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Guido N. J. Tytgat - One of the best experts on this subject based on the ideXlab platform.
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Subtypes of Intestinal Metaplasia and Helicobacter pylori.
Gut, 1992Co-Authors: M. E. Craanen, P. Blok, W. Dekker, J. Ferwerda, Guido N. J. TytgatAbstract:To determine whether there is a relationship between the presence of H pylori and the various subtypes of Intestinal Metaplasia in the gastric antrum, 2274 antral gastroscopic biopsies from 533 patients were examined. H pylori was found in 289 patients. Intestinal Metaplasia in general was found in 135 patients. Type I Intestinal Metaplasia was found in 133 patients (98.5%), type II in 106 patients (78.5%) and type III in 21 patients (15.6%). Ninety eight of these 135 patients (72.6%) were H pylori positive and 37 patients (27.4%) were H pylori negative. No statistically significant difference was found in the prevalence of type I and II Intestinal Metaplasia between the Intestinal Metaplasia positive and H pylori positive and Intestinal Metaplasia negative and H pylori negative patients. Type III Intestinal Metaplasia was found less often in the Intestinal Metaplasia positive and H pylori positive patients (11.2%) as compared with Intestinal Metaplasia positive and H pylori negative patients (27%) (p less than 0.05). In contrast with type I and II Intestinal Metaplasia type III Intestinal Metaplasia was found more often in moderate/severe Intestinal Metaplasia than in mild Intestinal Metaplasia (p less than 0.02). Within the group of patients with moderate/severe Intestinal Metaplasia, type III was found less often in the H pylori positive patients (p less than 0.05). We suggest that the gastric milieu for H pylori is less appropriate in type III Intestinal Metaplasia positive patients. As type III Intestinal Metaplasia might be regarded as a marker of possibly increased gastric cancer risk, the lower prevalence of H pylori in these type III Intestinal Metaplasia positive patients might be the result of severe changes in mucosal architecture.
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Intestinal Metaplasia and Helicobacter pylori: an endoscopic bioptic study of the gastric antrum.
Gut, 1992Co-Authors: M. E. Craanen, P. Blok, W. Dekker, J. Ferwerda, Guido N. J. TytgatAbstract:To study the relationship between Intestinal Metaplasia and Helicobacter pylori infection, 2274 gastroscopic antral biopsies taken from 533 patients were examined. Overall, Intestinal Metaplasia was found in 135 patients (25.3%) and H pylori in 289 patients (54.2%). The prevalence of Intestinal Metaplasia and H pylori was age related, being more common in patients greater than or equal to 50 years compared with patients less than 50 years (Intestinal Metaplasia, p less than 0.001 and H pylori, p less than 0.05). Intestinal Metaplasia was found more often in H pylori positive patients compared with H pylori negative patients (33.9% v 15.2%, p less than 0.001). The mean age of Intestinal Metaplasia positive patients who were also H pylori positive was 64 (13.3) years, whereas the mean age of Intestinal Metaplasia positive patients who were H pylori negative was 72 (14.7) years (p less than 0.005). The extent of Intestinal Metaplasia was not statistically different in the latter two groups. Although our data do not prove a causal relationship between H pylori infection and the histogenesis of Intestinal Metaplasia it is suggested that H pylori infection is an important factor in the development of Intestinal Metaplasia, which is generally recognised as a precursor lesion of Intestinal type gastric carcinoma.
Hashem B. El-serag - One of the best experts on this subject based on the ideXlab platform.
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Associations of Duration, Intensity, and Quantity of Smoking With Risk of Gastric Intestinal Metaplasia.
