Journal of Pathology and Translational Medicine

Review

Rare Gastric Lesions Associated with Helicobacter pylori Infection: A Histopathological Review: Mee Joo; J Pathol Transl Med. 2017;51(4):341-351. Published online June 5, 2017; DOI: https://doi.org/10.4132/jptm.2017.04.03

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Helicobacter pylori infection is associated with chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. However, some rare gastric lesions exhibiting distinctive histological features may also be associated with H. pylori infection, including lymphocytic gastritis, granulomatous gastritis, Russell body gastritis, or crystal-storing histiocytosis. Although diverse factors can contribute to their development, there is convincing evidence that H. pylori infection may play a pathogenic role. These findings are mainly based on studies in patients with these lesions who exhibited clinical and histological improvements after H. pylori eradication therapy. Thus, H. pylori eradication therapy might be indicated in patients with no other underlying disease, particularly in countries with a high prevalence of H. pylori infection. This review describes the characteristic histological features of these rare lesions and evaluates the evidence regarding a causative role for H. pylori infection in their pathogenesis.

Citations

Citations to this article as recorded by

Crystal-Storing Histiocytosis: The Iceberg of More Serious Conditions
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Diagnostics.2023; 13(2): 271. CrossRef
Acute systemic infection-associated Russell body gastroesophagitis: A case report and literature review
Elizaveta Flerova, Susan Inniss, Nneamaka Nwaoduah, Richard P. Denicola, Jialing Huang
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The Korean Journal of Gastroenterology.2023; 82(6): 269. CrossRef
H. pylori Infection and Virulence Factors cagA and vacA (s and m Regions) in Gastric Adenocarcinoma from Pará State, Brazil
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Original Articles

Helicobacter pylori Infection and Histopathological Features of Gastric Mucosa.: Gyung Hyuck Ko, Cheol Keun Park, Chun Sik Choi, Heung Bae Park, Jeong Hee Lee, Hye Jung Lee, Hyun Ju Kim, Kwang Ho Rhee; Korean J Pathol. 1996;30(3):199-209.

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Abstract PDF: A microscopic examination of 1,000 cases of gastroscopic biopsy specimens revealed that the prevalence and severity of chronic gastritis, neutrophilic infiltration, and Helicobacter pylori infection increased with advancing age until the age reached about 40, but they decreased thereafter in accordance with the increasing prevalence of intestinal metaplasia. The prevalence and severity of Helicobacter pylori infection, chronic gastritis, and neutrophilic infiltration were proportionately related to each other and to gastric peptic ulcer, but inversely related with intestinal metaplasia and gastric carcinoma. The results suggested that chronic gastritis and gastric peptic ulcer may be associated with Helicobacter pylori infection and that if these lesions persist, intestinal metaplasia may develop with decreased severity of chronic gastritis and Helicobacter pylori infection but, instead, increase of the risk of gastric carcinoma. And it is thought that the cause of the high incidence of gastric carcinoma in Korea may be related to the fact that chronic gastritis and Helicobacter pylori infection develop earlier in life and therefore the prevalence of intestinal metaplasia is higher in Korea than in other countries.

Histopathologic Analysis of Helicobacter Pylori Associated Gastritis.: Ho Jung Lee, Eun Sil Yu, In Chul Lee; Korean J Pathol. 1996;30(9):764-774.

