Gastric xanthelasma: case report

Xanthelasma, also known as Xanthoma or lipid island, is an uncommon gastrointestinal tract (GIT) tumor-like lesion and the stomach is its most frequent location in upper GI lesions, specifically in the gastric antrum, as a single lesion. The pathogenesis appears to be related to healing processes in response to tissue damage provoked by inflammation induced by Helicobacter pylori infection. Many studies have reported that successful H. pylori eradication helps prevent gastric cancer (GC) development. We present a case of a 77 years old patient that showed endoscopic diagnosis of erythematous gastropathy, a gastric antrum xanthelasma and H. Pylori infection. After confirmed H. pylori eradication, the lesion had complete regression. The successful eradication of H. pylori probably led to a total regression of the lesion. Gastric xanthelasma (GX) has been shown to be an independent predictive marker for early GC detection after H. pylori eradication. GX could be a useful marker for predicting the development of gastric cancer.

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Evaluation of the Epidemiologic Efficacy of Eradicating Helicobacter pylori on Development of Gastric Cancer

Epidemiologic Reviews ◽

10.1093/epirev/mxz006 ◽

2019 ◽

Vol 41 (1) ◽

pp. 97-108 ◽

Cited By ~ 2

Author(s):

Fujiao Duan ◽

Chunhua Song ◽

Jintao Zhang ◽

Peng Wang ◽

Hua Ye ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Population Attributable Risk ◽

Eradication Therapy ◽

Attributable Risk ◽

Chinese Patients ◽

Controlled Trials ◽

Mixed Effect ◽

H Pylori ◽

Development Of Gastric Cancer

Abstract Eradication of Helicobacter pylori colonization has been reported to affect the progression of gastric cancer. A comprehensive literature search was performed from 1997 to 2017 using electronic databases. All randomized controlled trials (RCTs) and nonrandomized controlled trials (non-RCT) evaluated the effect of H. pylori eradication on development of gastric cancer. Four RCTs and 9 non-RCTs were included (n = 40,740 participants; 321,269 person-years). Overall, H. pylori eradication therapy was associated with a significantly reduced risk of gastric cancer (incidence rate ratio (IRR) = 0.52, 95% confidence interval (CI): 0.41, 0.65). Results of mixed-effect Poisson regression meta-analysis were similar to those of traditional meta-analyses. In stratified analyses, the IRRs were 0.59 (95% CI: 0.41, 0.86) in RCTs and 0.48 (95% CI: 0.36, 0.64) in non-RCTs. The IRRs were 0.45 (95% CI: 0.34, 0.61) in patients and 0.63 (95% CI: 0.44, 0.90) in the general population. Moreover, the relative risk reduction was approximately 77% on the development of noncardiac gastric cancer with H. pylori eradication therapy in China. Attributable risk percentage and population attributable risk percentage for Chinese patients were 77.08% and 75.33%, respectively, and for Japanese patients were 57.80% and 45.99%, respectively. H. pylori eradication therapy reduces the risk of noncardiac gastric cancer development. The findings indicate the importance of early intervention with H. pylori eradication therapy from the perspective of epidemiology.

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Recent Advances inHelicobacter pyloriInfection in Children: From the Petri Dish to the Playgound

Canadian Journal of Gastroenterology ◽

10.1155/2003/809530 ◽

2003 ◽

Vol 17 (7) ◽

pp. 448-454 ◽

Cited By ~ 4

Author(s):

Peng-Yuan Zheng ◽

Nicola L Jones

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Peptic Ulcer ◽

Petri Dish ◽

Host Factors ◽

Causative Role ◽

Ulcer Disease ◽

Recent Advances ◽

H Pylori ◽

Development Of Gastric Cancer

Helicobacter pyloriinfection is acquired in childhood, plays a causative role in chronic gastritis and peptic ulcer disease, and is associated with the development of gastric cancer. The present review focuses on recent advances in the scientific knowledge ofH pyloriinfection in children, including clinical sequelae, diagnosis and treatment. In addition, recent insights regarding both bacterial and host factors that mediate human diseases associated withH pyloriinfection are discussed.