Journal of clinical gastroenterology, 2020Co-Authors: Aaron P. Thrift, Yan Liu, Mimi C. Tan, Andre G. Jove, Hashem B. El-seragAbstract:GOAL Determine whether various dimensions of smoking increase risk for gastric Intestinal Metaplasia. BACKGROUND Cigarette smoking has been implicated in the etiology of gastric cancer, but it is not clear if smoking is a risk factor for gastric Intestinal Metaplasia, a precursor lesion of gastric cancer. MATERIALS AND METHODS We compared data from 385 gastric Intestinal Metaplasia cases and 1577 controls without gastric Intestinal Metaplasia recruited into a cross-sectional study at the Michael E. DeBakey VA Medical Center in Houston, Texas. All participants completed standardized questionnaires and underwent a study endoscopy with gastric mapping biopsies. Gastric Intestinal Metaplasia cases included participants with Intestinal Metaplasia on any noncardia gastric biopsy. We calculated odds ratios and associated 95% confidence intervals using multivariable logistic regression models. RESULTS Compared with never smokers, current smokers had 2-fold increased risk for gastric Intestinal Metaplasia (odds ratio, 2.05; 95% confidence interval, 1.47-2.85). Among ever smokers, increasing duration and total dose were significantly associated with increased risk for gastric Intestinal Metaplasia (P-trend, 0.004 and 0.01, respectively). Among former smokers, risk for gastric Intestinal Metaplasia decreased over time and was no different to never smokers after 15 years smoking cessation. Cases with gastric Intestinal Metaplasia were more likely than controls to have Helicobacter pylori infection (53.2% vs. 21.7%); however, smoking effect on gastric Intestinal Metaplasia was not different by H. pylori infection status. CONCLUSIONS Cigarette smoking is a risk factor for gastric Intestinal Metaplasia. Risk of gastric Intestinal Metaplasia among former smokers remained significantly elevated until 15 years postcessation.
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Prevalence of Gastric Intestinal Metaplasia in a Multiethnic US Veterans Population.
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2020Co-Authors: Theresa Nguyen, Massimo Rugge, Mimi C. Tan, Yan Liu, Aaron P. Thrift, Hashem B. El-seragAbstract:Background & Aims There is a need to identify individuals with gastric Intestinal Metaplasia, a precursor to gastric cancer, so they can be offered screening and surveillance. We examined the prevalence of gastric Intestinal Metaplasia, detected by upper endoscopy biopsy analysis, in different race and ethnic subgroups. We also investigated the extent to which Helicobacter pylori infection, with or without acute and chronic gastritis, accounts for observed associations between race or ethnicity and risk of gastric Intestinal Metaplasia. Methods We used data from a cross-sectional study of consecutively recruited patients at the Michael E. DeBakey Veterans Affairs Medical Center in Houston, Texas, from February 2008 to August 2013. All participants completed a study questionnaire on sociodemographic and clinical characteristics and underwent upper endoscopy with gastric mapping (7 biopsy sites). Cases were classified as having gastric Intestinal Metaplasia if Intestinal Metaplasia was detected in 1 or more noncardia gastric biopsies; noncases were participants without evidence of gastric Intestinal Metaplasia. We used logistic regression models to estimate odds ratios (ORs) and 95% CI values to examine the association between race or ethnicity and gastric Intestinal Metaplasia and performed a mediation analysis to determine whether H pylori and gastritis affected observed associations. Results We included 415 cases with gastric Intestinal Metaplasia and 1764 noncases. The prevalence of gastric Intestinal Metaplasia was highest among Hispanic patients (29.5%; 95% CI, 23.7%–36.1%), followed by African American (25.5%; 95% CI, 22.4%–28.9%) and non-Hispanic white patients (13.7%; 95% CI, 11.9%–15.7%). After we adjusted for age, sex, and smoking, African American (OR, 1.87; 95% CI, 1.44–2.44) and Hispanic race or ethnicity (OR, 2.32; 95% CI, 1.61–3.34) and H pylori infection (OR, 3.65; 95% CI, 2.79–4.55) were associated with an increased risk of gastric Intestinal Metaplasia. H pylori infection alone accounted for 33.6% of the association of race or ethnicity with gastric Intestinal Metaplasia, and 55.5% of the association when combined with acute and chronic gastritis. Conclusions Hispanic and African American patients have an increased risk for gastric Intestinal Metaplasia, determined by upper endoscopy biopsy analysis, compared with non-Hispanic white patients. This increase in risk was partially independent of H pylori infection.
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Demographic and Lifestyle Risk Factors for Gastric Intestinal Metaplasia Among US Veterans.
