426 results on '"Genta RM"'
Search Results
2. Annurca Apple Polyphenol Extracts (APE) Suppress Polyp Development in Apcmin/+ Mice Fed Western or Balanced Diets
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Fini L, Selgrad M, Daoud Y, Garcia M, Fogliano V, Graziani G, Vitaglione P, Carmack SW, Genta RM, Boland CR, PIAZZI, GIULIA, RICCIARDIELLO, LUIGI, Fini L, Selgrad M, Piazzi G, Daoud Y, Garcia M, Fogliano V, Graziani G, Vitaglione P, Carmack SW, Genta RM, Boland CR, and Ricciardiello L.
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COLORECTAL CANCER ,POLYPHENOLS ,ApcMin/+ - Published
- 2009
3. JC Virus Infects the Enteric Glia of Patients with Chronic Idiopathic Intestinal Pseudo-Obstruction
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Selgrad M, Fini L, Williams S, Tonini M, Genta RM, Goel A, Boland CR, DE GIORGIO, ROBERTO, COGLIANDRO, ROSANNA FRANCESCA, STANGHELLINI, VINCENZO, BARBARA, GIOVANNI, CORINALDESI, ROBERTO, RICCIARDIELLO, LUIGI, Selgrad M, De Giorgio R, Fini L, Cogliandro R, Williams S, Stanghellini V, Barbara G, Tonini M, Corinaldesi R, Genta RM, Goel A, Boland CR, and Ricciardiello L.
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COLORECTAL CANCER ,LIVER TRANSPLANTATION ,jc virus - Published
- 2008
4. Epigenetic Silencing of Dll1 Regulates Notch Activation in Gastric Cancer
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Fini L, Garcia M, Selgrad M, Shin SK, Jascur T, Yao Y, Malfertheiner P, Wex T, Genta RM, Goel A, Sepulveda A, Boland CR, RICCIARDIELLO, LUIGI, Fini L, Garcia M, Selgrad M, Shin SK, Jascur T, Yao Y, Malfertheiner P, Wex T, Genta RM, Goel A, Sepulveda A, Boland CR, and Ricciardiello L.
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NOTCH ,COLORECTAL CANCER ,DNA METHYLATION - Published
- 2008
5. Premalignant lesions of the digestive system
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Odze, Rd, Riddell, Rh, Bosman, Ft, Carneiro, F, Fléjou J, F., Geboes, K, Genta, Rm, Hattori, T, Hruban, Rh, van Krieken JH, Lauwers, Gy, Offerhaus, Gja, Rugge, Massimo, Shimizu, M, Shimoda, T, Theise, Nd, and Vieth, M.
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- 2010
6. Update on Helicobacter pylori research. Malignancies
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Gasbarrini G, Genta RM, Anti M, Fox J, Caselli M, Doglioni C, Ierardi E, Masala G, Palli D, Fossi S, Corinaldesi R, Cammarota G., TESTONI , PIER ALBERTO, Gasbarrini, G, Genta, Rm, Anti, M, Fox, J, Caselli, M, Doglioni, C, Ierardi, E, Masala, G, Palli, D, Testoni, PIER ALBERTO, Fossi, S, Corinaldesi, R, and Cammarota, G.
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- 1997
7. Helicobacter pylori infection in patients with celiac disease
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Villanacci, V, Bassotti, Gabrio, Liserre, B, Lanzini, A, Lanzarotto, F, and Genta, Rm
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- 2006
8. Staging gastritis: An international proposal (vol 129, pg 1807, 2005)
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Rugge, Massimo and Genta, Rm
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- 2006
9. Gastric mucosal atrophy: interobserver consistency using new criteria for classification and grading
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Rugge, M, Correa, P, Dixon, Mf, Fiocca, Roberto, Hattori, T, Lechago, J, Leandro, G, Price, Ab, Sipponen, P, Solcia, E, Watanabe, H, and Genta, Rm
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Gastritis, Atrophic ,Observer Variation ,Gastric Mucosa ,Biopsy ,Pyloric Antrum ,Humans ,Reproducibility of Results ,Atrophy ,Severity of Illness Index - Abstract
Considerable difficulties persist amongst pathologists in agreeing on the presence and severity of gastric atrophy. An international group of pathologists pursued the following aims: (i) to generate an acceptable definition and a simple reproducible classification of gastric atrophy; and (ii) to develop guidelines for the recognition of atrophy useful for increasing agreement among observers.After redefining atrophy as the 'loss of appropriate glands' and examining histological samples from different gastric compartments, three categories were identified: (i) negative; (ii) indefinite; (iii) atrophy, with and without intestinalization. Atrophy was graded on a three-level scale. Interobserver reproducibility of the classification was tested by kappa statistics (general and weighted) in a series of 48 cases.The medians of the general agreement and weighted kappa values were 0.78 and 0.73, respectively. The weighted kappa coefficients, obtained by cross-tabulating the evaluation of each pathologist against all others, were, with only one exception,0.4 (moderate to excellent agreement).By using the definition of atrophy as the loss of appropriate glands and distinguishing the two main morphological entities of metaplastic and non-metaplastic types, a high level of agreement was achieved by a group of gastrointestinal pathologists trained in different cultural contexts.
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- 2002
10. Review article: pre-neoplastic states of the gastric mucosa - a practical approach for the perplexed clinician
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Genta, Rm and Rugge, Massimo
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- 2001
11. Topographic patterns of intestinal metaplasia and gastric cancer
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Cassaro, M, Rugge, Massimo, Gutierrez, O, Leandro, G, Graham, Dy, and Genta, Rm
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Adult ,Aged, 80 and over ,Male ,Metaplasia ,Hepatology ,Helicobacter pylori ,Gastroenterology ,Adenocarcinoma ,Middle Aged ,Helicobacter Infections ,Intestines ,Phenotype ,Risk Factors ,Stomach Neoplasms ,Prevalence ,Humans ,Female ,Dyspepsia ,Aged - Abstract
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.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.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) "Magenstrasse" (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.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.
