Review article: cellular and molecular mechanisms of NSAID‐induced peptic ulcers
Summary Background Nonsteroidal anti‐inflammatory drugs (NSAIDs) are some of the most prescribed drugs worldwide and have now probably overtaken Helicobacter pylori as the most common cause of gastrointestinal injury in Western countries. Further understanding of the pathogenesis of NSAID‐induced u...
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| Veröffentlicht in: | Alimentary pharmacology & therapeutics 2009-09, Vol.30 (6), p.517-531 |
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| container_title | Alimentary pharmacology & therapeutics |
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| creator | MUSUMBA, C. PRITCHARD, D. M. PIRMOHAMED, M. |
| description | Summary
Background Nonsteroidal anti‐inflammatory drugs (NSAIDs) are some of the most prescribed drugs worldwide and have now probably overtaken Helicobacter pylori as the most common cause of gastrointestinal injury in Western countries. Further understanding of the pathogenesis of NSAID‐induced ulcers is important to enable the development of novel and effective preventive strategies.
Aims To provide an update on recent advances in our understanding of the cellular and molecular mechanisms involved in the development of NSAID‐induced ulcers.
Methods A Medline search was performed to identify relevant literature using search terms including ‘nonsteroidal anti‐inflammatory drugs, aspirin, gastric ulcer, duodenal ulcer, pathogenesis, pharmacogenetics’.
Results The mechanisms of NSAID‐induced ulcers can be divided into topical and systemic effects and the latter may be prostaglandin‐dependent (through COX inhibition) or prostaglandin‐independent. Genetic factors may play an important role in determining individual predisposition.
Conclusions The pathogenesis of NSAID‐induced peptic ulcers is complex and multifactorial. Recent advances in cellular and molecular biology have highlighted the importance of various prostaglandin‐independent mechanisms. Pharmacogenetic studies may provide further insights into the pathogenetic mechanisms of NSAID‐induced ulcers and help identify patients at increased risk. |
| doi_str_mv | 10.1111/j.1365-2036.2009.04086.x |
| format | Article |
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Background Nonsteroidal anti‐inflammatory drugs (NSAIDs) are some of the most prescribed drugs worldwide and have now probably overtaken Helicobacter pylori as the most common cause of gastrointestinal injury in Western countries. Further understanding of the pathogenesis of NSAID‐induced ulcers is important to enable the development of novel and effective preventive strategies.
Aims To provide an update on recent advances in our understanding of the cellular and molecular mechanisms involved in the development of NSAID‐induced ulcers.
Methods A Medline search was performed to identify relevant literature using search terms including ‘nonsteroidal anti‐inflammatory drugs, aspirin, gastric ulcer, duodenal ulcer, pathogenesis, pharmacogenetics’.
Results The mechanisms of NSAID‐induced ulcers can be divided into topical and systemic effects and the latter may be prostaglandin‐dependent (through COX inhibition) or prostaglandin‐independent. Genetic factors may play an important role in determining individual predisposition.