The American journal of gastroenterology, 2020Co-Authors: Mimi C. Tan, Hashem B. El-serag, Niharika Mallepally, Yan Liu, Aaron P. ThriftAbstract:OBJECTIVES The risk of noncardia gastric cancer is increased in the presence of gastric Intestinal Metaplasia. We aimed to identify demographic and lifestyle factors independently associated with the risk of gastric Intestinal Metaplasia. METHODS We used data from a cross-sectional study of patients attending primary care and endoscopy clinics at the Michael E. DeBakey VA Medical Center in Houston, Texas, between February 2008 and August 2013. All patients completed standardized questionnaires and underwent endoscopy with gastric mapping biopsies. Gastric Intestinal Metaplasia cases included patients with Intestinal Metaplasia on any noncardia gastric biopsy; we defined extensive gastric Intestinal Metaplasia as antrum and corpus involvement. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic regression models. RESULTS We identified 423 cases with gastric Intestinal Metaplasia and 1,796 controls without gastric Intestinal Metaplasia. Older age (vs
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Characteristics of Intestinal Metaplasia in the gastric cardia
The American Journal of Gastroenterology, 1999Co-Authors: Hashem B. El-serag, Amnon Sonnenberg, M. Mazen Jamal, David C. Kunkel, Lida Crooks, Richard M. FeddersenAbstract:Abstract OBJECTIVE: Intestinal Metaplasia of the gastroesophageal junction is frequently grouped together with Barrett’s esophagus. The area of the gastroesophageal junction is comprised of the distal esophagus and the gastric cardia. The aim of the present study was to assess whether Intestinal Metaplasia in the distal esophagus and gastric cardia represent two different entities with a different set of risk factors. METHODS: Patients presenting for elective upper endoscopy were enrolled into a prospective study. The presence of gastritis and Intestinal Metaplasia was evaluated in gastric biopsies taken from the antrum, corpus, and cardia. Barrett’s esophagus was defined by the presence of any length of columnar mucosa above the gastroesophageal junction. RESULTS: Of 302 patients, 50 patients had Intestinal Metaplasia of the gastric cardia, 73 Barrett’s esophagus, and 116 erosive esophagitis. Men were more prone than women to develop Barrett’s esophagus or erosive esophagitis. Both conditions were also more common among whites than nonwhites. Smoking was particularly common among patients with Barrett’s esophagus. Patients with cardiac Intestinal Metaplasia did not share these demographic characteristics. The prevalence of daily reflux symptoms, erosive esophagitis, and Barrett’s esophagus was similar among patients both with and without cardiac Intestinal Metaplasia. However, atrophy and Intestinal Metaplasia of the gastric antrum and corpus were found more frequently among patients with than without cardiac Intestinal Metaplasia. CONCLUSIONS: Intestinal Metaplasia of the gastric cardia is different from Barrett’s esophagus. Although cardiac Intestinal Metaplasia is closely associated with signs of gastritis in other parts of the stomach, gastroesophageal reflux disease does not seem to be a risk factor. A diagnosis of Barrett’s esophagus should not be made based on the presence of Intestinal Metaplasia within the cardiac portion of the gastroesophageal junction.
Steven R. Demeester - One of the best experts on this subject based on the ideXlab platform.
