Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia
Background—The influence of gastrin on the colonic mucosa is still uncertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development. Aims—To evaluate the effect of g...
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Veröffentlicht in: | Gut 1997-09, Vol.41 (3), p.330-332 |
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description | Background—The influence of gastrin on the colonic mucosa is still uncertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development. Aims—To evaluate the effect of gastrin on colorectal cell proliferation, patients with chronic endogenous hypergastrinaemia underwent proctoscopy. Biopsy specimens were taken in order to study rectal cell kinetics. Patients and controls—Ten patients with chronic autoimmune gastritis (CAG), six patients with Zollinger-Ellison syndrome (ZES), and 16 hospital controls took part in this study. Patients with CAG and ZES had basal serum gastrin concentrations significantly higher than controls (p |
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Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development. Aims—To evaluate the effect of gastrin on colorectal cell proliferation, patients with chronic endogenous hypergastrinaemia underwent proctoscopy. Biopsy specimens were taken in order to study rectal cell kinetics. Patients and controls—Ten patients with chronic autoimmune gastritis (CAG), six patients with Zollinger-Ellison syndrome (ZES), and 16 hospital controls took part in this study. Patients with CAG and ZES had basal serum gastrin concentrations significantly higher than controls (p<0.001). Methods—Immunohistochemistry was performed on 3 μm sections of rectal biopsy specimens incubated with 5′-bromodeoxyuridine. Results—The percentage of proliferating cells in the entire crypts (overall labelling index) was similar in all the groups. However, the labelling frequency in the upper two fifths of the glands (φh value) was significantly higher in patients with CAG or ZES compared with controls (p<0.01 in both patient groups versus controls). Conclusions—Endogenous hypergastrinaemia is associated with rectal cell proliferation defects, similar to those observed in conditions at high risk for colon cancer. The effect of the increased serum concentrations of gastrin on the colorectal mucosa after treatment with drugs inhibiting gastric acid secretion should be investigated.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.41.3.330</identifier><identifier>PMID: 9378387</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Adult ; Age ; Aged ; Autoimmune Diseases - blood ; Autoimmune Diseases - pathology ; Biological and medical sciences ; Biopsy ; Cancer ; Cell Division ; Cell growth ; cell kinetics ; chronic autoimmune gastritis ; Chronic Disease ; colon cancer ; Colonic Neoplasms - etiology ; Colorectal cancer ; Female ; gastrin ; Gastrins - blood ; Gastritis - blood ; Gastritis - pathology ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Immunohistochemistry ; Laboratories ; Male ; Medical sciences ; Middle Aged ; Patients ; Rectum - pathology ; Risk Factors ; Rodents ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Studies ; Tumors ; Womens health ; Zollinger-Ellison syndrome ; Zollinger-Ellison Syndrome - blood ; Zollinger-Ellison Syndrome - pathology</subject><ispartof>Gut, 1997-09, Vol.41 (3), p.330-332</ispartof><rights>British Society of Gastroenterology</rights><rights>1997 INIST-CNRS</rights><rights>Copyright: 1997 British Society of Gastroenterology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b506t-d4ace0d4ba85b4b3cde5d1a1f7dfa318bec7a257e6d45ac79dd4ee0365f7af423</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891479/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891479/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2826672$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9378387$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Renga, M</creatorcontrib><creatorcontrib>Brandi, G</creatorcontrib><creatorcontrib>Paganelli, G