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Chiba N. Ulcer Disease and Helicobacter PyloriInfection: Current Treatment. EVIDENCE‐BASED GASTROENTEROLOGY AND HEPATOLOGY 4E 2019:68-85. [DOI: 10.1002/9781119211419.ch5] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
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Han Y, Jung HK, Chang JY, Moon CM, Kim SE, Shim KN, Jung SA, Kim JY, Bae JY, Kim SI, Lee JH, Park S. Identification of distinctive clinical significance in hospitalized patients with endoscopic duodenal mucosal lesions. Korean J Intern Med 2017; 32:827-835. [PMID: 28823115 PMCID: PMC5583440 DOI: 10.3904/kjim.2015.149] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/27/2015] [Revised: 07/13/2015] [Accepted: 07/30/2015] [Indexed: 11/27/2022] Open
Abstract
BACKGROUND/AIMS Duodenitis is not infrequent finding in patient undergoing endoscopy. However, hospitalized patients have a higher incidence of secondary duodenal mucosal lesions that might be related with inflammatory bowel disease (IBD), cytomegalovirus (CMV) infection, tuberculosis, immunologic disorders, or other rare infections. We aimed to identify clinicopathologic features of duodenal mucosal lesions in hospitalized patients. METHODS All hospitalized patients having duodenal mucosal lesions were identified by endoscopic registration data and pathologic data query from 2011 to 2014. The diagnostic index was designed to be sensitive; however, a detailed review of medical record and endoscopic findings was undertaken to improve specificity. Secondary duodenal lesion was defined as having specific reason to explain the duodenal lesion. RESULTS Among 6,334 hospitalized patients have undergone upper endoscopy, endoscopic duodenal mucosal lesions was detected in 475 patients. Secondary duodenal lesions was 21 patients (4.4%) and the most frequent secondary cause was IBD (n = 7). The mean age of secondary group was significantly lower than that in primary group (42.3 ± 18.9 years vs. 58.5 ± 16.8 years, p = 0.00), and nonsteroidal anti-inflammatory drugs were less frequently used in secondary group, but there was no differences of gender or presence of Helicobacter pylori. The involvement of distal part of duodenum including postbulbitis or panduodenitis was more frequently detected in secondary group than in primary group. By multivariate regression analysis, younger age of 29 years and the disease extent were significant predictors for the secondary mucosal lesions. CONCLUSIONS Secondary duodenal mucosal lesions with different pathophysiology, such as IBD or CMV infection, are rare. Disease extent and age seems the most distinctive feature of secondary duodenal mucosal lesions.
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Affiliation(s)
- Yeji Han
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Hye-Kyung Jung
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
- Correspondence to Hye-Kyung Jung, M.D. Department of Internal Medicine, Ewha Womans University Mokdong Hospital, 1071 Anyangcheon-ro, Yangcheon-gu, Seoul 07985, Korea Tel: +82-2-2650-2874 Fax: +82-2-2650-2874 E-mail:
| | - Ji Young Chang
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Chang Mo Moon
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Seong-Eun Kim
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Ki-Nam Shim
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Sung-Ae Jung
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Joo-Young Kim
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Ji-Yun Bae
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Sae-In Kim
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Ji-Hyun Lee
- Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea
| | - Sanghui Park
- Department of Pathology, Ewha Womans University School of Medicine, Seoul, Korea
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Chiba N. Ulcer Disease and Helicobacter pyloriInfection: Etiology and Treatment. EVIDENCE‐BASED GASTROENTEROLOGY AND HEPATOLOGY 2010:102-138. [DOI: 10.1002/9781444314403.ch6] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
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Pietroiusti A, Luzzi I, Gomez MJ, Magrini A, Bergamaschi A, Forlini A, Galante A. Helicobacter pylori duodenal colonization is a strong risk factor for the development of duodenal ulcer. Aliment Pharmacol Ther 2005; 21:909-15. [PMID: 15801926 DOI: 10.1111/j.1365-2036.2005.02423.x] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