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The gene expression profile of cardia Intestinal Metaplasia is similar to that of Barrett’s esophagus, not gastric Intestinal Metaplasia
Diseases of The Esophagus, 2011Co-Authors: Steven R. Demeester, Tom R. Demeester, Paul Marjoram, Hidekazu Kuramochi, Daniel Vallböhmer, K. Danenberg, Parakrama Chandrasoma, K. Tanaka, Jeffrey A. HagenAbstract:SUMMARY The etiology and significance of cardia Intestinal Metaplasia (CIM) is disputed. CIM may represent a form of Barrett's esophagus due to reflux or could reflect generalized gastric Intestinal Metaplasia due to Helicobacter pylori. The aim of this study was to utilize gene expression data to compare CIM to Barrett's and gastric Intestinal Metaplasia. Endoscopic biopsies were classified by endoscopic and histologic criteria as CIM (n= 33), Barrett's (n= 25), or gastric Intestinal Metaplasia of the antrum or body (n= 18). The squamocolumnar and gastroesophageal junctions were aligned in CIM patients and patients with diffuse gastric Intestinal Metaplasia were excluded. H. pylori was tested for in the biopsies of all patients. After laser-capture microdissection, quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to measure the mRNA expression of a panel of nine genes that has been shown to differentiate Barrett's from other foregut mucosa. Cluster analysis with linear discriminant analysis of the expression data was used to classify each sample into groups based solely on similarity of gene expression. Cluster analysis was performed for three groups (CIM vs. Barrett's vs. gastric Intestinal Metaplasia) and two groups (CIM + Barrett's vs. gastric Intestinal Metaplasia). There was no difference in H. pylori infection among groups (P= 0.66). Clustering into three groups resulted in frequent misclassification between CIM and Barrett's while misclassification of gastric Intestinal Metaplasia was uncommon. The CIM and Barrett's groups were then combined for two group clustering and linear discriminant analysis correctly predicted 95% of CIM and Barrett's samples and 83% of gastric Intestinal Metaplasia samples based on gene expression alone. In conclusion, the gene expression profiles of CIM and Barrett's esophagus were similar in 95% of biopsies and differed significantly from that of gastric Intestinal Metaplasia. The indistinguishable gene expression profile of CIM and BE suggests that they may share a common etiology in the majority of patients with a similar biology, and calls into question the perception that CIM is an innocuous process.
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The location of Intestinal Metaplasia within a columnar-lined esophagus
The American journal of gastroenterology, 2008Co-Authors: Steven R. DemeesterAbstract:TO THE EDITOR: Since Dr. Barrett's description of the columnar-lined esophagus in the 1950s there has been a substantial increase in our understanding of both the etiology and significance of this condition. In the June issue of The American Journal of Gastroenterology, Harrison and colleagues evaluated the efficacy of multiple biopsies to detect the presence of Intestinal Metaplasia in patients with a columnar-lined esophagus (1). However, the inconsistent use of the terms "Barrett's esophagus" and "columnar-lined esophagus" in the manuscript make it difficult to follow. Apparently within the group of 125 patients in this study there were some with known Intestinal Metaplasia, some with dysplasia, and presumably some without Intestinal Metaplasia and only a columnar-lined esophagus on endoscopy. It would be helpful to know the numbers of patients in each of these groups, and it would perhaps be useful to use the known Barrett's patients (those with documented Intestinal Metaplasia with or without dysplasia) as a positive control group in the study.
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The impact of an antireflux procedure on Intestinal Metaplasia of the cardia.
Annals of Surgery, 1998Co-Authors: Steven R. Demeester, Guilherme M. Campos, Tom R. Demeester, Cedric G. Bremner, Jeffrey A. Hagen, Jeffrey H. Peters, Peter F. CrookesAbstract:OBJECTIVE: The aim of this study was to determine whether antireflux surgery is more effective in producing loss of Intestinal Metaplasia located only at the gastroesophageal junction than it has been in patients with Intestinal Metaplasia extending up into the distal esophagus. SUMMARY BACKGROUND DATA: Biopsies of a normal appearing gastroesophageal junction will demonstrate cardiac mucosa containing goblet cells--the hallmark of Intestinal Metaplasia--in 10% to 15% of patients who are evaluated for symptoms of gastroesophageal reflux. The incidence of adenocarcinoma of the esophagus and cardia is rising faster than any other cancer in America, and most of these cancers are found adjacent to areas of Intestinal Metaplasia. Antireflux surgery in patients with Barrett's esophagus may provide protection from progression to dysplasia and cancer; however, it does not reliably cause regression of the Intestinal Metaplasia. Less is known about the potential for Intestinal Metaplasia limited to the cardia (CIM) to regress. METHODS: Sixty patients with Intestinal Metaplasia of the esophagus or cardia had antireflux surgery. Patients in the Intestinal (CIM) group (n = 15) had no endoscopically visible segment of columnar epithelium. Patients in the Barrett's group (n = 45) had columnar epithelium visible within the esophagus. Median follow-up was 25 months in each group. RESULTS: Postoperative biopsies showed complete loss of Intestinal Metaplasia in 73% of the patients with CIM compared with 4.4% of the patients with Barrett's. Low-grade dysplasia, present in 10 patients preoperatively, regressed in 7 patients (70%). No patient progressed to high-grade dysplasia or cancer. CONCLUSIONS: Loss of Intestinal Metaplasia after antireflux surgery is rare in patients with Barrett's, but occurred in most patients with CIM. This suggests that cardiac epithelium is dynamic and that microscopic areas of Intestinal Metaplasia are able to regress much more frequently than longer, visible segments of Intestinal Metaplasia.