M</creatorcontrib><creatorcontrib>Calabrese, C</creatorcontrib><creatorcontrib>Papa, S</creatorcontrib><creatorcontrib>Tosti, A</creatorcontrib><creatorcontrib>Tomassetti, P</creatorcontrib><creatorcontrib>Miglioli, M</creatorcontrib><creatorcontrib>Biasco, G</creatorcontrib><title>Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia</title><title>Gut</title><addtitle>Gut</addtitle><description>Background—The influence of gastrin on the colonic mucosa is still uncertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development. Aims—To evaluate the effect of gastrin on colorectal cell proliferation, patients with chronic endogenous hypergastrinaemia underwent proctoscopy. Biopsy specimens were taken in order to study rectal cell kinetics. Patients and controls—Ten patients with chronic autoimmune gastritis (CAG), six patients with Zollinger-Ellison syndrome (ZES), and 16 hospital controls took part in this study. Patients with CAG and ZES had basal serum gastrin concentrations significantly higher than controls (p<0.001). Methods—Immunohistochemistry was performed on 3 μm sections of rectal biopsy specimens incubated with 5′-bromodeoxyuridine. Results—The percentage of proliferating cells in the entire crypts (overall labelling index) was similar in all the groups. However, the labelling frequency in the upper two fifths of the glands (φh value) was significantly higher in patients with CAG or ZES compared with controls (p<0.01 in both patient groups versus controls). Conclusions—Endogenous hypergastrinaemia is associated with rectal cell proliferation defects, similar to those observed in conditions at high risk for colon cancer. The effect of the increased serum concentrations of gastrin on the colorectal mucosa after treatment with drugs inhibiting gastric acid secretion should be investigated.</description><subject>Adult</subject><subject>Age</subject><subject>Aged</subject><subject>Autoimmune Diseases - blood</subject><subject>Autoimmune Diseases - pathology</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Cancer</subject><subject>Cell Division</subject><subject>Cell growth</subject><subject>cell kinetics</subject><subject>chronic autoimmune gastritis</subject><subject>Chronic Disease</subject><subject>colon cancer</subject><subject>Colonic Neoplasms - etiology</subject><subject>Colorectal cancer</subject><subject>Female</subject><subject>gastrin</subject><subject>Gastrins - blood</subject><subject>Gastritis - blood</subject><subject>Gastritis - pathology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Laboratories</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Patients</subject><subject>Rectum - pathology</subject><subject>Risk Factors</subject><subject>Rodents</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Studies</subject><subject>Tumors</subject><subject>Womens health</subject><subject>Zollinger-Ellison syndrome</subject><subject>Zollinger-Ellison Syndrome - blood</subject><subject>Zollinger-Ellison Syndrome - pathology</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc9rFDEcxYModa3evAoDil6cNZkkk8xFkEWrWBRK7aGX8J3kO7vZzi-Tmdb-92bZZVEPnvKF9-Hx8h4hzxldMsbLd-t5Wgq25EvO6QOyYKLUOS-0fkgWlDKVSyWqx-RJjFtKqdYVOyEnFVeaa7UgFxdoJ2gzi22bjWFofYMBJj_0GfQus0ObLgu9xZAFH28y32dj0rGfYnbnp022uR8xrCFOwfeAnYen5FEDbcRnh_eU_Pj08XL1OT__fvZl9eE8ryUtp9wJsEidqEHLWtTcOpSOAWuUa4AzXaNVUEiFpRMSrKqcE4iUl7JR0IiCn5L3e99xrjt0NkUK0Jox-A7CvRnAm7-V3m_Merg1LHUgVJUMXh8MwvBzxjiZzsddEdDjMEeTEC051Ql8-Q-4HebQp88ZplRVCV4pnqi3e8qGIcaAzTEKo2a3lElLGcEMN2mphL_4M_4RPkyT9FcHHaKFtglpBB-PWKGLslS7FvI95uOEv44yhBtTKq6k-Xa1MmfXgurL6yvzNfFv9nzdbf8f8DdA6bqo</recordid><startdate>19970901</startdate><enddate>19970901</enddate><creator>Renga, M</creator><creator>Brandi, G</creator><creator>Paganelli, G M</creator><creator>Calabrese, C</creator><creator>Papa, S</creator><creator>Tosti, A</creator><creator>Tomassetti, P</creator><creator>Miglioli, M</creator><creator>Biasco, G</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19970901</creationdate><title>Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia</title><author>Renga, M ; Brandi, G ; Paganelli, G M ; Calabrese, C ; Papa, S ; Tosti, A ; Tomassetti, P ; Miglioli, M ; Biasco, G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b506t-d4ace0d4ba85b4b3cde5d1a1f7dfa318bec7a257e6d45ac79dd4ee0365f7af423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adult</topic><topic>Age</topic><topic>Aged</topic><topic>Autoimmune Diseases - blood</topic><topic>Autoimmune Diseases - pathology</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>Cancer</topic><topic>Cell Division</topic><topic>Cell growth</topic><topic>cell kinetics</topic><topic>chronic autoimmune gastritis</topic><topic>Chronic Disease</topic><topic>colon cancer</topic><topic>Colonic Neoplasms - etiology</topic><topic>Colorectal cancer</topic><topic>Female</topic><topic>gastrin</topic><topic>Gastrins - blood</topic><topic>Gastritis - blood</topic><topic>Gastritis - pathology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Laboratories</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Patients</topic><topic>Rectum - pathology</topic><topic>Risk Factors</topic><topic>Rodents</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Studies</topic><topic>Tumors</topic><topic>Womens health</topic><topic>Zollinger-Ellison syndrome</topic><topic>Zollinger-Ellison Syndrome - blood</topic><topic>Zollinger-Ellison Syndrome - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Renga, M</creatorcontrib><creatorcontrib>Brandi, G</creatorcontrib><creatorcontrib>Paganelli, G M</creatorcontrib><creatorcontrib>Calabrese, C</creatorcontrib><creatorcontrib>Papa, S</creatorcontrib><creatorcontrib>Tosti, A</creatorcontrib><creatorcontrib>Tomassetti, P</creatorcontrib><creatorcontrib>Miglioli, M</creatorcontrib><creatorcontrib>Biasco, G</creatorcontrib><collection>Istex</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Renga, M</au><au>Brandi, G</au><au>Paganelli, G M</au><au>Calabrese, C</au><au>Papa, S</au><au>Tosti, A</au><au>Tomassetti, P</au><au>Miglioli, M</au><au>Biasco, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>1997-09-01</date><risdate>1997</risdate><volume>41</volume><issue>3</issue><spage>330</spage><epage>332</epage><pages>330-332</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><eissn>1458-3288</eissn><coden>GUTTAK</coden><abstract>Background—The influence of gastrin on the colonic mucosa is still uncertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development. Aims—To evaluate the effect of gastrin on colorectal cell proliferation, patients with chronic endogenous hypergastrinaemia underwent proctoscopy. Biopsy specimens were taken in order to study rectal cell kinetics. Patients and controls—Ten patients with chronic autoimmune gastritis (CAG), six patients with Zollinger-Ellison syndrome (ZES), and 16 hospital controls took part in this study. Patients with CAG and ZES had basal serum gastrin concentrations significantly higher than controls (p<0.001). Methods—Immunohistochemistry was performed on 3 μm sections of rectal biopsy specimens incubated with 5′-bromodeoxyuridine. Results—The percentage of proliferating cells in the entire crypts (overall labelling index) was similar in all the groups. However, the labelling frequency in the upper two fifths of the glands (φh value) was significantly higher in patients with CAG or ZES compared with controls (p<0.01 in both patient groups versus controls). Conclusions—Endogenous hypergastrinaemia is associated with rectal cell proliferation defects, similar to those observed in conditions at high risk for colon cancer. The effect of the increased serum concentrations of gastrin on the colorectal mucosa after treatment with drugs inhibiting gastric acid secretion should be investigated.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>9378387</pmid><doi>10.1136/gut.41.3.330</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Age Aged Autoimmune Diseases - blood Autoimmune Diseases - pathology Biological and medical sciences Biopsy Cancer Cell Division Cell growth cell kinetics chronic autoimmune gastritis Chronic Disease colon cancer Colonic Neoplasms - etiology Colorectal cancer Female gastrin Gastrins - blood Gastritis - blood Gastritis - pathology Gastroenterology. Liver. Pancreas. Abdomen Humans Immunohistochemistry Laboratories Male Medical sciences Middle Aged Patients Rectum - pathology Risk Factors Rodents Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Studies Tumors Womens health Zollinger-Ellison syndrome Zollinger-Ellison Syndrome - blood Zollinger-Ellison Syndrome - pathology |
title | Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia |
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