Conclusions The pathogenesis of NSAID‐induced peptic ulcers is complex and multifactorial. Recent advances in cellular and molecular biology have highlighted the importance of various prostaglandin‐independent mechanisms. Pharmacogenetic studies may provide further insights into the pathogenetic mechanisms of NSAID‐induced ulcers and help identify patients at increased risk.</description><identifier>ISSN: 0269-2813</identifier><identifier>EISSN: 1365-2036</identifier><identifier>DOI: 10.1111/j.1365-2036.2009.04086.x</identifier><identifier>PMID: 19575764</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Anti-Inflammatory Agents, Non-Steroidal - adverse effects ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Biological and medical sciences ; Clinical Trials as Topic ; Cyclooxygenase 2 Inhibitors - adverse effects ; Digestive system ; Gastroenterology. Liver. Pancreas. Abdomen ; Genetic Predisposition to Disease - genetics ; Helicobacter pylori ; Humans ; Medical sciences ; Other diseases. Semiology ; Peptic Ulcer - chemically induced ; Pharmacology. Drug treatments ; Prostaglandins ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><ispartof>Alimentary pharmacology & therapeutics, 2009-09, Vol.30 (6), p.517-531</ispartof><rights>2009 Blackwell Publishing Ltd</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4956-57cf6b935e6c6c3a8f790788ce0cf3a25ddb9b90b8653aa1b91a0ed52874c7b33</citedby><cites>FETCH-LOGICAL-c4956-57cf6b935e6c6c3a8f790788ce0cf3a25ddb9b90b8653aa1b91a0ed52874c7b33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2036.2009.04086.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2036.2009.04086.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,1434,27929,27930,45579,45580,46414,46838</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21830314$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19575764$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MUSUMBA, C.</creatorcontrib><creatorcontrib>PRITCHARD, D. M.</creatorcontrib><creatorcontrib>PIRMOHAMED, M.</creatorcontrib><title>Review article: cellular and molecular mechanisms of NSAID‐induced peptic ulcers</title><title>Alimentary pharmacology & therapeutics</title><addtitle>Aliment Pharmacol Ther</addtitle><description>Summary
Background Nonsteroidal anti‐inflammatory drugs (NSAIDs) are some of the most prescribed drugs worldwide and have now probably overtaken Helicobacter pylori as the most common cause of gastrointestinal injury in Western countries. Further understanding of the pathogenesis of NSAID‐induced ulcers is important to enable the development of novel and effective preventive strategies.
Aims To provide an update on recent advances in our understanding of the cellular and molecular mechanisms involved in the development of NSAID‐induced ulcers.
Methods A Medline search was performed to identify relevant literature using search terms including ‘nonsteroidal anti‐inflammatory drugs, aspirin, gastric ulcer, duodenal ulcer, pathogenesis, pharmacogenetics’.
Results The mechanisms of NSAID‐induced ulcers can be divided into topical and systemic effects and the latter may be prostaglandin‐dependent (through COX inhibition) or prostaglandin‐independent. Genetic factors may play an important role in determining individual predisposition.
Conclusions The pathogenesis of NSAID‐induced peptic ulcers is complex and multifactorial. Recent advances in cellular and molecular biology have highlighted the importance of various prostaglandin‐independent mechanisms. Pharmacogenetic studies may provide further insights into the pathogenetic mechanisms of NSAID‐induced ulcers and help identify patients at increased risk.</description><subject>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Clinical Trials as Topic</subject><subject>Cyclooxygenase 2 Inhibitors - adverse effects</subject><subject>Digestive system</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Helicobacter pylori</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Other diseases. Semiology</subject><subject>Peptic Ulcer - chemically induced</subject><subject>Pharmacology. Drug treatments</subject><subject>Prostaglandins</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><issn>0269-2813</issn><issn>1365-2036</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMtu1DAUhi0EotPCKyBvSlcJx_b4VonFqNwqVbQqZW05zonIyEkGu-ll10fgGXkSks6o7BBnYx-d77ePPkIog5JN9W5dMqFkwUGokgPYEpZgVHn3jCyeBs_JAriyBTdM7JH9nNcAoDTwl2SPWamlVssFubzEmxZvqU_XbYh4TAPGOEafqO9r2g0Rw2PXYfjh-zZ3mQ4N_fptdfrh98Ovtq_HgDXd4GaK0zEGTPkVedH4mPH17jwg3z99vDr5Upydfz49WZ0VYWmlKqQOjaqskKiCCsKbRlvQxgSE0AjPZV1XtrJQGSWF96yyzAPWkhu9DLoS4oAcbd_dpOHniPnadW2e1_c9DmN2WggzFZiJfPtPkgOf_HE7gWYLhjTknLBxm9R2Pt07Bm4279ZuFuxmwW427x7Nu7sp-mb3x1h1WP8N7lRPwOEO8Dn42CTfhzY_cZwZAYLN3Pstd9tGvP_vBdzq4mq-iT_RiZ9D</recordid><startdate>200909</startdate><enddate>200909</enddate><creator>MUSUMBA, C.