Editing Peptic ulcer disease (section)

===NSAIDs===
Taking [[nonsteroidal anti-inflammatory drug]]s (NSAIDs) such as [[aspirin]]<ref>{{cite journal |last1=Chan |first1=F. K. L. |last2=Graham |first2=D. Y. |title=Review article: prevention of non-steroidal anti-inflammatory drug gastrointestinal complications--review and recommendations based on risk assessment. |journal=Aliment Pharmacol Ther |date=May 15, 2004 |volume=19 |issue=10 |pages=1051–61 |doi=10.1111/j.1365-2036.2004.01935.x |pmid=15142194 |s2cid=24654342 |url=https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2004.01935.x |access-date=27 February 2022}}</ref> can increase the risk of peptic ulcer disease by four times compared to non-users. The risk of getting a peptic ulcer is two times for aspirin users. Risk of bleeding increases if NSAIDs are combined with [[selective serotonin reuptake inhibitor]] (SSRI), [[corticosteroid]]s, [[antimineralocorticoid]]s, and [[anticoagulants]]. The gastric mucosa protects itself from [[gastric acid]] with a layer of mucus, the secretion of which is stimulated by certain [[prostaglandin]]s. NSAIDs block the function of [[cyclooxygenase]] 1 (''COX-1''), which is essential for the production of these prostaglandins. Besides this, NSAIDs also inhibit stomach mucosa cells proliferation and mucosal blood flow, reducing [[bicarbonate]] and mucus secretion, which reduces the integrity of the mucosa. Another type of NSAIDs, called COX-2 selective anti-inflammatory drugs (such as [[celecoxib]]), preferentially inhibit ''COX-2'', which is less essential in the gastric mucosa. This reduces the probability of getting peptic ulcers; however, it can still delay ulcer healing for those who already have a peptic ulcer.<ref name="Angel 2017"/> Peptic ulcers caused by NSAIDs differ from those caused by ''H. pylori'' as the latter's appear as a consequence of inflammation of the mucosa (presence of neutrophil and submucosal edema), the former instead as a consequence of a direct damage of the NSAID molecule against COX enzymes, altering the hydrophobic state of the mucus, the permeability of the lining epithelium and mitochondrial machinery of the cell itself. In this way NSAID's ulcers tend to complicate faster and dig deeper in the tissue causing more complications, often asymptomatically until a great portion of the tissue is involved.<ref>{{Cite web |title=NSAIDs: When To Use Them and for How Long |url=https://my.clevelandclinic.org/health/treatments/11086-non-steroidal-anti-inflammatory-medicines-nsaids |access-date=2024-06-07 |website=Cleveland Clinic |language=en}}</ref><ref>{{Citation |last1=Ghlichloo |first1=Ida |title=Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) |date=2024 |work=StatPearls |url=http://www.ncbi.nlm.nih.gov/books/NBK547742/ |access-date=2024-06-07 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=31613522 |last2=Gerriets |first2=Valerie}}</ref>