Relationship Between Low-Dose Aspirin-Induced Gastric Mucosal Injury and Intragastric pH in Healthy Volunteers
Background and Aims Gastric acid plays an important role in the pathogenesis of gastric mucosal lesions. We investigated whether aspirin-induced gastric mucosal injury might have any association with the intragastric pH. Materials and Methods Fifteen healthy, Helicobacter pylori -negative volunteers...
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creator | Nishino, Masafumi Sugimoto, Mitsushige Kodaira, Chise Yamade, Mihoko Shirai, Naohito Ikuma, Mutsuhiro Tanaka, Tatsuo Sugimura, Haruhiko Hishida, Akira Furuta, Takahisa |
description | Background and Aims
Gastric acid plays an important role in the pathogenesis of gastric mucosal lesions. We investigated whether aspirin-induced gastric mucosal injury might have any association with the intragastric pH.
Materials and Methods
Fifteen healthy,
Helicobacter pylori
-negative volunteers randomly underwent the four different 7-day regimens: (1) aspirin 100 mg, (2) rabeprazole 10 mg, (3) aspirin 100 mg + rabeprazole 10 mg, and (4) aspirin 100 mg + rabeprazole 40 mg. Gastric mucosal injury based on the modified Lanza score (MLS), 24-h intragastric pH, and histopathology of gastric mucosa were evaluated prior to the start and on day 7 of each regimen.
Results
The median MLSs were 0 in the baseline and the rabeprazole 10 mg regimen. The median MLS in the aspirin regimen was 3, while those in both aspirin + rabeprazole 10 mg and aspirin + rabeprazole 40 mg regimens were 0. Rabeprazole significantly prevented the gastric mucosal injury by aspirin (
P
= 0.001 for rabeprazole 10 mg and
P
= 0.005 for rabeprazole 40 mg). The MLSs were negatively correlated with the 24-h intragastric pH (
P
= −0.711, |
doi_str_mv | 10.1007/s10620-009-0920-3 |
format | Article |
fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_744620009</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A712949818</galeid><sourcerecordid>A712949818</sourcerecordid><originalsourceid>FETCH-LOGICAL-c565t-3a49f40d9b8f3cc14261204a1124e1e4b37e18aaabbf60630f9698b95168a5473</originalsourceid><addsrcrecordid>eNp1kV2L1DAUhoso7rj6A7yRoIhXXXPaNGkux1V3BkYEUW9Dmp7OZugks0nLMv_elBYXRclFDjnPez7yZtlLoFdAqXgfgfKC5pTKnMoUlI-yFVSizIuK14-zFQWeYgB-kT2L8UATKIA_zS5AclEIWq8y9w17PVjv4q09kQ843CM6svP3-UcfkazjyQbr8q1rR4MtudFxCNaQL6PxUfdk6w5jOBPt2hQOQe-X_GlDrCMb1P1weyY_fT-6ATHE59mTTvcRXyz3Zfbj86fv15t89_Vme73e5abi1ZCXmsmO0VY2dVcaA6zgUFCmAQqGgKwpBUKttW6ajlNe0k5yWTeyAl7rionyMns31z0FfzdiHNTRRoN9rx36MSrBWPq59B-JfP0XefBjcGk4VXJBK6hknaA3M7TXPSrrOp92NVNJtRZQSCZrmKirf1DptHi0xjvsbHr_QwCzwAQfY8BOnYI96nBWQNXksJodVmlQNTmsyqR5tcw7NkdsHxSLpQl4uwA6Gt13QTtj42-uSM2nxRJXzFxMKbfH8LD4_7v_Amzlu1o</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>367051598</pqid></control><display><type>article</type><title>Relationship Between Low-Dose Aspirin-Induced Gastric Mucosal Injury and Intragastric pH in Healthy Volunteers</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Nishino, Masafumi ; Sugimoto, Mitsushige ; Kodaira, Chise ; Yamade, Mihoko ; Shirai, Naohito ; Ikuma, Mutsuhiro ; Tanaka, Tatsuo ; Sugimura, Haruhiko ; Hishida, Akira ; Furuta, Takahisa</creator><creatorcontrib>Nishino, Masafumi ; Sugimoto, Mitsushige ; Kodaira, Chise ; Yamade, Mihoko ; Shirai, Naohito ; Ikuma, Mutsuhiro ; Tanaka, Tatsuo ; Sugimura, Haruhiko ; Hishida, Akira ; Furuta, Takahisa</creatorcontrib><description>Background and Aims
Gastric acid plays an important role in the pathogenesis of gastric mucosal lesions. We investigated whether aspirin-induced gastric mucosal injury might have any association with the intragastric pH.