Massimo Rugge - One of the best experts on this subject based on the ideXlab platform.
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Prevalence of Gastric Intestinal Metaplasia in a Multiethnic US Veterans Population.
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2020Co-Authors: Theresa Nguyen, Massimo Rugge, Mimi C. Tan, Yan Liu, Aaron P. Thrift, Hashem B. El-seragAbstract:Background & Aims There is a need to identify individuals with gastric Intestinal Metaplasia, a precursor to gastric cancer, so they can be offered screening and surveillance. We examined the prevalence of gastric Intestinal Metaplasia, detected by upper endoscopy biopsy analysis, in different race and ethnic subgroups. We also investigated the extent to which Helicobacter pylori infection, with or without acute and chronic gastritis, accounts for observed associations between race or ethnicity and risk of gastric Intestinal Metaplasia. Methods We used data from a cross-sectional study of consecutively recruited patients at the Michael E. DeBakey Veterans Affairs Medical Center in Houston, Texas, from February 2008 to August 2013. All participants completed a study questionnaire on sociodemographic and clinical characteristics and underwent upper endoscopy with gastric mapping (7 biopsy sites). Cases were classified as having gastric Intestinal Metaplasia if Intestinal Metaplasia was detected in 1 or more noncardia gastric biopsies; noncases were participants without evidence of gastric Intestinal Metaplasia. We used logistic regression models to estimate odds ratios (ORs) and 95% CI values to examine the association between race or ethnicity and gastric Intestinal Metaplasia and performed a mediation analysis to determine whether H pylori and gastritis affected observed associations. Results We included 415 cases with gastric Intestinal Metaplasia and 1764 noncases. The prevalence of gastric Intestinal Metaplasia was highest among Hispanic patients (29.5%; 95% CI, 23.7%–36.1%), followed by African American (25.5%; 95% CI, 22.4%–28.9%) and non-Hispanic white patients (13.7%; 95% CI, 11.9%–15.7%). After we adjusted for age, sex, and smoking, African American (OR, 1.87; 95% CI, 1.44–2.44) and Hispanic race or ethnicity (OR, 2.32; 95% CI, 1.61–3.34) and H pylori infection (OR, 3.65; 95% CI, 2.79–4.55) were associated with an increased risk of gastric Intestinal Metaplasia. H pylori infection alone accounted for 33.6% of the association of race or ethnicity with gastric Intestinal Metaplasia, and 55.5% of the association when combined with acute and chronic gastritis. Conclusions Hispanic and African American patients have an increased risk for gastric Intestinal Metaplasia, determined by upper endoscopy biopsy analysis, compared with non-Hispanic white patients. This increase in risk was partially independent of H pylori infection.
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diagnosis gastric Intestinal Metaplasia what to do next
Current Opinion in Gastroenterology, 2019Co-Authors: David Y. Graham, Massimo Rugge, Robert M. GentaAbstract:Purpose of review One of the most vexing problems for gastroenterologists is what actions to take after receiving a histological diagnosis of gastric Intestinal Metaplasia. We approach the problem by starting with suggesting a biopsy protocol that ensures obtaining the biopsies required for diagnosis, assessing the status of the gastric mucosa, and effective communication with the pathologist and patient. Recent findings The rediscovery and integration of the long history of gastric damage and repair resulting in pseudopyloric Metaplasia (called SPEM) into the thinking of investigators working with animal models of gastric cancer has resulted in improved ability to separate changes associated with benign repair from those associated with inflammation-associated gastric carcinogenesis. Summary Gastric Intestinal Metaplasia is a potential reversible product of injury and repair and not directly connected with carcinogenesis. Intestinal Metaplasia is a biomarker for prior gastric injury and repair. The risk of gastric cancer is best assessed in relation to the severity, extent, and, most importantly, the cause of the atrophic changes.
