AI Article Synopsis
- Inflammation is triggered by mediators like prostaglandins, cytokines, and tumor necrosis factor (TNF), and these contribute to tumorigenesis leading to colitis-associated cancer.
- Certain medications, primarily nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and biological factors, can lower these mediators and aid in treating acute flare-ups as well as help maintain long-term remission.
- Though NSAIDs show promise in chemoprevention for colorectal cancer in IBD patients, their use in high doses over extended periods raises concerns for side effects, highlighting the need for more research to determine effective, lower doses.
Article 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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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7306635 | PMC |
| http://dx.doi.org/10.7759/cureus.8240 | DOI Listing |
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