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Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection  [cached]
Lea Irene Veijola, Aino Mirjam Oksanen, Pentti Ilmari Sipponen, Hilpi Iris Kaarina Rautelin
World Journal of Gastroenterology , 2010,
Abstract: AIM: To study the association between Helicobacter pylori (H. pylori) infection and autoimmune type atrophic gastritis.METHODS: Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology, immunoblot-based serology, and histology to reveal a past or a present H. pylori infection. In addition, serum markers for gastric atrophy (pepsinogen I, pepsinogen I/II and gastrin) and autoimmunity [parietal cell antibodies (PCA), and intrinsic factor (IF), antibodies] were determined.RESULTS: Of the 14 patients with severe gastric atrophy, as demonstrated by histology and serum markers, and no evidence for an ongoing H. pylori infection, eight showed H. pylori antibodies by immunoblotting. All eight had elevated PCA and 4/8 also had IF antibodies. Of the six immunoblot-negative patients with severe corpus atrophy, PCA and IF antibodies were detected in four. Among the patients with low to moderate grade atrophic gastritis (all except one with an ongoing H. pylori infection), serum markers for gastric atrophy and autoimmunity were seldom detected. However, one H. pylori negative patient with mild atrophic gastritis had PCA and IF antibodies suggestive of a pre-atrophic autoimmune gastritis.CONCLUSION: Signs of H. pylori infection in autoimmune gastritis, and positive autoimmune serum markers in H. pylori gastritis suggest an etiological role for H. pylori in autoimmune gastritis.
How to assess the severity of atrophic gastritis  [cached]
Yan-Cheng Dai, Zhi-Peng Tang, Ya-Li Zhang
World Journal of Gastroenterology , 2011,
Abstract: Atrophic gastritis, is the main consequence of long-standing Helicobacter pylori infection, and is linked to the development of gastric cancer. The severity of atrophic gastritis is related to the lifetime risk of gastric cancer development, especially in terms of its degree and extent of mucosal damage. Therefore, it is important for clinicians to assess the severity of atrophic gastritis, interfere with the disease progress, and reverse gastric mucosal atrophy. In the article, we demonstrated some methods (conventional endoscopy, modern endoscopic technology and noninvasive methods) that may help assess the severity of atrophic gastritis and select the reasonable treatment protocols.
Mucosal patterns of Helicobacter pylori-related gastritis without atrophy in the gastric corpus using standard endoscopy  [cached]
Sheng-Lei Yan, Shwu-Tzy Wu, Chien-Hua Chen, Yeh-Huang Hung, Tsung-Hsun Yang, Vun-Siew Pang, Yung-Hsiang Yeh
World Journal of Gastroenterology , 2010,
Abstract: AIM: To identify the mucosal patterns of Helicobacter pylori (H. pylori)-related gastritis in the gastric corpus using standard endoscopy and to evaluate their reproducibility.METHODS: A total of 112 consecutive patients underwent upper gastrointestinal endoscopy. The endoscopists classified the endoscopic findings into 4 patterns. In the second part of the study, 90 images were shown to 3 endoscopists in order to evaluate the inter-observer and intra-observer variability in image assessment.RESULTS: The mucosal patterns of the gastric body were categorized into 4 types. Type 1 pattern was defined as cleft-like appearance, type 2 as regular arrangement of red dots, type 3 pattern as the mosaic mucosal pattern and type 4 pattern as the mosaic pattern with a focal area of hyperemia. Type 1 and type 2 mucosal patterns were statistically significant in predicting H. pylori-negative status as compared with other mucosal types (χ2 = 12.79 and 61.25 respectively, P < 0.01). Type 3 and type 4 mucosal patterns were statistically significant in predicting a H. pylori-positive status as compared with other mucosal types (χ2 = 21.22 and 11.02 respectively, P < 0.01). Furthermore, the sensitivity, specificity, positive and negative predictive values of type 3 plus type 4 patterns for predicting H. pylori-positive gastric mucosa were 100%, 86%, 94%, and 100%, respectively. The mean κ values for inter- and intra-observer agreement in assessing the various endoscopic patterns were 0.808 (95% CI, 0.678-0.938) and 0.826 (95% CI, 0.727-0.925) respectively.CONCLUSION: Our study suggests that mucosal patterns in H. pylori-infected gastric mucosa without atrophy can be reliably identified using standard endoscopy in the gastric corpus.