Materials and Methods
Fifteen healthy,
Helicobacter pylori
-negative volunteers randomly underwent the four different 7-day regimens: (1) aspirin 100 mg, (2) rabeprazole 10 mg, (3) aspirin 100 mg + rabeprazole 10 mg, and (4) aspirin 100 mg + rabeprazole 40 mg. Gastric mucosal injury based on the modified Lanza score (MLS), 24-h intragastric pH, and histopathology of gastric mucosa were evaluated prior to the start and on day 7 of each regimen.
Results
The median MLSs were 0 in the baseline and the rabeprazole 10 mg regimen. The median MLS in the aspirin regimen was 3, while those in both aspirin + rabeprazole 10 mg and aspirin + rabeprazole 40 mg regimens were 0. Rabeprazole significantly prevented the gastric mucosal injury by aspirin (
P
= 0.001 for rabeprazole 10 mg and
P
= 0.005 for rabeprazole 40 mg). The MLSs were negatively correlated with the 24-h intragastric pH (
P
= −0.711, < 0.001), whereas aspirin had no effect on the intragastric pH. Aspirin expanded the mean diameter of the microvessels of the gastric mucosa, which, in turn, was negatively correlated with the intragastric pH.
Conclusions
Aspirin might induce gastric mucosal injury by affecting the mucosal microvessels in an acid-dependent manner. Sustained maintenance of the intragastric pH at an elevated value is necessary to prevent gastric mucosal damage induced by aspirin.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1007/s10620-009-0920-3</identifier><identifier>PMID: 19672708</identifier><identifier>CODEN: DDSCDJ</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject><![CDATA[2-Pyridinylmethylsulfinylbenzimidazoles - administration & dosage ; 2-Pyridinylmethylsulfinylbenzimidazoles - metabolism ; Anti-Inflammatory Agents, Non-Steroidal - administration & dosage ; Anti-Inflammatory Agents, Non-Steroidal - adverse effects ; Aryl Hydrocarbon Hydroxylases - genetics ; Aryl Hydrocarbon Hydroxylases - metabolism ; Aspirin ; Aspirin - administration & dosage ; Aspirin - adverse effects ; Biochemistry ; Biological and medical sciences ; Biopsy ; Bones, joints and connective tissue. Antiinflammatory agents ; Cytochrome P-450 CYP2C19 ; Digestive system ; Dosage and administration ; Feeding. Feeding behavior ; Female ; Fundamental and applied biological sciences. Psychology ; Gastric Acid - metabolism ; Gastric Acidity Determination ; Gastric Mucosa - drug effects ; Gastric Mucosa - metabolism ; Gastric Mucosa - pathology ; Gastroenterology ; Gastroscopy ; Genotype ; Helicobacter ; Hepatology ; Humans ; Hydrogen-Ion Concentration ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Oncology ; Original Article ; Pharmacology. Drug treatments ; Phenotype ; Proton Pump Inhibitors - administration & dosage ; Proton Pump Inhibitors - metabolism ; Rabeprazole ; Severity of Illness Index ; Stomach Ulcer - chemically induced ; Stomach Ulcer - metabolism ; Stomach Ulcer - pathology ; Stomach Ulcer - prevention & control ; Transplant Surgery ; Vertebrates: anatomy and physiology, studies on body, several organs or systems ; Young Adult]]></subject><ispartof>Digestive diseases and sciences, 2010-06, Vol.55 (6), p.1627-1636</ispartof><rights>Springer Science+Business Media, LLC 2009</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 Springer</rights><rights>Springer Science+Business Media, LLC 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-3a49f40d9b8f3cc14261204a1124e1e4b37e18aaabbf60630f9698b95168a5473</citedby><cites>FETCH-LOGICAL-c565t-3a49f40d9b8f3cc14261204a1124e1e4b37e18aaabbf60630f9698b95168a5473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10620-009-0920-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10620-009-0920-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27911,27912,41475,42544,51306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22943670$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19672708$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishino, Masafumi</creatorcontrib><creatorcontrib>Sugimoto, Mitsushige</creatorcontrib><creatorcontrib>Kodaira, Chise</creatorcontrib><creatorcontrib>Yamade, Mihoko</creatorcontrib><creatorcontrib>Shirai, Naohito</creatorcontrib><creatorcontrib>Ikuma, Mutsuhiro</creatorcontrib><creatorcontrib>Tanaka, Tatsuo</creatorcontrib><creatorcontrib>Sugimura, Haruhiko</creatorcontrib><creatorcontrib>Hishida, Akira</creatorcontrib><creatorcontrib>Furuta, Takahisa</creatorcontrib><title>Relationship Between Low-Dose Aspirin-Induced Gastric Mucosal Injury and Intragastric pH in Healthy Volunteers</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><addtitle>Dig Dis Sci</addtitle><description>Background and Aims
Gastric acid plays an important role in the pathogenesis of gastric mucosal lesions. We investigated whether aspirin-induced gastric mucosal injury might have any association with the intragastric pH.
