Biomarkers in various types of atrophic gastritis and their diagnostic usefulness
Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic g...
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| Veröffentlicht in: | Digestive diseases and sciences 2005-03, Vol.50 (3), p.474-482 |
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| creator | REMBIASZ, Kazimierz KONTUREK, Peter C KARCZ, Danuta KONTUREK, Stanislaw J OCHMANSKI, Wladyslaw BIELANSKI, Wladyslaw BUDZYNSKI, Andrzej STACHURA, Jerzy |
| description | Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis. |
| doi_str_mv | 10.1007/s10620-005-2461-8 |
| format | Article |
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This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1007/s10620-005-2461-8</identifier><identifier>PMID: 15810629</identifier><identifier>CODEN: DDSCDJ</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Biomarkers - analysis ; Biopsy, Needle ; Cohort Studies ; Female ; Gastric Acid - metabolism ; Gastric Mucosa - pathology ; Gastrins - blood ; Gastritis, Atrophic - diagnosis ; Gastroenterology. Liver. Pancreas. Abdomen ; Helicobacter pylori ; Helicobacter pylori - isolation & purification ; Humans ; Immunohistochemistry ; Inflammation Mediators - analysis ; Male ; Medical sciences ; Middle Aged ; Other diseases. Semiology ; Pepsinogen A - blood ; Probability ; Prognosis ; Retrospective Studies ; Risk Assessment ; Sensitivity and Specificity ; Severity of Illness Index ; Statistics, Nonparametric ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><ispartof>Digestive diseases and sciences, 2005-03, Vol.50 (3), p.474-482</ispartof><rights>2005 INIST-CNRS</rights><rights>Springer Science + Business Media, Inc. 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-5c2a3c1f389f609002e8a28df55819f984f3d274d5bd3ed28b738ec4696a412f3</citedby><cites>FETCH-LOGICAL-c387t-5c2a3c1f389f609002e8a28df55819f984f3d274d5bd3ed28b738ec4696a412f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16684550$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15810629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>REMBIASZ, Kazimierz</creatorcontrib><creatorcontrib>KONTUREK, Peter C</creatorcontrib><creatorcontrib>KARCZ, Danuta</creatorcontrib><creatorcontrib>KONTUREK, Stanislaw J</creatorcontrib><creatorcontrib>OCHMANSKI, Wladyslaw</creatorcontrib><creatorcontrib>BIELANSKI, Wladyslaw</creatorcontrib><creatorcontrib>BUDZYNSKI, Andrzej</creatorcontrib><creatorcontrib>STACHURA, Jerzy</creatorcontrib><title>Biomarkers in various types of atrophic gastritis and their diagnostic usefulness</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><description>Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Biopsy, Needle</subject><subject>Cohort Studies</subject><subject>Female</subject><subject>Gastric Acid - metabolism</subject><subject>Gastric Mucosa - pathology</subject><subject>Gastrins - blood</subject><subject>Gastritis, Atrophic - diagnosis</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Helicobacter pylori</subject><subject>Helicobacter pylori - isolation & purification</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation Mediators - analysis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Other diseases. Semiology</subject><subject>Pepsinogen A - blood</subject><subject>Probability</subject><subject>Prognosis</subject><subject>Retrospective Studies</subject><subject>Risk Assessment</subject><subject>Sensitivity and Specificity</subject><subject>Severity of Illness Index</subject><subject>Statistics, Nonparametric</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Liver. Pancreas. Abdomen</topic><topic>Helicobacter pylori</topic><topic>Helicobacter pylori - isolation & purification</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammation Mediators - analysis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Other diseases. Semiology</topic><topic>Pepsinogen A - blood</topic><topic>Probability</topic><topic>Prognosis</topic><topic>Retrospective Studies</topic><topic>Risk Assessment</topic><topic>Sensitivity and Specificity</topic><topic>Severity of Illness Index</topic><topic>Statistics, Nonparametric</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>REMBIASZ, Kazimierz</creatorcontrib><creatorcontrib>KONTUREK, Peter C</creatorcontrib><creatorcontrib>KARCZ, Danuta</creatorcontrib><creatorcontrib>KONTUREK, Stanislaw J</creatorcontrib><creatorcontrib>OCHMANSKI, Wladyslaw</creatorcontrib><creatorcontrib>BIELANSKI, Wladyslaw</creatorcontrib><creatorcontrib>BUDZYNSKI, Andrzej</creatorcontrib><creatorcontrib>STACHURA, Jerzy</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><collection>MEDLINE - Academic</collection><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>REMBIASZ, Kazimierz</au><au>KONTUREK, Peter C</au><au>KARCZ, Danuta</au><au>KONTUREK, Stanislaw J</au><au>OCHMANSKI, Wladyslaw</au><au>BIELANSKI, Wladyslaw</au><au>BUDZYNSKI, Andrzej</au><au>STACHURA, Jerzy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biomarkers in various types of atrophic gastritis and their diagnostic usefulness</atitle><jtitle>Digestive diseases and sciences</jtitle><addtitle>Dig Dis Sci</addtitle><date>2005-03-01</date><risdate>2005</risdate><volume>50</volume><issue>3</issue><spage>474</spage><epage>482</epage><pages>474-482</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><coden>DDSCDJ</coden><abstract>Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>15810629</pmid><doi>10.1007/s10620-005-2461-8</doi><tpages>9</tpages></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Biological and medical sciences Biomarkers - analysis Biopsy, Needle Cohort Studies Female Gastric Acid - metabolism Gastric Mucosa - pathology Gastrins - blood Gastritis, Atrophic - diagnosis Gastroenterology. Liver. Pancreas. Abdomen Helicobacter pylori Helicobacter pylori - isolation & purification Humans Immunohistochemistry Inflammation Mediators - analysis Male Medical sciences Middle Aged Other diseases. Semiology Pepsinogen A - blood Probability Prognosis Retrospective Studies Risk Assessment Sensitivity and Specificity Severity of Illness Index Statistics, Nonparametric Stomach. Duodenum. Small intestine. Colon. Rectum. Anus |
| title | Biomarkers in various types of atrophic gastritis and their diagnostic usefulness |
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