Current Clinical Applications of Magnifying Endoscopy with Narrow Band Imaging in the Stomach  [PDF]
Hai-Yan Li,Zhi-Zheng Ge,Mitsuhiro Fujishiro,Xiao-Bo Li
Diagnostic and Therapeutic Endoscopy , 2012, DOI: 10.1155/2012/271914
Abstract: Narrow band imaging (NBI), in conjunction with magnifying endoscopy (ME), has arisen more and more attention in the area of advanced endoscopy. By enhancing the mucosal microvascular architecture and surface pattern, it is feasible to use ME-NBI to identify subtle changes associated with gastric inflammation, atrophy, intestinal metaplasia, and early gastric cancer. The new technique thus plays a valuable role in therapeutic decision-making, endoscopic treatment process, postoperative evaluation, and follow-up examination. To date, many criteria or evaluation method of ME-NBI has been proposed. This paper aims to summarize the various diagnosing classifications and the current clinical applications of ME-NBI in the stomach. 1. Introduction Magnifying endoscopy (ME), for the diagnosis of gastrointestinal tract, started in the late 1960s and it has been increasingly popular since electronic videoendoscopes gradually replaced fibreoptic endoscopes [1]. With a magnified observation, endoscopists were then able to visualize the fine details of mucosal surface pattern and vascular architecture. In the 1980s, another technique in the area of endoscopy came into use, namely, the chromoendoscopy, which brought about better delineation of tumor contours and identification of mucosal pit patterns [2]. Furthermore, by narrowing the bandwidth of spectral transmittance, a narrow band imaging (NBI) system was developed in the last decade [3]. This special technique can enhance the contrast between microvessels and background mucosal surface and allow better evaluation of faint or diminutive changes. With these ongoing developments, it becomes probable to detect and differentiate gastrointestinal tumors at an early stage and modern endoscopists are moving towards the role of pathologists, that is, the optical histology. As for stomach, it is the combination of magnifying endoscopy with narrow band imaging (ME-NBI) that highlights suspicious lesions and brings better diagnostic efficacy. We herein review the recent publications and present a wide extent of the clinical applications of ME-NBI in the stomach. In general, most diagnostic criteria of NBI for gastric lesions have been proposed on the basis of previous research of ME or chromoendoscopy. 2. Evaluation of Gastritis, Atrophy, Intestinal Metaplasia, and Adenoma Appearance of normal gastric mucosa without Helicobacter pylori (HP) infection has been confirmed by a series of studies. It differs depending on the location of the stomach. In gastric corpus (Figure 1(a)), ME shows small round pits which are surrounded
Chronic Gastritis in Dermatitis Herpetiformis: A Controlled Study
Anna Alakoski,Teea T. Salmi,Kaisa Hervonen,Hannu Kautiainen,Maarit Salo,Katri Kaukinen,Timo Reunala,Pekka Collin
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/640630
Abstract: Background and Objective. Previous small studies suggest that chronic atrophic gastritis is common in dermatitis herpetiformis (DH). We here examined the frequency and topography of chronic gastritis in 93 untreated DH subjects and in 186 controls with dyspepsia. Methods. Specimens were drawn from the gastric corpus and antrum and examined for atrophy, intestinal metaplasia, and Helicobacter pylori. Duodenal biopsies were taken. Results. Atrophic corpus gastritis was more frequent in DH than in controls (16.0% and 2.7%, resp., <0.001); atrophy in the antrum was rare in both groups (3.2% and 1.1%, =0.34). Intestinal metaplasia was present in 13 (14.0%) DH and 12 (6.5%) control patients (=0.038) and H. pylori in 17 (18.3%) and 17 (9.3%) (=0.028), respectively. Small-bowel villous atrophy was seen in 76% of the DH patients, equally in patients with and without chronic gastritis. One DH patient with atrophic gastritis developed gastric cancer. Conclusion. In DH, chronic atrophic gastritis was common in the corpus, but not in the antrum. H. pylori will partly explain this, but corpus atrophy is suggestive of an autoimmune etiology. Atrophic gastritis may increase the risk of gastric cancer. We advocate performing upper endoscopy with sufficient histologic samples in DH.
The Progression of Atrophic Gastritis to Gastric Cancer: A Retrospective Study in 61,810 Cases  [PDF]
Yi-Ren Hu, Ying Yu, Jian-Xin Li, Wei-Chun Lu, Qi-Jin Shu, Ying-Cong Yu
Journal of Cancer Therapy (JCT) , 2017, DOI: 10.4236/jct.2017.86047
Abstract: Background and Aim: Chronic atrophic gastritis is a known precancerous lesion for gastric cancer, with an overall 5-year survival less than 20%. However, there is few new data describing the progression rate from atrophic gastritis (AG) to gastric cancer in China. We retrospectively analyzed the risk of gastric cancer among patients with AG and aimed to determine the accuracy of endoscopy diagnosis of AG in China. Methods: Clinical features and endoscopic profiles of chronic atrophic gastritis patients from Wenzhou People’s Hospital between January 2006 and December 2016 were analyzed retrospectively. Results: There were 61,810 cases analyzed retrospectively. 3641 cases of atopic gastritis were diagnosed by endoscopy, in which 1704 cases were confirmed by pathological biopsy; the diagnostic coincidence rate was 46.80%; 2631 cases were diagnosed as atrophic gastritis by pathological biopsy, in which 927 cases were ignored by endoscopy; the miss diagnosis rate was 35.23%. The progression rate from chronic atrophic gastritis and non-atrophic gastritis to gastric cancer respectively was 0.79% and 0.43%. The rate of intestinal metaplasia in mild AG, moderate AG and severe AG respectively was 75.63%, 86.18% and 90.32%, 3.42%, 6.27% and 5.16% about dysplasia in three different degree atrophic gastritis. Conclusions: Endoscopy diagnosis and pathology diagnosis of AG were statistically different. Patients with atrophic gastritis have higher risk of developing into gastric cancer, but it needs further investigation. Different degrees of atrophic gastritis have the different proportions of intestinal metaplasia and dysplasia.