Materials and Methods
Fifteen healthy,
Helicobacter pylori
-negative volunteers randomly underwent the four different 7-day regimens: (1) aspirin 100 mg, (2) rabeprazole 10 mg, (3) aspirin 100 mg + rabeprazole 10 mg, and (4) aspirin 100 mg + rabeprazole 40 mg. Gastric mucosal injury based on the modified Lanza score (MLS), 24-h intragastric pH, and histopathology of gastric mucosa were evaluated prior to the start and on day 7 of each regimen.
Results
The median MLSs were 0 in the baseline and the rabeprazole 10 mg regimen. The median MLS in the aspirin regimen was 3, while those in both aspirin + rabeprazole 10 mg and aspirin + rabeprazole 40 mg regimens were 0. Rabeprazole significantly prevented the gastric mucosal injury by aspirin (
P
= 0.001 for rabeprazole 10 mg and
P
= 0.005 for rabeprazole 40 mg). The MLSs were negatively correlated with the 24-h intragastric pH (
P
= −0.711, < 0.001), whereas aspirin had no effect on the intragastric pH. Aspirin expanded the mean diameter of the microvessels of the gastric mucosa, which, in turn, was negatively correlated with the intragastric pH.
Conclusions
Aspirin might induce gastric mucosal injury by affecting the mucosal microvessels in an acid-dependent manner. Sustained maintenance of the intragastric pH at an elevated value is necessary to prevent gastric mucosal damage induced by aspirin.</description><subject>2-Pyridinylmethylsulfinylbenzimidazoles - administration & dosage</subject><subject>2-Pyridinylmethylsulfinylbenzimidazoles - metabolism</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - administration & dosage</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</subject><subject>Aryl Hydrocarbon Hydroxylases - genetics</subject><subject>Aryl Hydrocarbon Hydroxylases - metabolism</subject><subject>Aspirin</subject><subject>Aspirin - administration & dosage</subject><subject>Aspirin - adverse effects</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Bones, joints and connective tissue. Antiinflammatory agents</subject><subject>Cytochrome P-450 CYP2C19</subject><subject>Digestive system</subject><subject>Dosage and administration</subject><subject>Feeding. Feeding behavior</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastric Acid - metabolism</subject><subject>Gastric Acidity Determination</subject><subject>Gastric Mucosa - drug effects</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastric Mucosa - pathology</subject><subject>Gastroenterology</subject><subject>Gastroscopy</subject><subject>Genotype</subject><subject>Helicobacter</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Hydrogen-Ion Concentration</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pharmacology. Drug treatments</subject><subject>Phenotype</subject><subject>Proton Pump Inhibitors - administration & dosage</subject><subject>Proton Pump Inhibitors - metabolism</subject><subject>Rabeprazole</subject><subject>Severity of Illness Index</subject><subject>Stomach Ulcer - chemically induced</subject><subject>Stomach Ulcer - metabolism</subject><subject>Stomach Ulcer - pathology</subject><subject>Stomach Ulcer - prevention & control</subject><subject>Transplant Surgery</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><subject>Young Adult</subject><issn>0163-2116</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kV2L1DAUhoso7rj6A7yRoIhXXXPaNGkux1V3BkYEUW9Dmp7OZugks0nLMv_elBYXRclFDjnPez7yZtlLoFdAqXgfgfKC5pTKnMoUlI-yFVSizIuK14-zFQWeYgB-kT2L8UATKIA_zS5AclEIWq8y9w17PVjv4q09kQ843CM6svP3-UcfkazjyQbr8q1rR4MtudFxCNaQL6PxUfdk6w5jOBPt2hQOQe-X_GlDrCMb1P1weyY_fT-6ATHE59mTTvcRXyz3Zfbj86fv15t89_Vme73e5abi1ZCXmsmO0VY2dVcaA6zgUFCmAQqGgKwpBUKttW6ajlNe0k5yWTeyAl7rionyMns31z0FfzdiHNTRRoN9rx36MSrBWPq59B-JfP0XefBjcGk4VXJBK6hknaA3M7TXPSrrOp92NVNJtRZQSCZrmKirf1DptHi0xjvsbHr_QwCzwAQfY8BOnYI96nBWQNXksJodVmlQNTmsyqR5tcw7NkdsHxSLpQl4uwA6Gt13QTtj42-uSM2nxRJXzFxMKbfH8LD4_7v_Amzlu1o</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>Nishino, Masafumi</creator><creator>Sugimoto, Mitsushige</creator><creator>Kodaira, Chise</creator><creator>Yamade, Mihoko</creator><creator>Shirai, Naohito</creator><creator>Ikuma, Mutsuhiro</creator><creator>Tanaka, Tatsuo</creator><creator>Sugimura, Haruhiko</creator><creator>Hishida, Akira</creator><creator>Furuta, Takahisa</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7QL</scope><scope>C1K</scope></search><sort><creationdate>20100601</creationdate><title>Relationship