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Operative Link for Gastritis Assessment gastritis staging incorporates Intestinal Metaplasia subtyping.
Human Pathology, 2011Co-Authors: Massimo Rugge, Gianmaria Pennelli, Matteo Fassan, Marco Pizzi, Donato Nitti, Fabio FarinatiAbstract:Summary Both sulfomucin-type Intestinal Metaplasia (ie, types II and III Intestinal Metaplasia, colonic-type Intestinal Metaplasia) and gastritis in Operative Link for Gastritis Assessment stages III and IV are associated with an increased risk of Intestinal-type gastric cancer. This study aimed to verify the hypothesis that gastritis in Operative Link for Gastritis Assessment stages III and IV (both consistently associated with an increased cancer risk) is associated per se with types II and III Intestinal Metaplasia. Two hundred consecutive cases of atrophic gastritis (Operative Link for Gastritis Assessment stages I, II, III, and IV) were considered (50 cases for each stage). All cases were stained with high iron diamine, and Intestinal Metaplasia was subtyped accordingly (type I [ie, small-Intestinal type] and types II and III). Helicobacter pylori status was also considered, distinguishing H pylori –positive versus H pylori –negative versus H pylori –eradicated patients. A significant association was found between Intestinal Metaplasia subtype and the Operative Link for Gastritis Assessment stage of gastritis (the higher the stage, the more the colonic-type of Intestinal Metaplasia, and vice versa; Wilcoxon, P = .001). The strength of the association between Operative Link for Gastritis Assessment stages and the 3 Intestinal Metaplasia subtypes was confirmed by logistic regression analysis ( P P = .001) and H pylori status (Fisher exact, P
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topographic patterns of Intestinal Metaplasia and gastric cancer
The American Journal of Gastroenterology, 2000Co-Authors: M Cassaro, David Y. Graham, Massimo Rugge, Oscar Gutierrez, Gioacchino Leandro, Robert M. GentaAbstract:Abstract OBJECTIVE: The role of Intestinal Metaplasia in gastric oncogenesis has been demonstrated by both cross-sectional and longitudinal studies. This study was designed to determine whether, in a population at high risk for gastric cancer, different topographical patterns and phenotypes of Intestinal Metaplasia were associated with different degrees of cancer risk. METHODS: A total of 68 Colombian patients with gastric cancer and 67 controls with nonulcer dyspepsia were studied by an extensive biopsy protocol. Intestinal Metaplasia was assessed semiquantitatively by histology and was characterized histochemically. In both patients and controls, the Spearman’s correlation test was applied to the test if the gastric distribution of metaplastic lesions resulted in specific topographical patterns associated with different risks for cancer. RESULTS: Four topographical patterns of Intestinalization emerged: 1) “Focal,” in 14 cancer patients and 16 controls; 2) “Antrum-predominant,” in seven cancer patients and six controls; 3) “Magenstrase” (involving the lesser curvature from cardia to pylorus) in 25 cancer patients and four controls. This pattern was associated with higher cancer risk (OR = 5.7; 95% CI: 1.3–26) than were the two less extensive patterns; and 4) “Diffuse,” involving essentially the entire gastric mucosa with the exception of the fundus, was unique to 13 cancer patients. The OR for cancer was 12.2; 95% CI: 2.0–72.9. Incomplete-type Metaplasia significantly correlated with the extent of total Metaplasia and was also associated with greater cancer risk. CONCLUSIONS: In a population with high risk for gastric cancer, the extension of Intestinal Metaplasia correlates with the extent of its “incomplete” phenotype and is significantly associated with increased cancer risk. Both the extent and location of Intestinal Metaplasia along the lesser curvature (from the cardia to the prepyloric zones) identify patients with the highest cancer risk.
Hiroyuki Mutoh - One of the best experts on this subject based on the ideXlab platform.