AIM To test the hypothesis that duodenal colonization represents the final crucial step in the development of Helicobacter pylori related duodenal ulcer. METHODS Patients with non-ulcer dyspepsia who had gastric colonization by H. pylori were included in the study. At baseline endoscopy, we evaluated the prevalence of duodenal colonization (culture, urease testing and histology), and cytotoxin-associated gene A status (polymerase chain reaction). No patients received eradication during 1 year follow-up. At this time, endoscopy was repeated and the incidence of duodenal ulcer was assessed. RESULTS Among 181 patients completing follow-up, 53 (29%) had duodenal colonization: 72% of them were cytotoxin-associated gene A positive, versus 37% patients without duodenal colonization (P < 0.001). Duodenal ulcer developed in 12 (22.6%) patients with duodenal colonization and in two (1.6%) without duodenal colonization (odds ratio for duodenal ulcer: 6.29, 95% confidence intervals 2.44-17.45). The incidence of duodenal ulcer was similar among cytotoxin-associated gene A positive and cytotoxin-associated gene A negative subjects with duodenal colonization: 21.05% versus 26.6%. CONCLUSIONS The assessment of duodenal colonization by H. pylori in patients with non-ulcer dyspepsia is strongly predictive for the subsequent development of duodenal ulcer and may help to stratify patients at risk for this disease.
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Affiliation(s)
- A Pietroiusti
- Dipartimento di Medicina Interna, Università degli Studi di Roma Tor Vergata, 00133 Roma, Italy.
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Abstract
AIM: To investigate the ultrastructural and morphological changes of non-specific duodenitis (NSD) in an attempt to grade them according to the extent of the lesions.
METHODS: Biopsies were taken from the mucosa of duodenal bulb of 44 patients selected from the patients undergoing upper gastrointestinal endoscopy for epigastric discomforts. From each patient, two pinch biopsies on the same area were obtained from duodenal bulb. One was for scanning electron microscopy and the other was stained with hematoxylin-eosin, Warthin-Starry silver and both were then examined under light microscope. A total of 12 specimens (three from each degree of the normal and I-III of NSD diagnosed and graded by histology) selected from the 44 patients were dehydrated, critical point dried, coated with gold palladium and examined under a JEOL JSM-30 scanning electron microscope (SEM) at 20 kV.
RESULTS: According to the ultrastructural morphologic changes, non-specific duodenitis was divided into normal (as control group), mild, moderate and severe degrees according to results of SEM. The normal villi of duodenal bulb were less than 0.2 mm. There were inflammation cells, occasionally red blood cells and macrophages on the mucosal epithelial surface. Erosion and desquamation of epithelium could be seen. Three cases (25%, 3/12) had gastric metaplasia and Helicobacter pylori (H pylori) infection could be found in 5 cases (41.67%, 5/12) in duodenal bulb mucosa. The most distinctive feature was the ulcer-like defect on the surface of epithelial cells.
CONCLUSION: Non-specific duodenitis is a separate entity disease caused by different factors. SEM is of value as an aid in the diagnosis of mucosal diseases of duodenum.
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Affiliation(s)
- Cheng-Xin Wang
- Department of Pathology and Pathophysiology, School of Medicine and Life Sciences, Jianghan University, Wuhan 430056, Hubei Province, China.
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Ciancio G, Nuti M, Orsini B, Iovi F, Ortolani M, Palomba A, Amorosi A, Surrenti E, Ilani SM, Surrenti C. Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease. Dig Liver Dis 2002; 34:16-21. [PMID: 11926569 DOI: 10.1016/s1590-8658(02)80054-8] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
BACKGROUND It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS . Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS . The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.
