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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Veröffentlicht in:Digestive diseases and sciences 2010-06, Vol.55 (6), p.1627-1636
Hauptverfasser: Nishino, Masafumi, Sugimoto, Mitsushige, Kodaira, Chise, Yamade, Mihoko, Shirai, Naohito, Ikuma, Mutsuhiro, Tanaka, Tatsuo, Sugimura, Haruhiko, Hishida, Akira, Furuta, Takahisa
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container_issue 6
container_start_page 1627
container_title Digestive diseases and sciences
container_volume 55
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
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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, &lt; 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&amp;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, &lt; 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 &amp; dosage</subject><subject>2-Pyridinylmethylsulfinylbenzimidazoles - metabolism</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - administration &amp; 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 &amp; 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 &amp; Public Health</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pharmacology. 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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 &amp; Public Health</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pharmacology. 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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, &lt; 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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1573-2568
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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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