</creator><creator>PRITCHARD, D. M.</creator><creator>PIRMOHAMED, M.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>200909</creationdate><title>Review article: cellular and molecular mechanisms of NSAID‐induced peptic ulcers</title><author>MUSUMBA, C. ; PRITCHARD, D. M. ; PIRMOHAMED, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4956-57cf6b935e6c6c3a8f790788ce0cf3a25ddb9b90b8653aa1b91a0ed52874c7b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Clinical Trials as Topic</topic><topic>Cyclooxygenase 2 Inhibitors - adverse effects</topic><topic>Digestive system</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Helicobacter pylori</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Other diseases. Semiology</topic><topic>Peptic Ulcer - chemically induced</topic><topic>Pharmacology. Drug treatments</topic><topic>Prostaglandins</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MUSUMBA, C.</creatorcontrib><creatorcontrib>PRITCHARD, D. M.</creatorcontrib><creatorcontrib>PIRMOHAMED, M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Alimentary pharmacology & therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MUSUMBA, C.</au><au>PRITCHARD, D. M.</au><au>PIRMOHAMED, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Review article: cellular and molecular mechanisms of NSAID‐induced peptic ulcers</atitle><jtitle>Alimentary pharmacology & therapeutics</jtitle><addtitle>Aliment Pharmacol Ther</addtitle><date>2009-09</date><risdate>2009</risdate><volume>30</volume><issue>6</issue><spage>517</spage><epage>531</epage><pages>517-531</pages><issn>0269-2813</issn><eissn>1365-2036</eissn><abstract>Summary
Background Nonsteroidal anti‐inflammatory drugs (NSAIDs) are some of the most prescribed drugs worldwide and have now probably overtaken Helicobacter pylori as the most common cause of gastrointestinal injury in Western countries. Further understanding of the pathogenesis of NSAID‐induced ulcers is important to enable the development of novel and effective preventive strategies.
Aims To provide an update on recent advances in our understanding of the cellular and molecular mechanisms involved in the development of NSAID‐induced ulcers.
Methods A Medline search was performed to identify relevant literature using search terms including ‘nonsteroidal anti‐inflammatory drugs, aspirin, gastric ulcer, duodenal ulcer, pathogenesis, pharmacogenetics’.
Results The mechanisms of NSAID‐induced ulcers can be divided into topical and systemic effects and the latter may be prostaglandin‐dependent (through COX inhibition) or prostaglandin‐independent. Genetic factors may play an important role in determining individual predisposition.
Conclusions The pathogenesis of NSAID‐induced peptic ulcers is complex and multifactorial. Recent advances in cellular and molecular biology have highlighted the importance of various prostaglandin‐independent mechanisms. Pharmacogenetic studies may provide further insights into the pathogenetic mechanisms of NSAID‐induced ulcers and help identify patients at increased risk.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>19575764</pmid><doi>10.1111/j.1365-2036.2009.04086.x</doi><tpages>17</tpages></addata></record> |
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| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection) |
| subjects | Anti-Inflammatory Agents, Non-Steroidal - adverse effects Anti-Inflammatory Agents, Non-Steroidal - pharmacology Biological and medical sciences Clinical Trials as Topic Cyclooxygenase 2 Inhibitors - adverse effects Digestive system Gastroenterology. Liver. Pancreas. Abdomen Genetic Predisposition to Disease - genetics Helicobacter pylori Humans Medical sciences Other diseases. Semiology Peptic Ulcer - chemically induced Pharmacology. Drug treatments Prostaglandins Stomach. Duodenum. Small intestine. Colon. Rectum. Anus |
| title | Review article: cellular and molecular mechanisms of NSAID‐induced peptic ulcers |
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