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The Prevalence ofHelicobacter pyloriVirulence Factors in Bhutan, Vietnam, and Myanmar Is Related to Gastric Cancer Incidence

BioMed Research International ◽

10.1155/2015/830813 ◽

2015 ◽

Vol 2015 ◽

pp. 1-8 ◽

Cited By ~ 8

Author(s):

Tran Thi Huyen Trang ◽

Seiji Shiota ◽

Miyuki Matsuda ◽

Tran Thanh Binh ◽

Rumiko Suzuki ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Virulence Factors ◽

Cancer Incidence ◽

The Status ◽

The Difference ◽

H Pylori ◽

Significant Health ◽

Development Of Gastric Cancer

Gastric cancer is a significant health problem in Asia. Although the prevalence ofHelicobacter pyloriinfection is similar in Bhutan, Vietnam, and Myanmar, the incidence of gastric cancer is highest in Bhutan, followed by Vietnam and Myanmar. We hypothesized thatH. pylorivirulence factors contribute to the differences. The status ofcagA,vacA,jhp0562, andβ-(1,3)galT(jhp0563)was examined in 371H. pylori-infected patients from Bhutan, Vietnam, and Myanmar. Each virulence factor could not explain the difference of the incidence of gastric cancer. However, the prevalence of quadruple-positive forcagA,vacAs1,vacAm1, andjhp0562-positive/β-(1,3)galT-negative was significantly higher in Bhutan than in Vietnam and Myanmar and correlated with gastric cancer incidence. Moreover, gastritis-staging scores measured by histology of gastric mucosa were significantly higher in quadruple-positive strains. We suggest that thecagA,vacAs1,vacAm1, andjhp0562-positive/β-(1,3)galT-negative genotype may play a role in the development of gastric cancer.

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Eradication Treatment of Helicobacter pylori Infection: Its Importance and Possible Relationship in Preventing the Development of Gastric Cancer

ISRN Gastroenterology ◽

10.5402/2012/935410 ◽

2012 ◽

Vol 2012 ◽

pp. 1-9 ◽

Cited By ~ 7

Author(s):

Bruna Maria Roesler ◽

Sandra Cecília Botelho Costa ◽

José Murilo Robilotta Zeitune

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Genetic Factors ◽

Salt Intake ◽

Mucosal Damage ◽

Bacterial Virulence ◽

Host Genetic ◽

H Pylori ◽

Host Genetic Factors ◽

Development Of Gastric Cancer

Helicobacter pylori is the most important carcinogen for gastric adenocarcinoma. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of carcinogenesis in the stomach; host genetic factors contribute to the regulation of the inflammatory response and to the aggravation of mucosal damage. In terms of environmental factors, salt intake and smoking contribute to the development of lesions. Various therapeutic schemes are proposed to eradicate H. pylori infection, which could potentially prevent gastric cancer, offering the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred.

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Statins’ Regulation of the Virulence Factors of Helicobacter pylori and the Production of ROS May Inhibit the Development of Gastric Cancer

Antioxidants ◽

10.3390/antiox10081293 ◽

2021 ◽

Vol 10 (8) ◽

pp. 1293

Author(s):

Ting-Yu Lin ◽

Wen-Hsi Lan ◽

Ya-Fang Chiu ◽

Chun-Lung Feng ◽

Cheng-Hsun Chiu ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Virulence Factors ◽

Treatment Strategies ◽

Vacuolating Cytotoxin ◽

Cholesterol Levels ◽

Cytotoxin Associated Gene A ◽

H Pylori ◽

Cellular Components ◽

Development Of Gastric Cancer

Conventionally, statins are used to treat high cholesterol levels. They exhibit pleiotropic effects, such as the prevention of cardiovascular disease and decreased cancer mortality. Gastric cancer (GC) is one of the most common cancers, ranking as the third leading global cause of cancer-related deaths, and is mainly attributed to chronic Helicobacter pylori infection. During their co-evolution with hosts, H. pylori has developed the ability to use the cellular components of the host to evade the immune system and multiply in intracellular niches. Certain H. pylori virulence factors, including cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), and cholesterol-α-glucosyltransferase (CGT), have been shown to exploit host cholesterol during pathogenesis. Therefore, using statins to antagonize cholesterol synthesis might prove to be an ideal strategy for reducing the occurrence of H. pylori-related GC. This review discusses the current understanding of the interplay of H. pylori virulence factors with cholesterol and reactive oxygen species (ROS) production, which may prove to be novel therapeutic targets for the development of effective treatment strategies against H. pylori-associated GC. We also summarize the findings of several clinical studies on the association between statin therapy and the development of GC, especially in terms of cancer risk and mortality.