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- 2000
12. Identification of the phenotype of the gastric mucosa in patient's with Barrett's esophagus with and without H-pylori infection
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Russo, V, Rugge, Massimo, Cassaro, M, Genta, Rm, Parenti, ANNA ROSITA, DI MARIO, Francesco, Busatto, Graziella, and Graham, Dy
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- 1999
13. Distribution of smooth muscle cell bundles in the gastric mucosa with or without Helicobacter pylori infection and their relationship with mast cells
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Nakajima, S., primary, Hattori, T., additional, Krishnan, B., additional, Ota, H., additional, El-Zimaity, HMT, additional, Graham, DY., additional, and Genta, RM., additional
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- 1998
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14. Mast cell involvement in gastritis with or without Helicobacter pylori infection
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Nakajima, S, primary, Krishnan, B, additional, Ota, H, additional, Segura, AM, additional, Hattori, T, additional, Graham, DY, additional, and Genta, RM, additional
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- 1997
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15. Adherence of Helicobacter pylori to areas of incomplete intestinal metaplasia in the gastric mucosa
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Genta, RM, primary, Gurer, IE, additional, Graham, DY, additional, Krishnan, B, additional, Segura, AM, additional, Gutierrez, O, additional, Kim, JG, additional, and Burchette, JL, additional
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- 1996
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16. Effect of hepatocyte proliferation and cellular DNA synthesis on hepatitis B virus replication
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Ozer, A, primary, Khaoustov, VI, additional, Mearns, M, additional, Lewis, DE, additional, Genta, RM, additional, Darlington, GJ, additional, and Yoffe, B, additional
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- 1996
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17. Lesions indefinite for intraepithelial neoplasia and OLGA staging for gastric atrophy.
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Fassan M, Pizzi M, Farinati F, Nitti D, Zagonel V, Genta RM, and Rugge M
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- 2012
18. The gastric mucosa in gastric cancer patients in a low-incidence area.
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Genta RM and Pusztaszeri M
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- 2006
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19. Non-invasive neoplasia of the stomach.
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Rugge M, Nitti D, Farinati F, di Mario F, Genta RM, Rugge, Massimo, Nitti, Donato, Farinati, Fabio, di Mario, Francesco, and Genta, Robert M
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- 2005
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20. Gastric mucosa: long-term outcome after cure of Helicobacter pylori infection.
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Franceschi F, Genta RM, Sepulveda AR, Franceschi, Francesco, Genta, Robert M, and Sepulveda, Antonio R
- Abstract
The histopathological changes due to chronic Helicobacter pylori infection are well characterized. Nevertheless, the clinical and pathological outcomes resulting from the cure of this infection remain incompletely described. In particular, the influence of eradication of H. pylori on nonulcer dyspepsia, the long-term effects of H. pylori eradication on gastric atrophy and intestinal metaplasia, and the role of H. pylori eradication in the prevention of gastric cancer are still unclear. We reviewed 38 studies reported between 1993 and 1999 on the outcome of various disorders related to H. pylori infection after successful eradication. There is general agreement concerning the regression of chronic gastritis, lymphoid follicles, and limited-stage low-grade MALT lymphomas of the gastric mucosa after eradication of H. pylori infection. Conversely, there are still major questions on whether H. pylori eradication improves the outcome of premalignant lesions, such as atrophy, intestinal metaplasia, and dysplasia. Finally, some extragastric idiopathic diseases seem to improve in consequence of the eradication of the infection, although there are still no definitive data to support this. [ABSTRACT FROM AUTHOR]
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- 2002
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21. Parasites and Diarrhea. II: Helminths and Diarrhea.
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Hashmey, Rayhan, Genta, Robert M., White, A. Clinton, Hashmey, R, Genta, RM, and White Jr
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- 1997
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22. Parasites and Diarrhea. I: Protozoans and Diarrhea.
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Hashmey, Rayhan, Genta, Robert M., White, A. Clinton, Hashmey, R, Genta, RM, and White Jr
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- 1997
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23. No helicobacter left behind: detecting the infection in patients with partial gastrectomy.
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Genta RM
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- 2012
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24. The war of the worlds: metaplastic versus nonmetaplastic atrophic gastritis.
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Rugge M, Fassan M, Farinati F, and Genta RM
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- 2011
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25. Distribution of smooth muscle cell bundles in the gastric mucosa with or without Helicobacter pyloriinfection and their relationship with mast cells
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Nakajima, S., Hattori, T., Krishnan, B., Ota, H., El-Zimaity, HMT, Graham, DY., and Genta, RM.
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- 1998
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26. Epigenetic regulation of Delta-Like1 controls Notch1 activation in gastric cancer
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Peter Malfertheiner, Richard Meyer, Yahya Daoud, C. Richard Boland, Franco Bazzoli, Lucia Fini, Antonio Gasbarrini, Michael Selgrad, Thomas Wex, Marco Romano, Giulia Piazzi, James G. Fox, Luigi Ricciardiello, Robert M. Genta, Melissa Garcia, Piazzi G, Fini L, Selgrad M, Garcia M, Daoud Y, Wex T, Malfertheiner P, Gasbarrini A, Romano M, Meyer RL, Genta RM, Fox JG, Boland CR, Bazzoli F, Ricciardiello L., Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Division of Comparative Medicine, and Fox, James G.