Between Low-Dose Aspirin-Induced Gastric Mucosal Injury and Intragastric pH in Healthy Volunteers</title><author>Nishino, Masafumi ; Sugimoto, Mitsushige ; Kodaira, Chise ; Yamade, Mihoko ; Shirai, Naohito ; Ikuma, Mutsuhiro ; Tanaka, Tatsuo ; Sugimura, Haruhiko ; Hishida, Akira ; Furuta, Takahisa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-3a49f40d9b8f3cc14261204a1124e1e4b37e18aaabbf60630f9698b95168a5473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>2-Pyridinylmethylsulfinylbenzimidazoles - administration & dosage</topic><topic>2-Pyridinylmethylsulfinylbenzimidazoles - metabolism</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - administration & dosage</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</topic><topic>Aryl Hydrocarbon Hydroxylases - genetics</topic><topic>Aryl Hydrocarbon Hydroxylases - metabolism</topic><topic>Aspirin</topic><topic>Aspirin - administration & dosage</topic><topic>Aspirin - adverse effects</topic><topic>Biochemistry</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>Bones, joints and connective tissue. Antiinflammatory agents</topic><topic>Cytochrome P-450 CYP2C19</topic><topic>Digestive system</topic><topic>Dosage and administration</topic><topic>Feeding. Feeding behavior</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastric Acid - metabolism</topic><topic>Gastric Acidity Determination</topic><topic>Gastric Mucosa - drug effects</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastric Mucosa - pathology</topic><topic>Gastroenterology</topic><topic>Gastroscopy</topic><topic>Genotype</topic><topic>Helicobacter</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Hydrogen-Ion Concentration</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pharmacology. Drug treatments</topic><topic>Phenotype</topic><topic>Proton Pump Inhibitors - administration & dosage</topic><topic>Proton Pump Inhibitors - metabolism</topic><topic>Rabeprazole</topic><topic>Severity of Illness Index</topic><topic>Stomach Ulcer - chemically induced</topic><topic>Stomach Ulcer - metabolism</topic><topic>Stomach Ulcer - pathology</topic><topic>Stomach Ulcer - prevention & control</topic><topic>Transplant Surgery</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishino, Masafumi</creatorcontrib><creatorcontrib>Sugimoto, Mitsushige</creatorcontrib><creatorcontrib>Kodaira, Chise</creatorcontrib><creatorcontrib>Yamade, Mihoko</creatorcontrib><creatorcontrib>Shirai, Naohito</creatorcontrib><creatorcontrib>Ikuma, Mutsuhiro</creatorcontrib><creatorcontrib>Tanaka, Tatsuo</creatorcontrib><creatorcontrib>Sugimura, Haruhiko</creatorcontrib><creatorcontrib>Hishida, Akira</creatorcontrib><creatorcontrib>Furuta, Takahisa</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishino, Masafumi</au><au>Sugimoto, Mitsushige</au><au>Kodaira, Chise</au><au>Yamade, Mihoko</au><au>Shirai, Naohito</au><au>Ikuma, Mutsuhiro</au><au>Tanaka, Tatsuo</au><au>Sugimura, Haruhiko</au><au>Hishida, Akira</au><au>Furuta, Takahisa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relationship Between Low-Dose Aspirin-Induced Gastric Mucosal Injury and Intragastric pH in Healthy Volunteers</atitle><jtitle>Digestive diseases and sciences</jtitle><stitle>Dig Dis Sci</stitle><addtitle>Dig Dis Sci</addtitle><date>2010-06-01</date><risdate>2010</risdate><volume>55</volume><issue>6</issue><spage>1627</spage><epage>1636</epage><pages>1627-1636</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><coden>DDSCDJ</coden><abstract>Background and Aims
Gastric acid plays an important role in the pathogenesis of gastric mucosal lesions. We investigated whether aspirin-induced gastric mucosal injury might have any association with the intragastric pH.
