scholarly journals Eosinophilic Gastroenteritis as a Cause of Non-Helicobacter pylori, Non-gastrotoxic Drug Ulcers in Children

2020 ◽  
Author(s):  
Jung Yeon Joo ◽  
Jin Min Cho ◽  
In Hyuk Yoo ◽  
Hye Ran Yang
Keyword(s):  
Helicobacter Pylori ◽  
Atopic Dermatitis ◽  
Clinical Laboratory ◽  
Systemic Disease ◽  
Eosinophilic Gastroenteritis ◽  
Ulcer Recurrence ◽  
Blood Eosinophil ◽  
Iron Level ◽  
Peptic Ulcers ◽  
H Pylori

Abstract Background: While Helicobacter pylori (H. pylori) ulcers has declined recently, H. pylori-negative and/or gastrotoxic drug-negative peptic ulcers (HNGN-PU) has increased. This study aimed to analyze the etiology of peptic ulcers in children and the differences in clinical, laboratory, endoscopic, and histopathologic findings of peptic ulcers according to etiology, including eosinophilic gastroenteritis (EoGE).Methods: In total, 255 children (157 boys and 98 girls) with peptic ulcers were recruited. The subjects were categorized into 5 groups according to the etiology of the ulcer: 1) H. pylori infection (n = 51); 2) gastrotoxic drugs (n = 18); 3) idiopathic (n = 144); 4) systemic disease (n = 23); 5) EoGE (n = 19). Clinical data were reviewed and analyzed retrospectively.Results: Age at diagnosis, ulcer recurrence, atopic dermatitis history, white blood cell count, blood eosinophil count, platelet count, serum albumin level, iron level, erythrocyte sedimentation rate, and C-reactive protein level differed significantly among the 5 groups (all p < 0.05). Regarding endoscopic findings, multiple ulcers and gastric mucosal nodularity differed among the 5 groups (all p < 0.05). When comparing the EoGE ulcer group with the others, EoGE group revealed older ages (p = 0.022), higher rates of ulcer recurrence (p = 0.018), atopic dermatitis history (p = 0.001), and both blood and tissue eosinophilia (both p = 0.001).Conclusions: EoGE ulcers constituted 10.2% of HNGN-PU in pediatric patients. In children with HNGN-PU, peripheral eosinophilia, ulcer recurrence, and atopic dermatitis history might imply EoGE, necessitating thorough investigation of tissue eosinophils during endoscopic biopsy.Trial registration: A total of 255 children was retrospectively registered between between July 2003 and April 2017.

scholarly journals Eosinophilic Gastroenteritis as a Cause of Non-Helicobacter pylori, Non-gastrotoxic Drug Ulcers in Children

2020 ◽  
Author(s):  
Jung Yeon Joo ◽  
Jin Min Cho ◽  
In Hyuk Yoo ◽  
Hye Ran Yang
Keyword(s):  
Helicobacter Pylori ◽  
Atopic Dermatitis ◽  
Clinical Laboratory ◽  
Systemic Disease ◽  
Eosinophilic Gastroenteritis ◽  
Ulcer Recurrence ◽  
Blood Eosinophil ◽  
Iron Level ◽  
Peptic Ulcers ◽  
H Pylori

Abstract Background: While Helicobacter pylori (H. pylori) ulcers has declined recently, H. pylori-negative and/or gastrotoxic drug-negative peptic ulcers (HNGN-PU) has increased. This study aimed to analyze the etiology of peptic ulcers in children and the differences in clinical, laboratory, endoscopic, and histopathologic findings of peptic ulcers according to etiology, including eosinophilic gastroenteritis (EoGE). Methods: In total, 255 children (157 boys and 98 girls) with peptic ulcers were recruited. The subjects were categorized into 5 groups according to the etiology of the ulcer: 1) H. pylori infection (n = 51); 2) gastrotoxic drugs (n = 18); 3) idiopathic (n = 144); 4) systemic disease (n = 23); 5) EoGE (n = 19). Clinical data were reviewed and analyzed retrospectively. Results: Age at diagnosis, ulcer recurrence, atopic dermatitis history, white blood cell count, blood eosinophil count, platelet count, serum albumin level, iron level, erythrocyte sedimentation rate, and C-reactive protein level differed significantly among the 5 groups (all p < 0.05). Regarding endoscopic findings, multiple ulcers and gastric mucosal nodularity differed among the 5 groups (all p < 0.05). When comparing the EoGE ulcer group with the others, EoGE group revealed older ages (p = 0.022), higher rates of ulcer recurrence (p = 0.018), atopic dermatitis history (p = 0.001), and both blood and tissue eosinophilia (both p = 0.001). Conclusions: EoGE ulcers constituted 10.2% of HNGN-PU in pediatric patients. In children with HNGN-PU, peripheral eosinophilia, ulcer recurrence, and atopic dermatitis history might imply EoGE, necessitating thorough investigation of tissue eosinophils during endoscopic biopsy. Trial registration: 255 children retrospectively registered between between July 2003 and April 2017.