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Oncology ,Cellular differentiation ,medicine.disease_cause ,Epigenesis, Genetic ,Mice ,Basic Helix-Loop-Helix Transcription Factors ,Serrate-Jagged Proteins ,Receptor, Notch1 ,Promoter Regions, Genetic ,biology ,METHYLATION ,Cell Differentiation ,Research Papers ,Gene Expression Regulation, Neoplastic ,NOTCH ,DNA methylation ,embryonic structures ,Azacitidine ,Intercellular Signaling Peptides and Proteins ,Stem cell ,Signal Transduction ,medicine.medical_specialty ,Settore MED/12 - GASTROENTEROLOGIA ,Notch signaling pathway ,Decitabine ,Delta-like 1 ,Helicobacter Infections ,Stomach Neoplasms ,Delta like-1 ,Cell Line, Tumor ,Internal medicine ,medicine ,Animals ,Humans ,Homeodomain Proteins ,Helicobacter pylori ,Calcium-Binding Proteins ,gastric cancermed ,Membrane Proteins ,Cancer ,DNA Methylation ,Hepatology ,biology.organism_classification ,medicine.disease ,GASTRIC CANCER ,Immunology ,Transcription Factor HES-1 ,Carcinogenesis ,Jagged-1 Protein - Abstract
The Notch signaling pathway drives proliferation, differentiation, apoptosis, cell fate, and maintenance of stem cells in several tissues. Aberrant activation of Notch signaling has been described in several tumours and in gastric cancer (GC), activated Notch1 has been associated with de-differentiation of lineage-committed stomach cells into stem progenitors and GC progression. However, the specific role of the Notch1 ligand DLL1 in GC has not yet been elucidated. To assess the role of DLL1 in GC cancer, the expression of Notch1 and its ligands DLL1 and Jagged1, was analyzed in 8 gastric cancer cell lines (KATOIII, SNU601, SNU719, AGS, SNU16, MKN1, MKN45, TMK1). DLL1 expression was absent in KATOIII, SNU601, SNU719 and AGS. The lack of DLL1 expression in these cells was associated with promoter hypermethylation and 5-aza-2'dC caused up-regulation of DLL1. The increase in DLL1 expression was associated with activation of Notch1 signalling, with an increase in cleaved Notch1 intracellular domain (NICD) and Hes1, and down-regulation in Hath1. Concordantly, Notch1 signalling was activated with the overexpression of DLL1. Moreover, Notch1 signalling together with DLL1 methylation were evaluated in samples from 52 GC patients and 21 healthy control as well as in INS-GAS mice infected with H. pylori and randomly treated with eradication therapy. In GC patients, we found a correlation between DLL1 and Hes1 expression, while DLL1 methylation and Hath1 expression were associated with the diffuse and mixed type of gastric cancer. Finally, none of the samples from INS-GAS mice infected with H. pylori, a model of intestinal-type gastric tumorigenesis, showed promoter methylation of DLL1. This study shows that Notch1 activity in gastric cancer is controlled by the epigenetic silencing of the ligand DLL1, and that Notch1 inhibition is associated with the diffuse type of gastric cancer., Italian Association for Cancer Research (IG-10216)
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- 2011
27. JC virus infects the enteric glia of patients with chronic idiopathic intestinal pseudo-obstruction
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Luigi Ricciardiello, Marcello Tonini, Ajay Goel, S Williams, Rosanna Cogliandro, Roberto Corinaldesi, Robert M. Genta, Giovanni Barbara, Michael Selgrad, R Meyer, R. De Giorgio, Lucia Fini, R Domiati-Saad, Vincenzo Stanghellini, Clement Richard Boland, Selgrad M., De Giorgio R., Fini L., Cogliandro RF., Williams S., Stanghellini V., Barbara G., Tonini M., Corinaldesi R., Genta RM., Domiati-Saad R., Meyer R., Goel A., Boland CR., and Ricciardiello L.
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Intestinal pseudo-obstruction ,Adult ,Male ,Pathology ,medicine.medical_specialty ,Manometry ,viruses ,Chronic idiopathic intestinal pseudo-obstruction ,JC virus ,Myenteric Plexus ,Biology ,medicine.disease_cause ,Article ,Virus ,NO ,Young Adult ,T Antigen ,JC Virus, T Antigen, Chronic idiopathic intestinal pseudo-obstruction, myenteric plexus, Mad-1 ,Intestine, Small ,medicine ,Humans ,JC Virus ,myenteric plexus ,Mad-1 ,Cellular localization ,Myenteric plexus ,Gastrointestinal tract ,Polyomavirus Infections ,Enteric neuropathy ,Intestinal Pseudo-Obstruction ,Gastroenterology ,virus diseases ,Middle Aged ,medicine.disease ,nervous system diseases ,Tumor Virus Infections ,nervous system ,Immunology ,Chronic Disease ,DNA, Viral ,Female ,Microdissection ,Neuroglia - Abstract
Chronic idiopathic intestinal pseudo-obstruction (CIIP) is characterised by severe impairment of intestinal propulsive motility that mimics bowel obstruction. JC virus (JCV) is a polyomavirus that can infect brain glial cells causing a fatal disease, but may also be found throughout the normal gastrointestinal tract. The hypothesis that JCV infects the myenteric plexuses of patients with CIIP was tested. METHODS: 10 patients with CIIP and 61 normal specimens (30 ascending colon and 31 ileum) from patients with uncomplicated colon cancer were studied. DNA was extracted from the myenteric plexuses, and JCV T antigen (TAg) DNA and the viral regulatory region were detected by PCR and sequencing. Immunohistochemistry was performed to detect JCV viral protein expression, neuronal and glial markers. Fluorescence in situ hybridisation was performed for cellular localisation of the JCV infection. RESULTS: Clinical studies demonstrated neurogenic impairment, and pathological analyses showed neuropathy in each patient with CIIP. JCV TAg DNA was found in the myenteric plexuses of 8/10 (80%) of the patients with CIIP and 3/31 (9.7%) of the control patients (p
- Published
- 2008
28. Gastric Cancer and Its Precursor Lesions: Unraveling the Diversity in Asian Risk Profiles.
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Genta RM, Singhal A, Choi C, and Turner KO
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- Humans, Asian People statistics & numerical data, Risk Assessment, Stomach Neoplasms pathology
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- 2024
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29. Mast Cell Esophagitis: A Novel Entity in Patients with Unexplained Esophageal Symptoms.
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Ocampo AA, Genta RM, and Dellon ES
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- Humans, Female, Male, Retrospective Studies, Adult, Middle Aged, Esophagus pathology, Esophagus physiopathology, Mastocytosis complications, Mastocytosis physiopathology, Chest Pain etiology, Heartburn etiology, Biopsy, Prevalence, Cell Count, Mast Cells, Esophagitis complications, Esophagitis diagnosis, Esophagitis physiopathology, Deglutition Disorders etiology
- Abstract
It is not known whether esophageal mast cells may be a cause of unexplained esophageal symptoms. We aimed to determine the prevalence of esophageal mastocytosis in patients without other underlying causes of symptoms and assess the relationship between symptoms and mast cells. In this retrospective study, we identified adults with esophageal symptoms, a normal endoscopy, normal esophageal biopsies, and no definitive diagnosis during clinical evaluation. We quantified mast cell density (mast cells/mm
2 ) in archived esophageal biopsies using tryptase immunohistochemistry, and compared mast cell levels by clinical features and physiologic testing. In the 87 patients identified (mean age 37, 72% female, 63% white, 92% non-Hispanic), common symptoms were dysphagia (76%), heartburn (71%), and chest pain (25%). Overall, the mean esophageal epithelial mast cell count was 83.0 ± 51.8 mast cells/mm2 ; 60% of patients had ≥ 60 mast/mm2 , and 17% had ≥ 120 masts/mm2 . There were no differences in mast cell counts by type of esophageal testing. Mast cell levels did not differ significantly by type of symptoms, atopic status, medications, smoking status, or alcohol use. There were also no major differences in clinical characteristics by mast cell quartiles or thresholds. In conclusion, esophageal mast cell infiltration was common in patients with symptoms unexplained by prior testing, and levels were higher than previously published values for patients with no underlying esophageal condition. Mast cell esophagitis could be a novel cause of unexplained esophageal symptoms in a subset of patients, though it reamins to be determined if such patients benefit from mast cell-targeted treatment., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)- Published
- 2024
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30. Host-related low-prevalence gastritides: Epidemiological and clinical characterization.