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Affiliation(s)
- G Ciancio
- Department of Clinical Pathophysiology, Institute of Pathology, University of Florence, Italy
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Chang CC, Pan S, Lien GS, Chen SH, Cheng CJ, Liu JD, Cheng YS, Suk FM. Investigation of the extent of gastric metaplasia in the duodenal bulb by using methylene blue staining. J Gastroenterol Hepatol 2001; 16:729-33. [PMID: 11446879 DOI: 10.1046/j.1440-1746.2001.02521.x] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
BACKGROUND AND AIMS The existence of gastric metaplasia (GM) of the duodenal mucosa has been considered to be highly related to the recurrence of duodenal ulcers (DU). The aims of this study are to evaluate the usefulness of methylene blue staining in the detection of GM, and to clarify the relationship between GM and the deformity of the duodenal bulb. METHODS Fifteen patients with healed DU and four patients with symptoms of dyspepsia without evidence of ulcers were enrolled into this endoscopic study. During each endoscopy, methylene blue was sprayed evenly on the duodenal bulb, and biopsies were taken from blue-stained and unstained areas. The existence and extent of GM were assessed histologically and grossly. The correlation between duodenal bulb deformity and the extent of GM was also studied. RESULTS The mean score of methylene blue non-staining (MBNS) was 0, 1.30 +/- 0.15, and 3.00 +/- 0.00 in group A (non-ulcer patients), group B (patients with healed DU and with normal-shaped bulb) and C (patients with healed DU and with deformed duodenal bulb), respectively; showing significant differences among the groups (P < 0.05 in each). Both the existence and the grading of GM were higher in unstained specimens than in blue-stained specimens (100 vs 16.6%, P < 0.0001 and 3.62 +/- 0.09 vs 0.19 +/- 0.06, P < 0.001, respectively). CONCLUSIONS Methylene blue non-staining can be applied to investigate the existence and extent of GM in the duodenal bulb accurately. The incidence of GM in the duodenal bulb was higher in patients with healed ulcers than in non-ulcer patients. Patients with deformed duodenal bulbs have a higher extent of GM than those without deformed duodenal bulbs.
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Affiliation(s)
- C C Chang
- Department of Internal Medicine, Taipei Medical University Hospital, Taiwan
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Abstract
Peptic ulcers are accompanied by different patterns of chronic gastritis and duodenitis that generally run parallel to the topography of colonization by Helicobacter pylori (H. pylori). Duodenal ulcers arise on a background of a gastroduodenitis; the gastritis is antrum-predominant while the duodenitis requires acid-induced gastric metaplasia in the duodenal mucosa before bacterial colonization can occur. The colonized and inflamed metaplastic areas in the duodenum (and inflamed pre-pyloric antrum) are the initial sites of ulceration. Proximal gastric ulcers arise in a diffuse (pan-) gastritis or a corpus-predominant H. pylori gastritis when the weakened gastric mucosa (especially in the antrum-body transitional zone) is susceptible to ulceration even in the presence of subnormal acid production. These distinctive patterns of gastritis are sufficiently consistent for them to be used to predict ulcer risk.
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Affiliation(s)
- M F Dixon
- Division of Pathological Sciences, University of Leeds, UK
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Yang H, Wu SV, Pichuantes S, Song M, Wang J, Zhou D, Xu Z, Quan S, Polito A, Walsh JH. High prevalence of cagA-positive strains in Helicobacter pylori-infected, healthy, young Chinese adults. J Gastroenterol Hepatol 1999; 14:476-80. [PMID: 10355513 DOI: 10.1046/j.1440-1746.1999.01892.x] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
BACKGROUND Cytotoxin-associated gene A (cagA) has been implicated as a potential pathogenic marker for Helicobacter pylori-induced severe gastroduodenal diseases. Although the prevalence of cagA-positive strains has been reported in patient populations from developed countries, only limited information from developing countries is available. METHODS Polymerase chain reaction (PCR) in combination with immunoblot analysis was used to determine the prevalence of cagA and its adjacent cagE genes and to evaluate the expression of CagA protein in 55 H. pylori clinical isolates from China. RESULTS The expected PCR products derived from H. pylori cagA and cagE genes were identified in all Chinese H. pylori clinical isolates. Similarly, the CagA protein was detected in all 40 isolates tested. CONCLUSIONS These results demonstrated that the presence of the cagA gene correlated well with expression of the CagA protein in all surveyed Chinese H. pylori isolates and that infection with cagA-positive H. pylori strains is highly common in China and independent of clinical presentation.