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

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.

scholarly journals Helicobacter pylori and Metabolic Diseases

2020 ◽  
Vol 20 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Sung Eun Kim
Keyword(s):  
Helicobacter Pylori ◽  
Fatty Liver Disease ◽  
Metabolic Diseases ◽  
Gastrointestinal Disorders ◽  
Systemic Effects ◽  
Peptic Ulcers ◽  
Alcoholic Fatty Liver ◽  
H Pylori ◽  
The Relationship ◽  
Alcoholic Fatty Liver Disease

<i>Helicobacter pylori</i> (<i>H. pylori</i>) is one of the most common pathogens that can cause certain gastrointestinal disorders, such as gastritis, peptic ulcers, and gastric cancer. Recently, interest in the systemic effects of <i>H. pylori</i> on extragastric manifestations is increasing. Representative diseases include hematologic, cardiovascular, neurodegenerative, autoimmune, dermatologic, allergic, hepatobiliary, and metabolic diseases. Among them, since the prevalence of metabolic diseases is on the rise worldwide, the relationship between <i>H. pylori</i> infection and metabolic diseases has become an interesting research issue. Many studies have been conducted to clarify any association. However, the results of those studies still remain controversial. This review focuses on recently published studies to investigate the relationship between <i>H. pylori</i> infection and metabolic diseases, including diabetes mellitus, metabolic syndrome, obesity, and non-alcoholic fatty liver disease, and their associated pathophysiology.

scholarly journals Prevalence of vacA, cagA, and iceA Virulence Factors of Helicobacter Pylori Isolated from Gastro-duodenal Patients

2020 ◽  
Vol 14 (1) ◽  
pp. 72-79
Author(s):  
Ahmed Husham Salman ◽  
Aumed Arshad Hawezy
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Gastric Lymphoma ◽  
Signs And Symptoms ◽  
Molecular Technique ◽  
Peptic Ulcers ◽  
Back Ground ◽  
H Pylori ◽  
Pcr Test

Back ground: Helicobacter pylori are bacteria colonize in the human epithelial cells of the gastrointestinal tract. Its infection causes different diseases, including chronic gastritis, peptic ulcers, gastric lymphoma and adenocarcinoma. H. pylori have many virulence factors attributing in one or more biological functions. Objective: Detecting the prevalence of virulence factor genes vacA, cagA, iceA among strain of H. pylori using molecular technique (PCR). Materials and methods: Sixty patients (27 male and 33 female), aged 18 and above included in the present study who showed signs and symptoms of H. pylori, and undergo endoscopy between period of November 2019 and February 2020. RUT and PCR test done to detect the presence of H. pylori infection, also PCR used to detect the three virulence factors. Results: Result showed that 44 patients, 21 (47.7%) male and 23 (52.3%) female were detected as positive H. pylori infections, among them 13 (29.5%) above 50 years, and 31 (70.4%) were below 50 years. While prevalence of the virulence factors vacA, cagA, and iceA were (100%), (84.1%), and (34.1%) respectively. Conclusion: It can be concluded that the frequency and prevalence of these genes are differed and showed significant differences among them. Also, PCR test is sensitive and accurate for detection of H. pylori virulence genes.

scholarly journals Cross-sectional study of human coding- and non-coding RNAs in progressive stages of Helicobacter pylori infection

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Sergio Lario ◽  
María J. Ramírez-Lázaro ◽  
Aintzane González-Lahera ◽  
José L. Lavín ◽  
Maria Vila-Casadesús ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Expression Profiles ◽  
Gastric Carcinogenesis ◽  
Individual Response ◽  
Peptic Ulcers ◽  
Gastric Diseases ◽  
Sequence Of Events ◽  
Non Coding Rnas ◽  
H Pylori

Abstract Helicobacter pylori infects 4.4 billion individuals worldwide and is considered the most important etiologic agent for peptic ulcers and gastric cancer. Individual response to H. pylori infection is complex and depends on complex interactions between host and environmental factors. The pathway towards gastric cancer is a sequence of events known as Correa’s model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic-active gastritis, atrophy, metaplasia and gastric adenocarcinoma. This study examines gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profiles of coding- and non-coding RNAs that may have a role in Correa’s model of gastric carcinogenesis. We screened for differentially expressed genes in gastric biopsies by employing RNAseq, microarrays and qRT-PCR. Here we provide a detailed description of the experiments, methods and results generated. The datasets may help other scientists and clinicians to find new clues to the pathogenesis of H. pylori and the mechanisms of progression of the infection to more severe gastric diseases. Data is available via ArrayExpress.