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Genta RM and Rugge M
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Introduction: A recent consensus meeting (RE.GA.IN) addressed "host-related, low-prevalence gastritis": eosinophilic (EoG), lymphocytic (Hp-pos_LyG and Hp-neg_LyG), collagenous (CollG), and granulomatous gastritis (GrG). Our study evaluates their clinico-epidemiological characteristics., Materials and Methods: We extracted all patients with a diagnosis of EoG, LyG, CollG, and GrG from a clinicopathological database and compared their demographics, clinical and endoscopic characteristics, associated conditions, and clinical awareness to those of all other subjects in the database (controls)., Results: There were 1,781,005 unique patients (median age 57 years; 55.7 % female). Hispanics were overrepresented amongst those with Hp-pos_LyG. Subjects with GrG had a high prevalence of erosions and ulcers. Clinical awareness of these conditions was dismal (<1:10,000 patients). Some clinical manifestations were more common in patients with certain gastritides (e.g., vomiting and diarrhea in CollG; anemia in LyG), but none were sufficiently distinctive to suggest a clinical diagnosis. EoG was associated with EoE; LyG had a strong association with celiac disease; CollG with microscopic colitis; and GrG with Crohn disease., Conclusions: The diagnosis of these gastritides (between <1: in 1,000 and 1 in 5000 subjects) rests on histopathology. They remain poorly characterized and clinically neglected. Yet, their associations may herald other conditions: eosinophilic gastrointestinal diseases (EGID), celiac, and Crohn disease. Patients might benefit from increased detection and characterization., Competing Interests: Conflict of interest None., (Copyright © 2024 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.)
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- 2024
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31. Gastric cancer risk in autoimmune gastritis: evidence versus opinion.
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Rugge M, Genta RM, Malfertheiner P, and Graham DY
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- Humans, Stomach Neoplasms epidemiology, Stomach Neoplasms etiology, Gastritis complications, Helicobacter pylori, Helicobacter Infections complications, Gastritis, Atrophic complications
- Abstract
Competing Interests: Competing interests: None declared.
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- 2024
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32. RE.GA.IN.: the Real-world Gastritis Initiative-updating the updates.
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Rugge M, Genta RM, Malfertheiner P, Dinis-Ribeiro M, El-Serag H, Graham DY, Kuipers EJ, Leung WK, Park JY, Rokkas T, Schulz C, and El-Omar EM
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- Humans, Endoscopy, Gastric Mucosa pathology, Helicobacter Infections complications, Helicobacter Infections diagnosis, Helicobacter Infections pathology, Gastritis diagnosis, Gastritis epidemiology, Gastritis pathology, Stomach Neoplasms pathology, Helicobacter pylori
- Abstract
At the end of the last century, a far-sighted 'working party' held in Sydney, Australia addressed the clinicopathological issues related to gastric inflammatory diseases. A few years later, an international conference held in Houston, Texas, USA critically updated the seminal Sydney classification. In line with these initiatives, Kyoto Global Consensus Report, flanked by the Maastricht-Florence conferences, added new clinical evidence to the gastritis clinicopathological puzzle.The most relevant topics related to the gastric inflammatory diseases have been addressed by the Real-world Gastritis Initiative (RE.GA.IN.), from disease definitions to the clinical diagnosis and prognosis. This paper reports the conclusions of the RE.GA.IN. consensus process, which culminated in Venice in November 2022 after more than 8 months of intense global scientific deliberations. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus. After lively debates on the most controversial aspects of the gastritis spectrum, the RE.GA.IN. Faculty amalgamated complementary knowledge to distil patient-centred, evidence-based statements to assist health professionals in their real-world clinical practice. The sections of this report focus on: the epidemiology of gastritis; Helicobacter pylori as dominant aetiology of environmental gastritis and as the most important determinant of the gastric oncogenetic field; the evolving knowledge on gastric autoimmunity; the clinicopathological relevance of gastric microbiota; the new diagnostic horizons of endoscopy; and the clinical priority of histologically reporting gastritis in terms of staging. The ultimate goal of RE.GA.IN. was and remains the promotion of further improvement in the clinical management of patients with gastritis., Competing Interests: Competing interests: DSB has served as speaker for Abbott, AstraZeneca, Alfasigma, Biocodex, Pfizer, Reckitt Benckiser, Takeda, KRKA, PRO.MED.CS Praha and Dr Reddy’s Laboratories. LGC has served as speaker for Takeda and EMS. FDM has served as consultant for Biohit Healthcare. MD-R has served as consultant for Roche and Medtronic. DD has served as consultant for Reckits, Dr Reddy’s, Zentiva, AbbVie, Terapia and Takeda. EME-O is Editor of Gut. EJK is member of the Editorial Board of Gut. MLe has served as research consultant for Eiken Chemical. MLi has served as speaker for Abbott, AstraZeneca, Alfasigma, Biocodex, KRKA and PRO.MED.CS Praha. TM-B received research grants from: AstraZeneca, BMS, Biohit and Fujirebio; and has been involved in congresses and educational supported by AAA, AstraZeneca, MSD, BMS, Viatris and Pierre Fabre. FM has served as consultant for Phathom and Biocodex. ES has served as speaker for AbbVie, Agave, AGPharma, Alfasigma, Aurora Pharma, CaDiGroup, Celltrion, Dr Falk, EG Stada Group, Fenix Pharma, Fresenius Kabi, Galapagos, Janssen, JB Pharmaceuticals, Innovamedica/Adacyte, Malesci, Mayoly Biohealth, Omega Pharma, Pfizer, Reckitt Benckiser, Sandoz, SILA, Sofar, Takeda, Tillots and Unifarco; has served as consultant for AbbVie, Agave, Alfasigma, Biogen, Bristol-Myers Squibb, Celltrion, Diadema Farmaceutici, Dr Falk, Fenix Pharma, Fresenius Kabi, Janssen, JB Pharmaceuticals, Merck & Co, Nestlè, Reckitt Benckiser, Regeneron, Sanofi, SILA, Sofar, Synformulas, Takeda and Unifarco; and has received research support from Pfizer, Reckitt Benckiser, SILA, Sofar, Unifarco and Zeta Farmaceutici. NS has served as speaker for Astellas and consultant for Bristol-Myers Squibb. KS has served as consultant for Fuji Film Co. NU has served as speaker for lectures for: Olympus Co, Fuji Film Co, Boston Scientific Japan, Daiichi-Sankyo Co, Takeda Pharmaceutical Co, EA Pharma Co, Otsuka Pharmaceutical Co, AstraZeneca Co, Miyarisan Pharmaceutical Co and AI Medical Service Co., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.)