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Abstract PDF: Gastric mucosa shows continuous changes in surface epithelium as well as inflammatory reaction by various substances from the outside and their metabolic products. Gastric mucosal lesions are proven to be associated with bacterial infection by the discovery of Heliobacter pylori(H. pylori) and many studies about histopathologic changes of gastric mucosa associated H. pylori infection has been advanced. It is known that H. pylori associated gastritis displays surface foveolar epithelial changes, such as cytoplasmic vacuolation, mucin loss, juxtaluminal cytoplasm erosion, epithelial denudation, and mucosal irregularity. There have been many studies that H. pylori infection is associated with intestinal metaplasia, gastric dysplasia, and carcinoma. Also chronic H. pylori infection with its induction of gastric lymphoid follicle has been implicated as a precursor of gastric lymphoma of the unique B-cell type that arises from mucosa-associated lymphoid tissue(MALT). However, these gastric mucosal changes are also observed in gastritis with other causes. In this study, we aimed to define specific histopathiologic findings associated with H. pylori infection. A total of 463 gastric biopsy specimens were reviewed. They were Helicobacter-associated gastritis and were divided as many (MH), a few (AH), and no (NH), according to the number of H. pylori. 210 (MH), 131 (AH), and 122 (NH) biopsy specimens were included. Lymphocytes, plasma cells in lamina propria, eosinophils and neutrophils in surface epithelium and crypt as well as lamina propria were graded from 0 to 3. Surface epithelial changes including cytoplasmic vacuolation, mucin loss, juxtaluminal erosion, epithelial denudation and mucosal irregrarity were observed in 200 of 210 cases(95%) in MH group, 34 of 131 cases(26%) in AH group, and 6 of 122 cases(5%) in NH group. This result indicates there is significant difference in surface epithelial changes according to the number of H. pylori(p<0.001). Severity of eosinophil, neutrophil, lymphocyte, and plasma cell infiltration is increased in proportion to the number of H. pylori. Especially, neutrophilic infiltration is not identified in 95 of 122 cases(78%) in NH group, whereas MH group shows severe infitration (grade 3) in 127 of 210 cases(61%), and no (grade 0) in 11 of 210 cases(5%). This data well explains that the severity of neutrophil infiltration is associated with, the degree of H. pylori infection in chronic active gastritis, with statistical significance. The prevalence of lymphoid follicle formation was 17 of 120 cases(14%) in NH group, 24 of 131 cases(18%) in AH group, and 52 of 210 cases(25%) in MH group. This shows that lymphoid follicle formation correlates with the number of H. pylori, but without statistical significance. The prevalence of intestinal metaplasia in NH, AH, and MH was 43 of 122 cases(35%), 46 of 131 cases(35%), and 69 of 210 cases(33%), showing no association between intestinal metaplasia and H. pylori. In summary, H. pylori associated gastritis dispays characteristic histopathological changes in gastric mucosa, in which surface epithelial changes and various inflammatory infiltrates are increased in proportion to the number of H. pylori. Especially vacuolization of surface foveolar epithelium, cryptitis, and crypt abscess are specific findings of H. pylori associated gastritis.

Correlation between Helicobacter pylori Infection and Lymphoid Follicle Formation in Gastrectomy Specimens.: Won Ae Lee, Hye Sung Hahn, Woo Ho Kim, Yong Il Kim; Korean J Pathol. 1998;32(3):162-168.

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Abstract PDF: Histopathologic studies for Helicobacter pylori (H. pylori)-associated chronic gastritis have been mostly undertaken with endoscopic biopsy specimens, often leading to an inappropriate evaluation of the gastric mucosal alterations. The purpose of this paper was designed to investigate the actual prevalence of lymphoid follicle formation by H. pylori infection using the resected stomachs. A total of 16 fresh gastrectomy specimens bearing gastric carcinoma were examined under the quick and gentle procedure, with which H. pylori was detected in 12 cases (75%) and lymphoid follicles in 14 cases (87.5%), while the detection rate of H. pylori remained 56.3% in the control group which comprised the same 16 resected stomachs and were examined by routine tissue preparation procedure without any special care. There was a significant correlation between the presence of H. pylori and lymphoid follicle formation (p=0.05), but no correlation was found between the grades of H. pylori and lymphoid follicles. The topographical distribution of H. pylori or lymphoid follicles in antrum and body gave no statistical difference. Similarly, there was no correlation between H. pylori infection and intestinal metaplasia, activity of chronic gastritis or histologic types of accompanying adenocarcinoma. We conclude that studies of the gastric mucosal change by H. pylori infection using the gastrectomy specimens provide a useful information for analysis of lymphoid follicle formation which is a consistent morphological characteristic of H. pylori infection.