scholarly journals RECURRENCE RATE OF HELICOBACTER PYLORI IN PATIENTS WITH PEPTIC ULCER FIVE YEARS OR MORE AFTER SUCCESSFUL ERADICATION

2016 ◽  
Vol 53 (3) ◽  
pp. 152-155 ◽  
Author(s):  
Yuri Costa Farago FERNANDES ◽  
Gabriel da Rocha BONATTO ◽  
Mauro Willeman BONATTO
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Recurrence Rate ◽  
Early Recurrence ◽  
Peptic Ulcers ◽  
Ulcer Disease ◽  
Gastroduodenal Mucosa ◽  
H Pylori

ABSTRACT Background Infection with Helicobacter pylori is highly prevalent worldwide, especially in developing countries. Its presence in the gastroduodenal mucosa is related with development of peptic ulcer and other illnesses. The eradication of H. pylori improves mucosal histology in patients with peptic ulcers. Objective This study was aimed to verify if H. pylori recurrence occurs five years or more after confirmed eradication in patients with peptic ulcer. Moreover, we sought to determine the recurrence rate. Methods Retrospective and longitudinal, this study was based on a sample of 201 patients from western Paraná, Brazil. The patients were diagnosed with peptic ulcer disease, in the period of 1990-2000, and followed for five years or more after successful H. pylori eradication. Patients with early recurrence - prior to five years after eradication - were excluded from the sample. Results During an average follow-up of 8 years, 180 patients (89.55%) remained negative, and 21 (10.45%) became positive for H. pylori infection. New ulcers appeared in two-thirds of the patients with H. pylori recurrence. Conclusion The recurrence of H. pylori in patients with peptic ulcer can occur in the long-term - even if the infection had been successfully eradicated and the patients had remained free of recurrence in the first years of follow-up.

scholarly journals Nitazoxanide in Treatment of Helicobacter pylori: a Clinical and In Vitro Study

2003 ◽  
Vol 47 (12) ◽  
pp. 3780-3783 ◽  
Author(s):  
Yvonne Guttner ◽  
Helen M. Windsor ◽  
Charlie H. Viiala ◽  
Leon Dusci ◽  
Barry J. Marshall
Keyword(s):  
Helicobacter Pylori ◽  
Clinical Laboratory ◽  
Single Agent ◽  
Eradication Therapy ◽  
In Vitro Study ◽  
Laboratory Evaluation ◽  
Microbiological Characteristics ◽  
String Test ◽  
H Pylori

ABSTRACT Nitazoxanide (NTZ) is an antibiotic with microbiological characteristics similar to those of metronidazole but without an apparent problem of resistance. The aim of this study was the prospective evaluation of NTZ given as a single agent in the treatment of Helicobacter pylori infection. Twenty culture-positive patients with dyspepsia who had previously failed at least one course of H. pylori eradication therapy were enrolled. Subjects received 1 g of NTZ twice daily for 10 days. The safety and tolerability of the drug were assessed by physical examination, monitoring of adverse events, and clinical laboratory evaluation. Urea breath tests (UBTs) were performed 6 weeks posttreatment. H. pylori was isolated from UBT-positive patients by the string test or endoscopy with biopsy, and the MICs for these isolates were compared to those for isolates obtained pretherapy. The levels of tizoxanide, the active deacylated derivative of NTZ, were measured in blood, saliva, and tissue from two patients during treatment. The UBT results were positive for all 20 patients after completion of NTZ therapy. The MIC results demonstrated that the NTZ susceptibilities of none of the strains isolated from the patients posttherapy had changed significantly. No major adverse reactions were observed, but frequent minor side effects were observed. In conclusion, NTZ did not eradicate H. pylori when it was given as a single agent.

scholarly journals Relationship between Helicobacter pylori iceA, cagA, and vacA Status and Clinical Outcome: Studies in Four Different Countries

1999 ◽  
Vol 37 (7) ◽  
pp. 2274-2279 ◽  
Author(s):  
Yoshio Yamaoka ◽  
Tadashi Kodama ◽  
Oscar Gutierrez ◽  
Jong G. Kim ◽  
Kei Kashima ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Clinical Outcome ◽  
Clinical Presentation ◽  
The United States ◽  
Peptic Ulcers ◽  
Predominant Genotype ◽  
Clinical Presentations ◽  
Geographic Differences ◽  
H Pylori