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- 2024
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33. Quantification of Mucosal Mast Cells in the Gastrointestinal Tract: A Primer for Practicing Pathologists.
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Genta RM, Turner KO, Collins MH, Wechsler JB, Arva NC, Pletneva MA, Dellon ES, and Walker MM
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- Humans, Mast Cells pathology, Pathologists, Gastrointestinal Tract pathology, Mastocytosis diagnosis, Mastocytosis pathology, Gastrointestinal Diseases pathology
- Abstract
Context.—: Mast cells are essential components of the immune system and play crucial pathogenetic roles in several digestive diseases, including mastocytic enterocolitis and eosinophilic gastrointestinal disorders. Pathologists have rarely been asked to evaluate the distribution and density of mast cells in gastrointestinal (GI) biopsy specimens. However, such requests are becoming more common because of an increasing awareness of the role of mast cells in functional GI disease and in both esophageal and nonesophageal eosinophilic gastrointestinal disorders., Objective.—: To provide pathologists with tools to incorporate the assessment of mast cells in the evaluation of esophageal, gastric, and intestinal specimens by developing a systematic approach to their evaluation, counting, and reporting., Design.—: This study consisted of a review of the literature followed by multiple consensus sessions to decide where to count mast cells and what a countable mast cell is., Results.—: We reviewed 135 papers addressing the content of mast cells in the digestive tract, selected 21 that detailed how cells were counted (microscope lens, area of high-power fields, locations evaluated, type of cells considered as countable), and summarized their data in a table. Then, drawing from both the acceptable literature and our own extensive experience, we reached a tentative consensus on: (1) the normal numbers in the different segments of the GI tract; (2) the morphology of countable mast cells; and (3) the locations and strategies for counting them., Conclusions.—: The result is a set of suggestions for reporting mast cell counts, their distribution, and their location in a way clinicians can understand and use for management decisions., (© 2024 College of American Pathologists.)
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- 2024
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34. Determination of Optimal Eosinophil Thresholds for Diagnosis of Eosinophilic Gastritis and Duodenitis: A Pooled Analysis of 4 Prospective Studies.
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Dellon ES, Bortey E, Chang AT, Paterson CA, Turner K, and Genta RM
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- Humans, Eosinophils pathology, Prospective Studies, Duodenitis diagnosis, Duodenitis pathology, Eosinophilia diagnosis, Enteritis, Gastritis
- Abstract
Introduction: Consensus is lacking regarding the number of eosinophils (eos) required for the diagnosis of eosinophilic gastritis (EoG) and eosinophilic duodenitis (EoD). In addition, thresholds that require multiple high-power fields (HPFs) may not be practical for clinical use, resulting in delayed or missed diagnoses. This pooled analysis of 4 prospective studies assessed thresholds for multiple and single HPFs used to diagnose EoG and EoD., Methods: Studies included the phase 2 ENIGMA1, the phase 3 ENIGMA2, an EoG/EoD prevalence study and a healthy volunteer study. Eos were quantified in the epithelium and lamina propria for controls and symptomatic participants. Symptomatic participants were further divided by histologic diagnosis of EoG/EoD. Peak eos counts were assessed, and the area under the receiver operating characteristic curve was analyzed to identify eos cutoffs for detection of EoG/EoD using the Youden index and sensitivity and specificity equality approaches., Results: Based on the highest specificity analysis in 740 patients, the optimal eos threshold was determined to be 20 eos/HPF in 5 gastric HPFs for EoG (71% sensitivity and 94% specificity) and 33 eos/HPF in 3 duodenal HPFs for EoD (49% sensitivity and 100% specificity). For single-field analysis, the optimal eos thresholds were 33 eos/HPF (EoG) and 37 eos/HPF (EoD), both corresponding to 93% sensitivity and 93% specificity., Discussion: Highly specific single gastric and duodenal HPF thresholds may have more clinical applicability than thresholds requiring multiple HPFs and could better facilitate development of practical histopathologic guidelines to aid pathologists and clinicians in the detection and diagnosis of EoG and/or EoD., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)
- Published
- 2024
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35. Atrophic autoimmune gastritis: 'a muddled or misguided core concept compromises our overall comprehension of the problem'.
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Rugge M, Genta RM, Malfertheiner P, and Graham DY
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- Humans, Comprehension, Gastritis, Atrophic, Gastritis, Helicobacter pylori, Helicobacter Infections drug therapy
- Abstract
Competing Interests: Competing interests: None declared.
- Published
- 2023
- Full Text
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36. Proximity to Swine Farming Operations as a Risk Factor for Eosinophilic Esophagitis.
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Cotton CC, Jensen ET, Hoffman K, Green DJ, Tapia AL, Turner KO, Genta RM, and Dellon ES
- Abstract
We aimed to determine whether residential proximity to permitted swine facilities was associated with an increased risk of eosinophilic esophagitis (EoE) by conducting a case-control study using 2 complementary data sources: 1 from a tertiary care center (n = 401 cases and 1805 controls) and 1 from a large pathology group (n = 904 cases and 4074 controls). Addresses of the subjects and swine facilities were geocoded, and adjusted odds of EoE relative to proximity to and density of swine facilities were calculated. We observed a positive association between proximity to a permitted swine facility (<1 mile) and odds of EoE (adjusted odds ratio R, 2.56; 95% CI, 1.33-4.95) in the tertiary center data; density of farms (>10 farms/census tract) was also positively associated (adjusted odds ratio, 2.76; 95% CI, 1.30-5.84). However, this association was not observed in the pathology database. Though proximity to and density of swine operations were associated with EoE, associations were sensitive to the database used., Competing Interests: The authors report no conflicts of interest., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition.)
- Published
- 2023
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37. Steps forward in understanding gastric cancer risk.
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Rugge M, Genta RM, Malfertheiner P, and Graham DY
- Subjects
- Humans, Gastric Mucosa, Parietal Cells, Gastric, Stomach Neoplasms diagnosis, Stomach Neoplasms epidemiology, Stomach Neoplasms etiology, Helicobacter pylori, Helicobacter Infections complications
- Abstract
Competing Interests: Competing interests: None declared.
- Published
- 2023
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38. Do General Pathologists Assess Gastric and Duodenal Eosinophilia?