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DNA Methylation Silencing of microRNA Gene Methylater in the Precancerous Background Mucosa with and without Gastric Cancer: Analysis of Effects of Helicobacter pylori Eradication and Long-Term Aspirin Use

10.20944/preprints201902.0070.v1 ◽

2019 ◽

Author(s):

Jiro Watari ◽

Chiyomi Ito ◽

Tadakazu Shimoda ◽

Toshihiko Tomita ◽

Tadayuki Oshima ◽

...

Keyword(s):

Gastric Cancer ◽

Dna Methylation ◽

Helicobacter Pylori ◽

Early Stage ◽

Surrogate Marker ◽

Predictive Marker ◽

Microrna Gene ◽

H Pylori ◽

Background Mucosa

The risk of gastric cancer (GC) declines after Helicobacter pylori (H. pylori) eradication and long-term aspirin use. We evaluated the effects of H. pylori eradication (Cohort 1) and aspirin use (Cohort 2) on the methylation of microRNAs (miRNAs) such as miR-34c, miR-124a-3, miR-129-2, and miR-137 in the gastric mucosa with and without GC, i.e., atrophic mucosa (AM) and intestinal metaplasia (IM). DNA was isolated from AM and IM separately using laser caption microdissection. In Cohort 1, H. pylori eradication was associated with a significant reduction of miR-124a-3 methylation only in AM, but not in IM. miR-129-2 methylation in AM may be a surrogate marker of GC in H. pylori-infected patients. In Cohort 2, aspirin did not reverse miRNA methylation in either AM or IM irrespective of H. pylori infection. miR-129-2 methylation in AM was an independent predictive marker of GC in H. pylori-infected but not -eradicated patients. These results indicate that H. pylori eradication and aspirin use were less effective in improving methylation in IM compared with AM; thus, these interventions are recommended at an early stage prior to the development of IM to prevent GC development.

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Complete Genome Sequence of Helicobacter pylori Strain 29CaP Isolated from a Mexican Patient with Gastric Cancer

Genome Announcements ◽

10.1128/genomea.01512-15 ◽

2016 ◽

Vol 4 (1) ◽

Cited By ~ 2

Author(s):

Eduardo Mucito-Varela ◽

Gonzalo Castillo-Rojas ◽

Miguel A. Cevallos ◽

Luis Lozano ◽

Enrique Merino ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Genome Sequence ◽

Complete Genome Sequence ◽

Complete Genome ◽

Prophage Sequence ◽

Genomic Data Analysis ◽

H Pylori ◽

Mexican Patient ◽

Development Of Gastric Cancer

Helicobacter pylori infection is a risk factor for the development of gastric cancer and other gastroduodenal diseases. We report here the complete genome sequence of H. pylori strain 29CaP, isolated from a Mexican patient with gastric cancer. The genomic data analysis revealed a cag -negative H. pylori strain that contains a prophage sequence.

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Increased Production of Matrix Metalloproteinases in Helicobacter pylori Infection that Stimulates Gastric Cancer Stem Cells

International Journal of Veterinary Science ◽

10.37422/ijvs/20.043 ◽

2020 ◽

Keyword(s):

Gastric Cancer ◽

Stem Cells ◽

Helicobacter Pylori ◽

Cancer Stem Cells ◽

Histopathological Examination ◽

Physiological Saline ◽

Rrna Gene ◽

Peptic Ulcers ◽

Gastric Cancer Stem Cells ◽

H Pylori

Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.

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The correlation between lncRNAs and Helicobacter pylori in gastric cancer

Pathogens and Disease ◽

10.1093/femspd/ftaa004 ◽

2019 ◽

Vol 77 (9) ◽

Author(s):

Narges Dastmalchi ◽

Seyed Mahdi Banan Khojasteh ◽

Mirsaed Miri Nargesi ◽

Reza Safaralizadeh

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Molecular Mechanisms ◽

Gastrointestinal Diseases ◽

Mechanisms Of Action ◽

Molecular Pathways ◽

Gastric Diseases ◽

Non Coding Rnas ◽

H Pylori ◽

The Relationship

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.

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Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

International Journal of Molecular Sciences ◽

10.3390/ijms22094823 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4823

Author(s):

María Fernanda González ◽

Paula Díaz ◽

Alejandra Sandoval-Bórquez ◽

Daniela Herrera ◽

Andrew F. G. Quest

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Outer Membrane ◽

Extracellular Vesicles ◽

Membrane Vesicles ◽

Outer Membrane Vesicles ◽

Host Cells ◽

Gastric Epithelium ◽

Infected Cells ◽

H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

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