proinflammatory bacteria, and to generally be triggered by an event such as infectious gastroenteritis, in which there is an imbalance between commensal bacteria and pathogens, to perpetuate an alteration in the epithelial intestinal barrier, causing translocation of bacteria and their products in genetically susceptible individuals.9 The current review aims to describe treatment aspects of ulcerative colitis, role of disturbed normal flora in the pathogenesis of UC and significant role of prebiotics in the treatment of UC. Complete blood count, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) also known as inflammation markers serum electrolytes, liver function tests, stool samples for microbiologic analysis should be ordered for all UC suspected patients.10 The data of anaemia, leukocytosis, and thrombocytosis is revealed by complete blood count. Medical therapy of acute UC flares depends mainly on their severity. [...]mild flares are usually managed with oral and/or topical aminosalicylates, whereas for severe attacks intravenous corticosteroids (CSs) remain as the first-line therapy.12 To optimize clinical outcomes in these patients, response to any treatment should be assessed in a timely manner; in this sense, it is widely accepted that response to aminosalicylates should be evaluated in 2 to 4 weeks, whereas response to intravenous CS should be assessed in 3 to 5 days in severe attacks.13 Acute severe UC is treated with cyclosporine and Mesalazine. According to the recent data suggested PPAR increases expression of phosphatase and tensin homologue (PTEN) which is a tumor suppressor protein that inhibits PI3K signaling.24 Very limited data are available on the capacity of vedolizumab to induce mucosal and histological healing.