There is continuing interest in identifying Helicobacter pylori virulence factors that might predict the risk for symptomatic clinical outcomes. It has been proposed thaticeA and cagA genes are such markers and can identify patients with peptic ulcers. We compared H. pylori isolates from four countries, looking at thecagA and vacA genotypes, iceAalleles, and presentation of the infection. We used PCR to examineiceA, vacA, and cagA status of 424H. pylori isolates obtained from patients with different clinical presentations (peptic ulcer, gastric cancer, and atrophic gastritis). The H. pylori isolates examined included 107 strains from Bogota, Colombia, 70 from Houston, Tex., 135 from Seoul, Korea, and 112 from Kyoto, Japan. The predominant genotype differed among countries: the cagA-positive iceA1 vacA s1c-m1 genotype was predominant in Japan and Korea, thecagA-positive iceA2 vacA s1b-m1 genotype was predominant in the United States, and the cagA-positiveiceA2 vacA s1a-m1 genotype was predominant in Colombia. There was no association between the iceA,vacA, or cagA status and clinical outcome in patients in the countries studied. iceA status shows considerable geographic differences, and neither iceA nor combinations of iceA, vacA, andcagA were helpful in predicting the clinical presentation of an H. pylori infection.

scholarly journals Structural basis for the peptidoglycan recognition by Helicobacter pylori Csd4

2014 ◽  
Vol 70 (a1) ◽  
pp. C817-C817
Author(s):  
Hyoun Sook Kim ◽  
Byung Woo Han ◽  
Byung Il Lee ◽  
Se Won Suh
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Cell Shape ◽  
Gastrointestinal Diseases ◽  
Structural Basis ◽  
Free Form ◽  
Peptic Ulcers ◽  
Carboxypeptidase H ◽  
Ligand Free ◽  
H Pylori

Helicobacter pylori infection causes a variety of gastrointestinal diseases including peptic ulcers and gastric cancer. The colonization of this bacterium in the gastric mucosa is required for the survival in the stomach. Its colonization of the gastric mucosa of human stomach depends on its motility, which is facilitated by the helical cell shape. In H. pylori, crosslinking relaxation or trimming of peptidoglycan muropeptide affects the helical shape. Among several cell shape-determining peptidoglycan hydrolases identified in H. pylori, Csd4 is a Zn2+-dependent D,L-carboxypeptidase that cleaves the bond between the γ-D-Glu and mDAP bond of the uncrosslinked tripeptide of peptidoglycan (L-Ala-γ-D-Glu-mDAP) to produce L-Ala-γ-D-Glu dipeptide and mDAP, promoting the helical cell shape. Inhibition of D,L-carboxypeptidase activity of Csd4 may represent a novel therapeutic approach. We report here the crystal structures of H. pylori Csd4 in three different states: the ligand-free form, the substrate-bound form, and the product-bound form. H. pylori Csd4 consists of three domains: an N-terminal D,L-carboxypeptidase domain, a novel β-barrel domain, and a C-terminal immunoglobulin-like domain. Our ligand-bound structures provide structural basis of peptidoglycan recognition by D,L-carboxypeptidase. H. pylori Csd4 recognizes primarily the terminal mDAP of the tripeptide substrate and undergoes a significant structural change upon binding either mDAP or mDAP-containing tripeptide.

scholarly journals Mucosal FOXP3-Expressing CD4+ CD25high Regulatory T Cells in Helicobacter pylori-Infected Patients

2005 ◽  
Vol 73 (1) ◽  
pp. 523-531 ◽  
Author(s):  
Anna Lundgren ◽  
Erika Strömberg ◽  
Åsa Sjöling ◽  
Catharina Lindholm ◽  
Karin Enarsson ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Regulatory T Cells ◽  
Gastric Adenocarcinoma ◽  
Cytotoxic T Lymphocyte ◽  
Duodenal Mucosa ◽  
Peptic Ulcers ◽  
Low Levels ◽  
H Pylori ◽  
And Function

ABSTRACT Helicobacter pylori chronically colonizes the stomach and duodenum and causes peptic ulcers or gastric adenocarcinoma in 10 to 20% of infected individuals. We hypothesize that the inability of patients to clear H. pylori infections is a consequence of active suppression of the immune response. Here we show that H. pylori-infected individuals have increased frequencies of CD4+ CD25high T cells in both the stomach and duodenal mucosa compared to uninfected controls. These cells have the phenotype of regulatory T cells, as they express FOXP3, a key gene for the development and function of regulatory T cells, as well as high levels of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) protein. In contrast, mucosal CD4+ CD25low and CD4+ CD25− cells express little FOXP3 mRNA and low levels of the CTLA-4 protein. Mucosal CD4+ CD25high T cells are present in individuals with asymptomatic H. pylori infections as well as in duodenal ulcer patients. The frequencies of CD4+ CD25high cells are also increased in the stomachs of H. pylori-infected patients with gastric adenocarcinoma, particularly in cancer-affected tissues. These findings suggest that regulatory T cells may suppress mucosal immune responses and thereby contribute to the persistence of H. pylori infections.

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