Histopathologic Analysis of Helicobacter pylori-associated Chronic Gastritis between cagA-positive and cagA-negative Strains.: Hun Kyung Lee, Gyeong Hoon Kang, Hwoon Yong Jung, On Ja Kim; Korean J Pathol. 1998;32(7):504-510.

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Abstract: Infection with Helicobacter pylori (H. pylori) leads to gastritis, but the majority of infected persons are asymptomatic, and it has been recently described that the ability of H. pylori to cause more severe disease is related to the presence of the cytotoxin-associated gene A (cagA). We investigated the prevalence of cagA-bearing strains in a group of H. pylori-positive gastritis, and compared the morphologic differences between cagA-positive and cagA-negative cases on H&E stained slides. Polymerase chain reaction (PCR) assays for detection of H. pylori and cagA of 62 gastric biopsy specimens were performed. All the slides were analyzed by the updated Sydney system. Forty eight (77.4%) were PCR positive for H. pylori and thirty four (54.8%) were positive for cagA. There were no significant differences in numbers of H. pylori, degree of infiltration of mononuclear cells and degree of atrophy between cagA-positive and cagA-negative groups. The rates of neutrophilic infiltration and intestinal metaplasia were significantly higher in cagA-positive group than in cagA-negative group. In conclusion, the detection of H. pylori by PCR method is more sensitive than that of microscopic examination and H. pylori strains possessing cagA are associated with an enhanced induction of severe gastritis.

Case Reports

A Case of Gastric Inverted Hyperplastic Polyp Associated with Gastritis Cystica Profunda and Early Gastric Carcinoma.: Min Sung Choi, So Young Jin, Dong Won Kim, Dong Wha Lee, Sang Mo Park; Korean J Pathol. 2007;41(1):55-58.

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Abstract PDF: A gastric inverted hyperplastic polyp is characterized by downward growth of the hyperplastic mucosal components into the submucosa. Lesions are composed of hyperplastic foveolar-type glands, and sometimes coexist with gastritis cystica profunda (GCP). Adenocarcinoma frequen- tly can coexist, but the relationship is not clear. A 71-year-old male was admitted to hospital because of dyspepsia for one month. He underwent a wedge resection of the stomach, after endoscopic biopsies. The gross finding showed a slightly elevated papillary lesion with central depression. Microscopically, the elevated lesion was composed of hyperplastic fundic glands and foveolar cells, and the central depressed lesion showed a nodular inverted proliferation of normal appearing gastric epithelium and glands in the submucosa. An additional proximal gastrectomy specimen exhibited marked GCP and a minute adenocarcinoma at the proximal margin with p53 protein overexpression.

Acute Corrosive Esophago-Gastritis: A Case of Drain-cleansing Liquid-induced Transmural Inflammation.: Tae Jin Kim, Jeong Wook Seo, Yong Il Kim; Korean J Pathol. 1990;24(3):294-298.

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Abstract PDF: The pathologic features of acute corrosive esophago-gastritis by ingestion of "Trapunc", a common commercial drain cleansing liquid, is presented. A 37-year-old woman ingested abut 30 ml of Trapunc (3 gm NaOH/100 ml) to commit suicide and received piecemeal esophagectomy and total gastrectomy 9 days after the episode. The esophagus and stomach were extremely friable and necrotic. The most part of the stomach showed acute toxic necrotizing gastritis which was manifested by extensive greenish brown discoloration due to liquefaction necrosis of the mucosa except for a few rugae along the greater curvature. The antrum and distal body revealed severe mucosal detachment and even transmural necrosis. The tissue reaction was basically the same as those of NaOH-induced corrosive esophago-gastritis of acute stage, although it appeared to be severer probably due to sodium hypochlorite, and additive constituent of the ingested cleanser. A unique distribution pattenr of mucosal involvement is discussed.

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