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Saad AJ, Genta RM, Turner KO, Kamboj AP, Dellon ES, and Chehade M
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- Humans, Pathologists, Duodenum pathology, Eosinophilia diagnosis, Eosinophilia pathology, Gastritis diagnosis, Gastritis pathology, Duodenitis diagnosis
- Abstract
Context.—: Eosinophilic diseases of the gastrointestinal tract (EGIDs), eosinophilic gastritis (EoG), and eosinophilic duodenitis (EoD) are rarely suspected clinically and infrequently detected by pathologists., Objective.—: To determine whether histories of allergic or eosinophilic disorders and requests to rule out EoG and EoD affect pathologists' awareness of eosinophils in gastrointestinal biopsies., Design.—: Thirty-one community-based pathologists were given 16 sets of biopsies from gastric and duodenal mucosa with elevated eosinophils, Helicobacter pylori gastritis, atrophic gastritis, normal stomach and duodenum, lymphocytosis, and celiac disease. Participants were assigned to 3 groups: group A did not receive histories of allergic or eosinophilic conditions; group B received similar histories plus a clue of possible allergic or eosinophilic conditions; and group C received the same histories as B and was asked to rule out EoG/EoD. A list of gastric and duodenal diagnoses and a space for comments were provided. Results were analyzed descriptively., Results.—: Pathologists correctly diagnosed most noneosinophilic gastrointestinal disorders, indicating competence in gastrointestinal pathology. With respect to EoG and EoD, pathologists in group C performed significantly better that those in groups A and B. The combined odds ratio with 95% CI was 12.34 (2.87-53.04), P < .001, for A versus C and 4.02 (1.60-10.09), P < .02, for B versus C., Conclusions.—: Most pathologists neither reported gastric/duodenal eosinophilia nor diagnosed EoG/EoD, even when provided histories of eosinophilic disorders. Requests to rule out EoG/EoD resulted in only 4 of 11 participants evaluating and counting eosinophils in some cases. Simple evidence-based histopathologic criteria are needed before pathologists can be expected to consider and diagnose EGIDs., (© 2023 College of American Pathologists.)
- Published
- 2023
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39. Editorial: the other bug.
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Turner KO and Genta RM
- Published
- 2023
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40. The Occurrence of Gastritis in Microscopic Colitis and Inflammatory Bowel Disease.
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Sonnenberg A, Turner KO, Saboorian H, Singhal A, and Genta RM
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- Humans, Helicobacter Infections complications, Helicobacter Infections epidemiology, Helicobacter pylori, Gastritis complications, Gastritis epidemiology, Inflammatory Bowel Diseases complications, Inflammatory Bowel Diseases epidemiology, Crohn Disease complications, Colitis, Microscopic epidemiology, Colitis, Microscopic complications
- Abstract
Multiple studies have shown that Helicobacter pylori infection is associated with a lower prevalence of inflammatory bowel disease (IBD).
1,2 Besides chronic active gastritis (CAG) resulting from gastric infection with H pylori, pathologists have noticed another form of CAG, which is unrelated to H pylori infection and seems to cluster in patients with IBD.3-5 The aim of the present study was to compare the prevalence of H pylori-negative and H pylori-positive CAG in patients with IBD, and microscopic colitis (MC)., (Published by Elsevier Inc.)- Published
- 2023
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41. Case-control study of the concurrence of coeliac disease with inflammatory bowel disease.
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Sonnenberg A and Genta RM
- Subjects
- Humans, Case-Control Studies, Celiac Disease complications, Celiac Disease diagnosis, Celiac Disease epidemiology, Inflammatory Bowel Diseases complications, Inflammatory Bowel Diseases epidemiology, Inflammatory Bowel Diseases pathology, Crohn Disease epidemiology, Colitis, Ulcerative epidemiology, Colitis, Microscopic complications, Colitis, Microscopic epidemiology
- Abstract
Background and Aims: Previous studies suggested that inflammatory bowel disease (IBD) is associated with an increased prevalence of comorbid coeliac disease. Our case-control study aimed to test this association using a large histopathology database., Methods: The Inform Diagnostics database is a repository of histopathologic records from patients distributed throughout the United States. In a case-control study among patients with bidirectional endoscopy, we compared the occurrence of coeliac disease in case subjects with IBD or microscopic colitis (MC) and control subjects without inflammatory colitis, calculating odds ratios (OR) and their 95% confidence intervals (CI) adjusted to the varying age, gender and ethnic distributions of case and control subjects., Results: The study population was split into 12,816 IBD cases and 6486 MC cases, who were compared to 345,733 control subjects without colitis. A total of 2892 patients were diagnosed with coeliac disease. Of 12,816 IBD patients, 57 patients (0.4%) harboured coeliac disease compared to 0.7% (2548/345,733) in the control population. The prevalence of coeliac disease among MC patients was 4.4% (288/6486). The corresponding ORs were significantly decreased in IBD (OR: 0.50, CI: 0.38-0.64) and significantly increased in MC patients (6.78, 5.96-7.69). Further stratification of the case populations into subtypes of IBD (Crohn's disease or ulcerative colitis) and MC (collagenous or lymphocytic colitis) similarly revealed significantly decreased and increased ORs for each subtype., Conclusions: The previously reported positive association between coeliac disease and IBD may have been possibly biased by the inclusion of MC cases in the IBD patient population., (© 2023 John Wiley & Sons Ltd. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.)
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- 2023
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42. Editorial: concurrence of coeliac disease with inflammatory bowel disease - is big data the final arbiter? Authors' reply.
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Sonnenberg A and Genta RM
- Subjects
- Humans, Big Data, Celiac Disease, Inflammatory Bowel Diseases
- Published
- 2023
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43. High Discovery Rate of Duodenal and Gastric Eosinophilia in Patients With Unexplained Moderate-Severe Abdominal Symptoms: A Prospective US Multisite Study.
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Talley NJ, Peterson KA, Genta RM, Chang AT, Dellon ES, Sandborn WJ, Lacy BE, Chehade M, Hirano I, Gonsalves N, Lembo A, Schmitt CM, Rothenberg ME, Jain N, Pletneva MA, Turner KO, and Youngblood BA
- Subjects
- Humans, Duodenum diagnostic imaging, Prospective Studies, Case-Control Studies, Eosinophilia diagnosis, Stomach
- Published
- 2023
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44. Incomplete Intestinal Metaplasia Is Rare in Autoimmune Gastritis.