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Affiliation(s)
- H Yang
- Center for Ulcer Research, Department of Medicine, UCLA School of Medicine and Veterans Affairs West Los Angeles Medical Center, California 90073, USA
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Hamlet A, Thoreson AC, Nilsson O, Svennerholm AM, Olbe L. Duodenal Helicobacter pylori infection differs in cagA genotype between asymptomatic subjects and patients with duodenal ulcers. Gastroenterology 1999; 116:259-68. [PMID: 9922305 DOI: 10.1016/s0016-5085(99)70121-6] [Citation(s) in RCA: 109] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]
Abstract
BACKGROUND & AIMS It is unclear why only a minority of subjects infected by Helicobacter pylori develop duodenal ulcers (DU). The aim of this study was to investigate whether the number and type of H. pylori strains in the duodenum of patients with DU may play a critical role. METHODS Twenty-one patients with DU and 20 asymptomatic subjects with antral H. pylori infection were studied. Paired biopsy specimens were taken from the antrum and from each quadrant of the duodenal bulb. Analyses included extent of duodenal gastric metaplasia, severity of duodenitis, bacterial density, presence of the cagA gene, and vacuolating cytotoxin activity. RESULTS H. pylori was cultured from duodenal biopsy specimens in 95% of patients with DU and 80% of asymptomatic subjects. Both groups had a similar bacterial density and proportion of cagA-positive strains in the antrum (86% vs. 75%), but patients with DU had a 20-fold higher density of H. pylori and a higher proportion of cagA-positive strains in the duodenal bulb (81% vs. 30%). Active duodenitis was present only in patients with DU infected by cagA positive strains in the duodenum. CONCLUSIONS The results suggest that a high density of cagA-positive strains in the duodenum with severe duodenitis are important determinants of DU disease.
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Affiliation(s)
- A Hamlet
- Centre for Gastroenterological Research, Sahlgrenska University Hospital, Göteborg, Sweden.
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Mertz H, Kovacs T, Thronson M, Weinstein W. Gastric metaplasia of the duodenum: identification by an endoscopic selective mucosal staining technique. Gastrointest Endosc 1998; 48:32-8. [PMID: 9684661 DOI: 10.1016/s0016-5107(98)70125-7] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
Abstract
BACKGROUND To understand the pathophysiology of duodenal ulcer disease, it is important to identify and quantitate gastric metaplasia of the duodenum. Methylene blue dye is absorbed well by intestinal mucosa, but not by gastric mucosa. Our aim was to validate a methylene blue staining technique for measurement of gastric metaplasia in the duodenum. METHODS Eight subjects with chronic duodenal ulcer disease and seven subjects with other upper intestinal disorders underwent duodenal methylene blue staining after application of a mucolytic agent. Biopsy specimens were obtained from blue-stained and pale unstained areas and assessed for gastric metaplasia histologically. RESULTS Pink or pale unstained duodenal areas had more gastric surface cell metaplasia than blue-stained areas. Unstained duodenum was also more likely to have extensive (more than 25% of the biopsy specimens) gastric metaplasia (60%) than blue-stained areas (9%). Subjects with duodenal ulcer disease had more unstained mucosa than controls. CONCLUSION Methylene blue staining of the duodenum is useful to identify and quantitate gastric metaplasia.
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Affiliation(s)
- H Mertz
- Vanderbilt University Department of Medicine, CURE Gastroenteric Biology Center, Nashville, TN 37232, USA
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Savarino V, Mela GS, Zentilin P, Mele MR, Lapertosa L, Patetta R, Dallorto E, Vassallo A, Mansi C, Vigneri S, Celle G. Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum. Gut 1996; 39:508-12. [PMID: 8944557 PMCID: PMC1383261 DOI: 10.1136/gut.39.4.508] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
BACKGROUND The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.
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Affiliation(s)
- V Savarino
- Dipartimento di Medicina Interna, Università di Genova, Italy
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