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Cell lineage dynamics in the process leading to Intestinal Metaplasia
Journal of gastroenterology, 2011Co-Authors: Hirotsugu Sakamoto, Hiroyuki Mutoh, Hiroko Hayakawa, Miho Sashikawa, Kentaro SuganoAbstract:Background Gene expression in the early stage of the transition to Intestinal Metaplasia in human gastric mucosa has not been determined. In this study, we investigated the temporal relationship between cell lineage changes and intestine-specific gene expression in the process leading to Intestinal Metaplasia, using Cdx2-transgenic mice.
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a close relationship between Intestinal Metaplasia and cdx2 expression in human gallbladders with cholelithiasis
Human Pathology, 2007Co-Authors: Hirotsugu Sakamoto, Hiroyuki Mutoh, Kenichi Ido, Kiichi Satoh, Hiroko Hayakawa, Kentaro SuganoAbstract:We previously reported a case of a human gallbladder with cholelithiasis consisting of Intestinal Metaplasia with the expression of caudal-related homeobox transcription factor (Cdx2). However, it is unclear how often Intestinal Metaplasia and Cdx2 expression occur in human, nontumorous gallbladders with cholelithiasis. We studied the incidence of Intestinal Metaplasia and Cdx2 expression in human gallbladders with cholelithiasis. Gallbladders were resected under laparoscopy from 103 patients with cholelithiasis between September 2003 and March 2005. The mean age of the patients was 59.6 ± 15.0 years (range, 22-92 years). We retrospectively reviewed these cases to look for the presence of Intestinal Metaplasia and the expression of Cdx2. In addition, the characteristics of Intestinal Metaplasia were examined by immunostaining for Muc2, chromogranin A, and serotonin. Intestinal Metaplasia was found in 11.7% (12/103) of the gallbladders with cholelithiasis. The mean ages of patients with and without Intestinal Metaplasia were 60.8 ± 15.4 and 59.4 ± 14.9 years, respectively. Cdx2, Muc2, chromogranin A, and serotonin were expressed in 91.7% (11/12), 91.7% (11/12), 83.3% (10/12), and 50.0% (6/12) in Intestinal metaplastic mucosa, respectively. Only one case (1.1%) that expressed Cdx2 without Intestinal Metaplasia did not express Muc2, chromogranin A, and serotonin. We found that 10.7% (11/103) of nontumorous gallbladders resected because of cholelithiasis under laparoscopy revealed Intestinal Metaplasia with Cdx2 expression.
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development of gastric carcinoma from Intestinal Metaplasia in cdx2 transgenic mice
Cancer Research, 2004Co-Authors: Hiroyuki Mutoh, Kiichi Satoh, Shinji Sakurai, Kiichi Tamada, Hiroto Kita, Hiroyuki Osawa, Takeshi Tomiyama, Yukihiro Sato, Hironori Yamamoto, Norio IsodaAbstract:In the progression of chronic gastritis, gastric mucosal cells deviate from the normal pathway of gastric differentiation to an Intestinal phenotype. Many epidemiologic studies have found an association between the formation of Intestinal Metaplasia and the development of gastric carcinoma. However, there is no direct evidence that shows Intestinal Metaplasia is a precursor lesion of gastric carcinoma, to date. We periodically examined the Intestinal metaplastic mucosa of Cdx2-transgenic mice we have previously generated. Gastric polyps developed from Intestinal metaplastic mucosa in all stomachs of Cdx2-transgenic mice examined. These gastric polyps consisted of Intestinal-type adenocarcinoma that invaded the submucosa and muscularis propria and occasionally spread into the subserosa. p53 and APC gene mutations were recognized in the adenocarcinomas. The participation of APC and p53 gene mutations in gastric carcinogenesis from the Intestinal Metaplasia was verified by the Cdx2-transgenic mice, carrying ApcMin mutation or p53 deficiency, that developed gastric polyps much earlier than Cdx2 alone. We successfully showed that long-term Intestinal Metaplasia induces invasive gastric carcinoma. These results indicate that Intestinal Metaplasia itself plays a significant role in the genesis and progression of gastric carcinoma.