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Genta RM, Turner KO, Robiou C, Singhal A, and Rugge M
- Subjects
- Humans, Gastric Mucosa pathology, Metaplasia complications, Metaplasia pathology, Gastritis epidemiology, Gastritis complications, Gastritis pathology, Gastritis, Atrophic epidemiology, Gastritis, Atrophic pathology, Stomach Neoplasms pathology, Precancerous Conditions pathology, Helicobacter Infections complications, Helicobacter Infections epidemiology, Helicobacter pylori
- Abstract
Background: Incomplete intestinal metaplasia (IM) is reportedly associated with higher gastric cancer (GC) risk than its complete variant. AGA Guidelines recommend including IM subtyping in routine pathology reports. This study assesses the prevalence of complete versus incomplete IM in gastric conditions with different GC risks., Methods: IM subtyping (complete vs. incomplete) and grading (IM extension: G1: ≤30%; G2: >30%) were assessed in 386 patients with IM + ve gastric biopsy sets that included both antral and oxyntic samples. Cases were categorized as: (a) IM foci in otherwise normal mucosa (n = 59); (b) Helicobacter pylori gastritis (n = 138); (c) reactive gastropathy (141); and (d) autoimmune atrophic gastritis (AIG, n = 48). Odds ratios (OR) and their 95% CI were used in comparing the prevalence of incomplete IM and the correlation between subtype and IM extension., Results: Incomplete IM was present in 37.7% of patients with H. pylori gastritis, 8.3% of those with AIG 5.0% of those with reactive gastropathy, and none of those with otherwise normal mucosa. Incomplete IM was strongly associated with more extensive (G2-IM) mucosal intestinalization (OR = 6.69; 95% CI = 2.77-9.40)., Conclusion: Incomplete IM is significantly more prevalent in conditions (H. pylori gastritis) known to carry a higher risk of GC and is strongly associated with its extension. The low prevalence of incomplete IM in AIG (8.3%) and reactive gastropathy (5.2%) is in keeping with the low GC risk associated with these conditions., (© 2023 S. Karger AG, Basel.)
- Published
- 2023
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45. Autoimmune gastritis: long-term natural history in naïve Helicobacter pylori -negative patients.
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Rugge M, Bricca L, Guzzinati S, Sacchi D, Pizzi M, Savarino E, Farinati F, Zorzi M, Fassan M, Dei Tos AP, Malfertheiner P, Genta RM, and Graham DY
- Subjects
- Humans, Hyperplasia, Follow-Up Studies, Atrophy complications, Inflammation complications, Metaplasia, Helicobacter pylori, Gastritis pathology, Gastritis, Atrophic epidemiology, Precancerous Conditions pathology, Helicobacter Infections complications, Helicobacter Infections pathology, Stomach Neoplasms complications
- Abstract
Objective: Autoimmune gastritis (AIG) is an immunomediated disease targeting parietal cells, eventually resulting in oxyntic-restricted atrophy. This long-term follow-up study aimed at elucidating the natural history, histological phenotype(s), and associated cancer risk of patients with AIG consistently tested H. pylori -negative (naïve H. pylori -negative subjects)., Design: Two-hundred eleven naïve H. pylori -negative patients (tested by serology, histology, molecular biology) with AIG (F:M=3.15:1; p<0.001) were prospectively followed up with paired biopsies (T1 vs T2; mean follow-up years:7.5 (SD:4.4); median:7). Histology distinguished non-atrophic versus atrophic AIG. Atrophy was further subtyped/scored as non-metaplastic versus metaplastic (pseudopyloric (PPM) and intestinal (IM)). Enterochromaffin-like-cell (ECL) status was categorised as diffuse versus adenomatoid hyperplasia/dysplasia, and type 1 neuroendocrine tumours (Type1-NETs)., Results: Over the long-term histological follow-up, AIG consistently featured oxyntic-predominant-mononuclear inflammation. At T1, PPM-score was greater than IM (200/211 vs 160/211, respectively); IM scores increased from T1 to T2 (160/211 to 179/211), with no changes in the PPM prevalence (T1=200/211; T2=201/211). At both T1/T2, the prevalence of OLGA-III-stage was <5%; no Operative Link on Gastritis Assessment (OLGA)-IV-stage occurred. ECL-cell-status progressed from diffuse to adenomatoid hyperplasia/dysplasia (T1=167/14 vs T2=151/25). Type1-NETs (T1=10; T2=11) always coexisted with extensive oxyntic-atrophy, and ECL adenomatoid-hyperplasia/dysplasia. No excess risk of gastric or other malignancies was found over a cumulative follow-up time of 10 541 person years, except for (marginally significant) thyroid cancer (SIR=3.09; 95% CI 1.001 to 7.20)., Conclusions: Oxyntic-restricted inflammation, PPM (more than IM), and ECL-cell hyperplasia/neoplasia are the histological AIG hallmarks. Compared with the general population, corpus-restricted inflammation/atrophy does not increase the GC risk. The excess of GC risk reported in patients with AIG could plausibly result from unrecognised previous/current H. pylori comorbidity., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.)
- Published
- 2023
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46. Gastro-oesophageal junction: a conceptual agreement at last?
- Author
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Genta RM
- Abstract
Competing Interests: Competing interests: None declared.
- Published
- 2022
- Full Text
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47. Prevalence of Mismatch-Repair Deficiency in Rectal Adenocarcinomas.
- Author
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Papke DJ Jr, Yurgelun MB, Noffsinger AE, Turner KO, Genta RM, and Redston M
- Subjects
- Humans, Neoplastic Syndromes, Hereditary epidemiology, Neoplastic Syndromes, Hereditary genetics, Neoplastic Syndromes, Hereditary pathology, Prevalence, Adenocarcinoma epidemiology, Adenocarcinoma genetics, Adenocarcinoma pathology, Colorectal Neoplasms epidemiology, Colorectal Neoplasms genetics, Colorectal Neoplasms pathology, DNA Mismatch Repair genetics