Gastritis and Gastric Cancer: Time for gastric cancer prevention  [cached]
E.D. Papavassilliou,S. Savva
Annals of Gastroenterology , 2009,
Abstract: Gastric cancer represents a major clinical problem, associated with significant morbidity and mortality. Work over several decades has identified multiple risk factors for gastric cancer, which can be best classified as environmental and host-related factors. Gastric cancer is divided into intestinal-type and diffuse type. Precursor lesions for intestinal–type cancer are atrophic gastritis, intestinal metaplasia and dysplasia, while for diffuse type, that are less common, is the lack of intracellular adhesions (loss of E-cadherin protein). Currently, there are neither surveillance strategies nor clear-cut estimates of the benefits and risks of endoscopic surveillance. Thus gastroenterologists must individualize their approach to each patient, which may include frequent endoscopy, topographic mapping of the entire stomach, chromoendoscopy and magnifying endoscopy. In all cases of course the wishes of the patient must be factored in, but a frank discussion with patients and their relatives can be immensely helpful. Unlike colon cancer, for which clear and generally accepted guidelines have been developed over the years, the situation for gastric cancer remains still incompletely developed, reflecting, no doubt, our still limited understanding of gastric cancer pathogenesis. More work is needed to develop a rational and effective approach to the prevention of gastric cancer, mainly in the areas of the detection of early lesions and optimal allocation of limited resources to an effective screening program.
Extensive Atrophic Gastritis Increases Intraduodenal Hydrogen Gas  [PDF]
Yoshihisa Urita,Toshiyasu Watanabe,Tadashi Maeda,Tomohiro Arita,Yosuke Sasaki,Takamasa Ishii,Tatsuhiro Yamamoto,Akiro Kugahara,Asuka Nakayama,Makie Nanami,Kaoru Domon,Susumu Ishihara,Hirohito Kato,Kazuo Hike,Norikok Hara,Shuji Watanabe,Kazushige Nakanishi,Motonobu Sugimoto,Kazumasa Miki
Gastroenterology Research and Practice , 2008, DOI: 10.1155/2008/584929
Abstract: Objective. Gastric acid plays an important part in the prevention of bacterial colonization of the gastrointestinal tract. If these bacteria have an ability of hydrogen (H2) fermentation, intraluminal H2 gas might be detected. We attempted to measure the intraluminal H2 concentrations to determine the bacterial overgrowth in the gastrointestinal tract. Patients and methods. Studies were performed in 647 consecutive patients undergoing upper endoscopy. At the time of endoscopic examination, we intubated the stomach and the descending part of the duodenum without inflation by air, and 20 mL of intraluminal gas samples of both sites was collected through the biopsy channel. Intraluminal H2 concentrations were measured by gas chromatography. Results. Intragastric and intraduodenal H2 gas was detected in 566 (87.5%) and 524 (81.0%) patients, respectively. The mean values of intragastric and intraduodenal H2 gas were 8.5±15.9 and 13.2±58.0 ppm, respectively. The intraduodenal H2 level was increased with the progression of atrophic gastritis, whereas the intragastric H2 level was the highest in patients without atrophic gastritis. Conclusions. The intraduodenal hydrogen levels were increased with the progression of atrophic gastritis. It is likely that the influence of hypochlorhydria on bacterial overgrowth in the proximal small intestine is more pronounced, compared to that in the stomach.
