Effect of cyclooxygenase-2 inhibition on human Helicobacter pylori gastritis: mechanisms underlying gastrointestinal safety and implications for cancer chemoprevention
dc.contributor.author | Scheiman, James M. | en_US |
dc.contributor.author | Greenson, Joel K. | en_US |
dc.contributor.author | Lee, J. | en_US |
dc.contributor.author | Cryer, B. | en_US |
dc.date.accessioned | 2010-06-01T22:11:21Z | |
dc.date.available | 2010-06-01T22:11:21Z | |
dc.date.issued | 2003-06 | en_US |
dc.identifier.citation | Scheiman, J. M.; Greenson, J. K.; Lee, J.; Cryer, B. (2003). "Effect of cyclooxygenase-2 inhibition on human Helicobacter pylori gastritis: mechanisms underlying gastrointestinal safety and implications for cancer chemoprevention." Alimentary Pharmacology & Therapeutics 17(12): 1535-1543. <http://hdl.handle.net/2027.42/75208> | en_US |
dc.identifier.issn | 0269-2813 | en_US |
dc.identifier.issn | 1365-2036 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/75208 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12823157&dopt=citation | en_US |
dc.description.abstract | Cyclooxygenase (COX)-2 expression and prostaglandin production is increased by Helicobacter pylori infection. Non-selective COX inhibitors reduce prostaglandins and mucosal proliferation in infected mucosa and may reduce gastric cancer risk, but ulceration precludes their use. COX-2 inhibitors cause fewer ulcers and may be chemopreventive. Physiological studies of COX-2 inhibitors in humans with H. pylori infection have not been performed. Aim: To study the impact of COX-2 specific inhibition on gastric prostaglandin levels, H. pylori gastritis and proliferation. Methods: Twenty infected (eight males, 12 females; age 38 1.8) and six uninfected (four males, two females; age 36 3.5) healthy volunteers received rofecoxib 25 mg daily for 14 days. Endoscopic biopsies were evaluated for prostaglandin E 2 (PGE 2 ) content, gastritis and proliferation. Results: Before drug therapy, compared to uninfected, H. pylori -infected subjects had significantly higher: (a) gastric mucosal PGE 2 (pg mg tissue) in the gastric body and antrum, (b) H. pylori score in body and antrum and (c) mid-gland proliferation index in antrum and body. The COX-2 inhibitor did not significantly affect PGE 2 levels, gastritis scores or proliferation indices in the body or antrum in the H. pylori- positive or -negative subjects. Conclusion: The predominant source of increased gastric PGE 2 in H. pylori infection appears to be COX-1-derived. In non-ulcerated H. pylori gastritis, COX-2 inhibition does not affect cellular proliferation. Rofecoxib's lack of effect on gastric prostaglandin levels and proliferation in H. pylori -infected mucosa may explain the absence of an increased ulcer risk among COX-2 inhibitor users with H. pylori infection. The lack of significant effect on intermediate biomarkers raises uncertainty regarding the potential of specific COX-2 inhibitors for chemoprevention of gastric cancer. | en_US |
dc.format.extent | 102731 bytes | |
dc.format.extent | 3109 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Science Ltd | en_US |
dc.rights | 2003 Blackwell Publishing Ltd | en_US |
dc.title | Effect of cyclooxygenase-2 inhibition on human Helicobacter pylori gastritis: mechanisms underlying gastrointestinal safety and implications for cancer chemoprevention | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Otolaryngology | en_US |
dc.subject.hlbsecondlevel | Pharmacy and Pharmacology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan, USA; | en_US |
dc.contributor.affiliationother | Division of Gastroenterology, Department of Internal Medicine, | en_US |
dc.contributor.affiliationother | Department of Pathology, and the | en_US |
dc.contributor.affiliationother | Division of Gastroenterology, Department of Internal Medicine, University of Texas South-western, Dallas Veteran Affairs Medical Center, Dallas, Texas, USA | en_US |
dc.identifier.pmid | 12823157 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/75208/1/j.1365-2036.2003.01587.x.pdf | |
dc.identifier.doi | 10.1046/j.1365-2036.2003.01587.x | en_US |
dc.identifier.source | Alimentary Pharmacology & Therapeutics | en_US |
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dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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