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      Role of Using Nonsteroidal Anti-Inflammatory Drugs in Chemoprevention of Colon Cancer in Patients With Inflammatory Bowel Disease

      review-article
      1 , , 2 , 2 , 3 , 4 , 5 , 1
      ,
      Cureus
      Cureus
      ibd, colitis associated cancer, colorectal cancer, nsaids, mesalazine, chemoprevention

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          Abstract

          The process of inflammation occurs due to inflammatory mediators, including prostaglandins, cytokines, and tumor necrosis factor (TNF). All these mediators activate the process of tumorigenesis and dysplasia, leading to colitis-associated cancer. Several drugs used to decrease these mediators will help in the treatment of acute attacks and also help in prolonged remissions of the disease by using nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and biological factors. Reducing these inflammatory mediators also have a role in chemoprevention and prevent progression to colorectal carcinoma. The most researched drugs in this process of chemoprevention are NSAIDs as it has both cyclooxygenase-2 (COX-2) inhibitory and non-inhibitory effects. These drugs should be taken for a long time and in large doses to reach this effect, which puts the patient at risk for various side effects. Researchers will need to do more research in the future to find the lowest effective dose that can reach the chemopreventive effect. We used database Pubmed as the main source for data search and extracted articles exploring the relationship between NSAIDs and their role in chemoprevention of colorectal carcinoma in inflammatory bowel disease (IBD) patients. We chose 23 studies which included seven review articles. We found that inflammatory mediators have a key role in colitis-associated cancer.

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          Most cited references20

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          Cancers complicating inflammatory bowel disease.

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            Colorectal cancer in inflammatory bowel disease: the risk, pathogenesis, prevention and diagnosis.

            Patients with inflammatory bowel disease (IBD) are at increased risk for developing colorectal cancer (CRC), although the overall incidence of IBD-associated CRC has been diminishing in recent decades in western countries. As demonstrated in previous studies, the risk of CRC in IBD increases with longer duration, extent of colitis, a familial history of CRC, coexistent primary sclerosing cholangitis, and the degree of inflammation. The pathogenesis of CRC in IBD is poorly understood. Similar to sporadic CRC, IBD-associated CRC is a consequence of sequential episodes of genomic alteration. Multiple inter-related pathways, including immune response by mucosal inflammatory mediators, oxidative stress, and intestinal microbiota, are also involved the pathogenesis of IBD-associated CRC. Continuing colonic inflammation appears to be a factor in the development of CRC; therefore, anti-inflammatory agents such as 5-aminosalicylate compounds and immune modulators have been considered as potential chemopreventive agents. Colonoscopic surveillance is widely accepted as being effective in reducing the risk of IBD-associated CRC, although no clear evidence has confirmed that surveillance colonoscopy prolongs survival in patients with extensive colitis. The traditional recommendation has been quadrantic random biopsies throughout the entire colon; however, several guidelines now have endorsed chromoendoscopy with a target biopsy because of increasing diagnostic yields and reduced workloads for endoscopists and pathologists. New technologies such as narrow band imaging, confocal endomicroscopy, and autofluorescence imaging have not yet been confirmed as surveillance strategies in IBD.
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              Toll-like Receptors and Inflammatory Bowel Disease

              Inflammatory bowel disease (IBD) is one relapsing and lifelong disease that affects millions of patients worldwide. Increasing evidence has recently highlighted immune-system dysfunction, especially toll-like receptors (TLRs)-mediated innate immune dysfunction, as central players in the pathogenesis of IBD. TLRs and TLR-activated signaling pathways are involved not only in the pathogenesis but also in the efficacy of treatment of IBD. By understanding these molecular mechanisms, we might develop a strategy for relieving the experience of long-lasting suffering of those patients and improving their quality of life. The purpose of this review article is to summarize the potential mechanisms of TLR signaling pathways in IBD and the novel potential therapeutic strategies against IBD.
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                Author and article information

                Journal
                Cureus
                Cureus
                2168-8184
                Cureus
                Cureus (Palo Alto (CA) )
                2168-8184
                22 May 2020
                May 2020
                : 12
                : 5
                : e8240
                Affiliations
                [1 ] Internal Medicine, California Institute of Behavioral Neurosciences and Psychology, Fairfield, USA
                [2 ] Psychology, California Institute of Behavioral Neurosciences and Psychology, Fairfield, USA
                [3 ] Business & Management, University Sultan Zainal Abidin, Terengganu, MYS
                [4 ] Family Medicine, California Institute of Behavioral Neurosciences and Psychology, Fairfield, USA
                [5 ] Family Medicine, Lagos State Health Service Commission/Alimosho General Hospital, Lagos, NGA
                Author notes
                Article
                10.7759/cureus.8240
                7306635
                82aa0ca9-fb30-435d-b0c7-54b1a6e10533
                Copyright © 2020, Abdalla et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 21 April 2020
                : 22 May 2020
                Categories
                Gastroenterology

                ibd,colitis associated cancer,colorectal cancer,nsaids,mesalazine,chemoprevention

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