- Published
- 2022
- Full Text
- View/download PDF
48. International Consensus Recommendations for Eosinophilic Gastrointestinal Disease Nomenclature.
- Author
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Dellon ES, Gonsalves N, Abonia JP, Alexander JA, Arva NC, Atkins D, Attwood SE, Auth MKH, Bailey DD, Biederman L, Blanchard C, Bonis PA, Bose P, Bredenoord AJ, Chang JW, Chehade M, Collins MH, Di Lorenzo C, Dias JA, Dohil R, Dupont C, Falk GW, Ferreira CT, Fox AT, Genta RM, Greuter T, Gupta SK, Hirano I, Hiremath GS, Horsley-Silva JL, Ishihara S, Ishimura N, Jensen ET, Gutiérrez-Junquera C, Katzka DA, Khoury P, Kinoshita Y, Kliewer KL, Koletzko S, Leung J, Liacouras CA, Lucendo AJ, Martin LJ, McGowan EC, Menard-Katcher C, Metz DC, Miller TL, Moawad FJ, Muir AB, Mukkada VA, Murch S, Nhu QM, Nomura I, Nurko S, Ohtsuka Y, Oliva S, Orel R, Papadopoulou A, Patel DA, Pesek RD, Peterson KA, Philpott H, Putnam PE, Richter JE, Rosen R, Ruffner MA, Safroneeva E, Schreiner P, Schoepfer A, Schroeder SR, Shah N, Souza RF, Spechler SJ, Spergel JM, Straumann A, Talley NJ, Thapar N, Vandenplas Y, Venkatesh RD, Vieira MC, von Arnim U, Walker MM, Wechsler JB, Wershil BK, Wright BL, Yamada Y, Yang GY, Zevit N, Rothenberg ME, Furuta GT, and Aceves SS
- Subjects
- Humans, Consensus, Enteritis diagnosis, Enteritis complications, Gastritis diagnosis, Gastritis complications, Eosinophilia diagnosis, Eosinophilia complications, Eosinophilic Esophagitis complications
- Abstract
Background & Aims: Substantial heterogeneity in terminology used for eosinophilic gastrointestinal diseases (EGIDs), particularly the catchall term "eosinophilic gastroenteritis," limits clinical and research advances. We aimed to achieve an international consensus for standardized EGID nomenclature., Methods: This consensus process utilized Delphi methodology. An initial naming framework was proposed and refined in iterative fashion, then assessed in a first round of Delphi voting. Results were discussed in 2 consensus meetings, and the framework was updated and reassessed in a second Delphi vote, with a 70% threshold set for agreement., Results: Of 91 experts participating, 85 (93%) completed the first and 82 (90%) completed the second Delphi surveys. Consensus was reached on all but 2 statements. "EGID" was the preferred umbrella term for disorders of gastrointestinal (GI) tract eosinophilic inflammation in the absence of secondary causes (100% agreement). Involved GI tract segments will be named specifically and use an "Eo" abbreviation convention: eosinophilic gastritis (now abbreviated EoG), eosinophilic enteritis (EoN), and eosinophilic colitis (EoC). The term "eosinophilic gastroenteritis" is no longer preferred as the overall name (96% agreement). When >2 GI tract areas are involved, the name should reflect all of the involved areas., Conclusions: This international process resulted in consensus for updated EGID nomenclature for both clinical and research use. EGID will be the umbrella term, rather than "eosinophilic gastroenteritis," and specific naming conventions by location of GI tract involvement are recommended. As more data are developed, this framework can be updated to reflect best practices and the underlying science., (Copyright © 2022. Published by Elsevier Inc.)
- Published
- 2022
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49. Trends of Colonic Neoplasia in US Outpatient Endoscopy Centers.
- Author
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Sonnenberg A, Turner KO, and Genta RM
- Subjects
- Aged, Colonoscopy, Cross-Sectional Studies, Humans, Outpatients, Adenoma pathology, Colonic Neoplasms pathology, Colonic Polyps diagnosis, Colorectal Neoplasms diagnosis
- Abstract
Background: A variety of studies have shown rising trends in the occurrence of colorectal cancer in younger patients as opposed to falling trends among older patients aged 55 years or more. We hypothesized that the time trends of benign colonic precursor lesions would reveal similar patterns., Aims: The present study was designed to test this hypothesis in a large nationwide sample of the US population undergoing colonoscopy in community-based endoscopy centers., Methods: The Inform Diagnostics database is an electronic repository of histopathologic records of patients distributed throughout the USA. A cross-sectional study analyzed the detection rates of sessile serrated adenomas (SSA), hyperplastic polyps (HP), tubular adenomas (TA), traditional serrated adenomas (TSA), or adenocarcinomas (colorectal cancer, CRC) in 2,910,174 colonoscopies done 2008-2020., Results: During the 13-year time period, the rate of SSA showed a significant rise, both in patients younger and older than 55 years. HP and TA both showed a significant decline during the same time period. The trends of CRC in the older age group decreased significantly between 2008 (or its peak in 2012) and 2020. The trends of CRC in the younger age group increased significantly between 2008 and its peak in 2017., Conclusions: The age-specific time trends of benign and malignant colonic neoplasia are characterized by dissimilar temporal patterns. Such dissimilarity could suggest that besides a set of shared risk factors that affect all types of colonic neoplasia alike, there is yet another set of environmental risk factors that specifically influence malignant transformation., (© 2021. This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.)
- Published
- 2022
- Full Text
- View/download PDF
50. Temporal changes in the histology of microscopic colitis.
- Author
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Sonnenberg A and Genta RM
- Subjects
- Chronic Disease, Colonoscopy, Cross-Sectional Studies, Humans, Colitis, Collagenous epidemiology, Colitis, Collagenous pathology, Colitis, Lymphocytic epidemiology, Colitis, Lymphocytic pathology, Colitis, Microscopic diagnosis, Inflammatory Bowel Diseases pathology
- Abstract
Background: In a subgroup of patients with microscopic colitis [MC], its histopathology changed from lymphocytic [LC] to collagenous colitis [CC] and vice versa. Previous studies have also observed histopathological transitions between MC and inflammatory bowel disease [IBD]., Aims: The aim of the present study was to analyse the prevalence of such transitions in a large population of MC patients., Methods: The Inform Diagnostics database is an electronic repository of histopathology records of patients distributed throughout the USA. In a cross-sectional study, we analysed the prevalence of changes in MC histology. Each prevalence was expressed as the rate per 100 MC patients with its 95% Poisson confidence interval., Results: In a total population of 29 307 MC patients, our cross-sectional study focused on a subgroup of 4363 patients who underwent two or more consecutive colonoscopies between December 2008 and March 2020. Overall, 1.6% [95% CI 1.2-2.0%] of patients changed their MC phenotype from LC to CC, and 0.5% [0.3-0.7%] from CC to LC. Of 4363 MC patients, 414 [9.5%] were also diagnosed with IBD. In 2.9% [2.4-3.5%], MC and IBD were diagnosed as synchronous mucosal lesions. In 2.1% [1.7-2.6%], MC changed to IBD, and in 4.5% [3.9-5.2%] IBD changed to MC., Conclusions: The analysis confirmed the synchronous occurrence of MC and IBD and transitions between the two diagnoses. In patients who fail therapy for either one of the two diseases, the gastroenterologist should search for changes in the underlying phenotype as a possible explanation., (Published by Oxford University Press on behalf of European Crohn’s and Colitis Organisation (ECCO) 2022.)
- Published
- 2022
- Full Text
- View/download PDF
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