Materials and Methods
Fifteen healthy,
Helicobacter pylori
-negative volunteers randomly underwent the four different 7-day regimens: (1) aspirin 100 mg, (2) rabeprazole 10 mg, (3) aspirin 100 mg + rabeprazole 10 mg, and (4) aspirin 100 mg + rabeprazole 40 mg. Gastric mucosal injury based on the modified Lanza score (MLS), 24-h intragastric pH, and histopathology of gastric mucosa were evaluated prior to the start and on day 7 of each regimen.
Results
The median MLSs were 0 in the baseline and the rabeprazole 10 mg regimen. The median MLS in the aspirin regimen was 3, while those in both aspirin + rabeprazole 10 mg and aspirin + rabeprazole 40 mg regimens were 0. Rabeprazole significantly prevented the gastric mucosal injury by aspirin (
P
= 0.001 for rabeprazole 10 mg and
P
= 0.005 for rabeprazole 40 mg). The MLSs were negatively correlated with the 24-h intragastric pH (
P
= −0.711, < 0.001), whereas aspirin had no effect on the intragastric pH. Aspirin expanded the mean diameter of the microvessels of the gastric mucosa, which, in turn, was negatively correlated with the intragastric pH.
Conclusions
Aspirin might induce gastric mucosal injury by affecting the mucosal microvessels in an acid-dependent manner. Sustained maintenance of the intragastric pH at an elevated value is necessary to prevent gastric mucosal damage induced by aspirin.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>19672708</pmid><doi>10.1007/s10620-009-0920-3</doi><tpages>10</tpages></addata></record> |
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source | MEDLINE; Springer Nature - Complete Springer Journals |
subjects | 2-Pyridinylmethylsulfinylbenzimidazoles - administration & dosage 2-Pyridinylmethylsulfinylbenzimidazoles - metabolism Anti-Inflammatory Agents, Non-Steroidal - administration & dosage Anti-Inflammatory Agents, Non-Steroidal - adverse effects Aryl Hydrocarbon Hydroxylases - genetics Aryl Hydrocarbon Hydroxylases - metabolism Aspirin Aspirin - administration & dosage Aspirin - adverse effects Biochemistry Biological and medical sciences Biopsy Bones, joints and connective tissue. Antiinflammatory agents Cytochrome P-450 CYP2C19 Digestive system Dosage and administration Feeding. Feeding behavior Female Fundamental and applied biological sciences. Psychology Gastric Acid - metabolism Gastric Acidity Determination Gastric Mucosa - drug effects Gastric Mucosa - metabolism Gastric Mucosa - pathology Gastroenterology Gastroscopy Genotype Helicobacter Hepatology Humans Hydrogen-Ion Concentration Male Medical sciences Medicine Medicine & Public Health Oncology Original Article Pharmacology. Drug treatments Phenotype Proton Pump Inhibitors - administration & dosage Proton Pump Inhibitors - metabolism Rabeprazole Severity of Illness Index Stomach Ulcer - chemically induced Stomach Ulcer - metabolism Stomach Ulcer - pathology Stomach Ulcer - prevention & control Transplant Surgery Vertebrates: anatomy and physiology, studies on body, several organs or systems Young Adult |
title | Relationship Between Low-Dose Aspirin-Induced Gastric Mucosal Injury and Intragastric pH in Healthy Volunteers |
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