Narrow-band imaging with magnifying endoscopy is accurate for detecting gastric intestinal metaplasia  [cached]
Edoardo Savarino,Marina Corbo,Pietro Dulbecco,Lorenzo Gemignani
World Journal of Gastroenterology , 2013, DOI: 10.3748/wjg.v19.i17.2668
Abstract: AIM: To investigate the predictive value of narrow-band imaging with magnifying endoscopy (NBI-ME) for identifying gastric intestinal metaplasia (GIM) in unselected patients. METHODS: We prospectively evaluated consecutive patients undergoing upper endoscopy for various indications, such as epigastric discomfort/pain, anaemia, gastro-oesophageal reflux disease, suspicion of peptic ulcer disease, or chronic liver diseases. Patients underwent NBI-ME, which was performed by three blinded, experienced endoscopists. In addition, five biopsies (2 antrum, 1 angulus, and 2 corpus) were taken and examined by two pathologists unaware of the endoscopic findings to determine the presence or absence of GIM. The correlation between light blue crest (LBC) appearance and histology was measured. Moreover, we quantified the degree of LBC appearance as less than 20% (+), 20%-80% (++) and more than 80% (+++) of an image field, and the semiquantitative evaluation of LBC appearance was correlated with IM percentage from the histological findings. RESULTS: We enrolled 100 (58 F/42 M) patients who were mainly referred for gastro-esophageal reflux disease/dyspepsia (46%), cancer screening/anaemia (34%), chronic liver disease (9%), and suspected celiac disease (6%); the remaining patients were referred for other indications. The prevalence of Helicobacter pylori (H. pylori) infection detected from the biopsies was 31%, while 67% of the patients used proton pump inhibitors. LBCs were found in the antrum of 33 patients (33%); 20 of the cases were classified as LBC+, 9 as LBC++, and 4 as LBC+++. LBCs were found in the gastric body of 6 patients (6%), with 5 of them also having LBCs in the antrum. The correlation between the appearance of LBCs and histological GIM was good, with a sensitivity of 80% (95%CI: 67-92), a specificity of 96% (95%CI: 93-99), a positive predictive value of 84% (95%CI: 73-96), a negative predictive value of 95% (95%CI: 92-98), and an accuracy of 93% (95%CI: 90-97). The NBI-ME examination overlooked GIM in 8 cases, but the GIM was less than 5% in 7 of the cases. Moreover, in the 6 false positive cases, the histological examination showed the presence of reactive gastropathy (4 cases) or H. pylori active chronic gastritis (2 cases). The semiquantitative correlation between the rate of LBC appearance and the percentage of GIM was 79% (P < 0.01). CONCLUSION: NBI-ME achieved good sensitivity and specificity in recognising GIM in an unselected population. In routine clinical practice, this technique can reliably target gastric biopsies.
The Regenerating Gene I Is Overexpressed in Atrophic Gastritis Rats with Hypergastrinemia  [PDF]
Shujie Chen,Jing Zhong,Qunyan Zhou,Xiaofeng Lu,Liangjing Wang,Jianmin Si
Gastroenterology Research and Practice , 2011, DOI: 10.1155/2011/403956
Abstract: The role of gastrin on the development of atrophic gastritis (AG) and its relationship with the expression of RegIα??in vivo remain unclear. We established experimental AG in rats by combination administration with sodium salicylate, alcohol, and deoxycholate sodium. The mean score of inflammation in gastric antrum in AG rats was significantly elevated ( ), while the number of glands dramatically decreased ( ). In addition, the cell proliferation in gastric glands was increased in experimental AG rats, as determined by immunohistochemistry staining of PCNA and GS II. The level of serum gastrin in AG rats was significantly elevated relative to that of normal rats ( ). Moreover, the expression of RegIα protein and its receptor mRNA was increased in gastric tissues in AG rats ( ). Taken together, we demonstrated that the overexpression of Reglα is related with hypergastrinemia in AG rats. 1. Introduction Atrophic gastritis (AG) was defined as the loss of glands and/or replacement by intestinal glands in gastric mucosa, which has been recognized as initial step in the process of AG-dysplasia—gastric cancer (intestinal type) consequence [1, 2]. AG is classified as two major types, autoimmune atrophic gastritis and multifocal atrophic gastritis, and the later disease involves both the antrum and corpus of stomach and represents an increased risk for gastric cancer [1, 3]. Among multiple regulators, growing evidences indicated that growth factors may play an important role in the progression from chronic AG to gastric cancer [4]. The polypeptide hormone gastrin has been demonstrated to be an essential growth factor in gastric carcinogenesis [5]. In corpus-associated gastric atrophy, the maintenance of G cells and the loss of parietal cells could lead to hypergastrinaemia [5]. In contrast, in antrum-predominant AG, though the reduction of G cells inhibits the release of gastrin [6], the increase of inflammation in antrum mucosa induces gastric gland atrophy, intestinal metaplasia, and even tumorigenesis [7]. However, the roles of gastrin in the development of AG are not fully understood. The regenerating gene (Reg) Iα was originally isolated from regenerating pancreatic islet cells [8]. In the stomach, RegIα is expressed in the enterochromaffin-like (ECL) cells in response to water immersion stress-induced gastric mucosa damage [9–12]. It has been revealed that gastrin stimulates the ECL cells proliferation in Helicobacter pylori (H. pylori-)associated gastritis. Studies also demonstrated that gastrin and H. pylori could stimulate the expression of RegIα
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