Helicobacter suis-Associated Gastritis Mimicking Conventional H. pylori-Associated Atrophic Gastritis

Iwamuro, Masaya; Murayama, Somay Yamagata; Nakamura, Masahiko; Hamada, Kenta; Tanaka, Takehiro; Okada, Hiroyuki

doi:10.1155/2022/4254605

Cited by 3 publications

(2 citation statements)

References 15 publications

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“…The gastric MALT lymphomas are most probably the consequence of the continuous long-term stimulation of lymphocyte proliferation and are naturally not related to hypergastrinemia, since lymphocytes do not express the gastrin receptor or receptors for any of the ECL cell mediators (no lymphoma was detected in patients with gastrinoma). Interestingly, Helicobacter suis can infect humans and give rise to gastric MALT lymphoma ( 42 ), and may also induce gastritis, mimicking H. pylori gastritis ( 43 ).…”

Section: Gastric Cancermentioning

confidence: 99%

The central role of gastrin in gastric cancer

Waldum,

Mjønes

2023

Front. Oncol.

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The prevalence of gastric cancer has markedly declined, but due to the high mortality rates associated with gastric cancer, it is still a serious disease. The preferred classification of gastric cancer is according to Lauren into either the intestinal type, which has a glandular growth pattern, or the diffuse type, which does not have glandular structures. Both types have been classified as adenocarcinomas, with the latter type based on periodic acid–Schiff (PAS) positivity presumed to reflect mucin. However, the presence of mucin in the diffuse type, in contrast to neuroendocrine/enterochromaffin-like (ECL) cell markers, has not been confirmed by immunohistochemistry and in situ hybridization. The ECL cells are probably prone to becoming cancerous because they do not express E-cadherin. Gastric cancer is unique in that a bacterium, Helicobacter pylori, is thought to be its main cause. H. pylori predisposes infected individuals to cancer only after having caused oxyntic atrophy leading to gastric hypoacidity and hypergastrinemia. No single H. pylori factor has been convincingly proved to be carcinogenic. It is probable that gastrin is the pathogenetic factor for gastric cancer due to H. pylori, autoimmune gastritis, and long-term prolonged inhibition of gastric acid secretion. Hypergastrinemia induces ECL cell hyperplasia, which develops into neuroendocrine tumors (NETs) and then into neuroendocrine carcinomas in rodents, a sequence that has also been described in humans. During carcinogenesis, the tumor cells lose specific traits, requiring that sensitive methods be used to recognize their origin. Gastric cancer occurrence may hopefully be prevented by H. pylori eradication at a young age, and by the reduced use of inhibitors of acid secretion and use of a gastrin antagonist in those with previous long-term H. pylori infection and those with autoimmune gastritis.

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Section: Gastric Cancermentioning

confidence: 99%

The central role of gastrin in gastric cancer

Waldum,

Mjønes

2023

Front. Oncol.

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“…They concluded that H. suis was the most common NHPH that infected human stomachs 13 . The H. suis infection leads to diseases such as gastric mucosa-associated lymphoid tissue (MALT) lymphoma, nodular gastritis, chronic gastritis, and peptic ulcer [14][15][16][17][18][19][20] . However, the above reports did not provide proof of H. suis or other NHPH infection because they only used PCR assay and did not isolate the bacteria or analyze the isolated bacteria's genome to identify the infecting bacteria.…”

Section: Introductionmentioning

confidence: 99%

Development of serological assays to identifyHelicobacter suisandHelicobacter pyloriinfections

Matsui

Rimbara²,

Suzuki

et al. 2022

Preprint

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BackgroundHelicobacter suis hosted by hogs is the most-prevalent gastric non-Helicobacter pylori Helicobacter species (NHPH) found in humans with gastric diseases. However, there is no reliable method for diagnosing H. suis infection in clinical practice without gastric biopsy specimens. MethodsHelicobacter infection was diagnosed by using routine methods for detecting H. pylori infection and three other methods (PCR, culture accompanied by genomic analyses, and microscopy) for detecting NHPH and H. pylori infection using gastric biopsy specimens. Then, an ELISA was developed to detect serum anti-H. suis and anti-H. pylori antibody titers. Findings The serum specimens (n=101) were divided into specimens with (n=20) and without H. suis infection (n=81), or into specimens with (n=17) or without H. pylori infection (n=64) after excluding H. pylori infection-eradicated specimens (n=20). The cut-off values of the optical density in the ELISA were used to judge Helicobacter infections. The sensitivity and specificity were 100% and 92.5%, respectively, for identifying H. suis infection, or 88.2% and 87.5%, respectively, for identifying H. pylori infection, and these levels were considered acceptable for clinical application. We detected no other NHPH infections by PCR or culture in this study. Interpretation We developed the world′s first ELISA to simultaneously diagnose H. suis and H. pylori infection, which is available for large-scale medical examination. The eradication of H. suis was confirmed by the time-dependent decline of anti-H. suis antibody titers. Funding This work was supported by MEXT/JSPS KAKENHI (JP19H03474, JP20K08365) and AMED (JP20fk0108148, JP20fk0108133).

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