Histologic Findings in “Ex- Helicobacter pylori” Gastric Biopsies of Pediatric Patients

2005 ◽  
Vol 8 (4) ◽  
pp. 420-426 ◽  
Author(s):  
Marta Cohen ◽  
Eduardo Cueto Rúa ◽  
Norma Balcarce ◽  
Ricardo Drut
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Pediatric Patients ◽  
Clinical Course ◽  
Final Treatment ◽  
Gastric Biopsies ◽  
H Pylori ◽  
Lymphoid Aggregates

Long-term sequelae of Helicobacter pylori–associated chronic gastritis (HpCG) have been described in adult patients. In the present study we report the histology of gastric mucosa biopsies in 6 asymptomatic pediatric patients (5 male and 1 female; mean age 9.5 years) with previous HpCG. Preceding H. pylori was histologically proved and confirmed by culture, direct visualization, and/or serology before delivering treatment. In 5 of 6 cases the HpCG followed a protracted clinical course, with various therapeutic series needed before H. pylori eradication. Time from final treatment for HpCG to actual biopsy ranged from 3 months to almost 3 years. Gastric mucosa showed mild chronic gastritis with absence of H. pylori organisms (6 of 6), focal loss of gland units with collagenous replacement (6 of 6), serrated foveolae (3 of 6), regenerative changes at elongated glandular necks with cells having enlarged and hyper-chromatic nuclei (5 of 6), lymphoid aggregates (2 of 6), and presence of sulfomucins in isolated epithelial cells of glands and foveolae (2 of 6). None of these features were noticed in 10 normal gastric mucosa biopsies used as controls. The referred findings in “ex– H. pylori” pediatric patients may represent very early sequelae from HpCG at this age.

scholarly journals Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease

1993 ◽  
Vol 35 (2) ◽  
pp. 117-121 ◽  
Author(s):  
A. J. A. Barbosa ◽  
D. M. M. Queiroz ◽  
A. M. M. F. Nogueira ◽  
M. J. A. Roquette Reis ◽  
E. N. Mendes ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Chagas Disease ◽  
Chronic Gastritis ◽  
Antral Mucosa ◽  
Common Cause ◽  
Superficial Gastritis ◽  
H Pylori ◽  
Inflammatory Changes

Patients with the digestive form of Chagas'disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4% neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1%) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9%) while atrophic gastritis was present in 8 (47.1%) patients. H. pylori was present on gastric mucosa of 8 (100%) patients with atrophic gastritis and of 8 (88.8%) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

Long-term Clinical Outcome of Helicobacter pylori-negative Gastric Mucosa-associated Lymphoid Tissue Lymphoma is Comparable to That of H. pylori-positive Lymphoma

2009 ◽  
Vol 43 (4) ◽  
pp. 312-317 ◽  
Author(s):  
Su Jin Chung ◽  
Joo Sung Kim ◽  
Hansoo Kim ◽  
Sang Gyun Kim ◽  
Chul Woo Kim ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Clinical Outcome ◽  
Lymphoid Tissue ◽  
H Pylori

scholarly journals Downregulation of Interleukin- (IL-) 17 through Enhanced Indoleamine 2,3-Dioxygenase (IDO) Induction by Curcumin: A Potential Mechanism of Tolerance towards Helicobacter pylori

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Tiziana Larussa ◽  
Serena Gervasi ◽  
Rita Liparoti ◽  
Evelina Suraci ◽  
Raffaella Marasco ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Antimicrobial Properties ◽  
Human Gastric Mucosa ◽  
T Cell Apoptosis ◽  
Indoleamine 2,3 Dioxygenase ◽  
Treated Sample ◽  
Tryptophan Catabolism ◽  
Gastric Biopsies ◽  
H Pylori

The anti-inflammatory and antimicrobial properties of curcumin suggest its use as an anti-Helicobacter pylori (H. pylori) agent, but mechanisms underlying its helpful activity are still not clear. Indoleamine 2,3-dioxygenase (IDO) promotes the effector T cell apoptosis by catalyzing the rate-limiting first step in tryptophan catabolism, and its high expression in H. pylori-infected human gastric mucosa attenuates Th1 and Th17 immune response. The aim of this study was to investigate the role of curcumin in modulating the expression of IL-17 and IDO in H. pylori-infected human gastric mucosa. In an organ culture chamber, gastric biopsies from 35 patients were treated with and without 200 μM curcumin. In H. pylori-infected patients (n=21), IL-17 was significantly lower, both in gastric biopsies (p=0.0003) and culture supernatant (p=0.0001) while IDO significantly increased (p<0.00001) in curcumin-treated sample compared with untreated samples. In a subgroup of H. pylori-infected patients (n=15), samples treated with curcumin in addition to IDO inhibitor 1-methyl-L-tryptophan (1-MT) showed a higher expression of IL-17 compared with untreated samples and curcumin-treated alone (p<0.00001). Curcumin downregulates IL-17 production through the induction of IDO in H. pylori-infected human gastric mucosa, suggesting its role in dampening H. pylori-induced immune-mediated inflammatory changes.

scholarly journals Interleukin-12 Drives the Th1 Signaling Pathway in Helicobacter pylori-Infected Human Gastric Mucosa

2007 ◽  
Vol 75 (4) ◽  
pp. 1738-1744 ◽  
Author(s):  
Antonia Pellicanò ◽  
Ladislava Sebkova ◽  
Giovanni Monteleone ◽  
Giovanni Guarnieri ◽  
Maria Imeneo ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Transcription Factors ◽  
Gastric Mucosa ◽  
Enzyme Linked Immunosorbent Assay ◽  
Human Gastric Mucosa ◽  
Organ Cultures ◽  
Gastric Biopsies ◽  
Ifn Γ ◽  
H Pylori ◽  
Cell Commitment

ABSTRACT In this study we examined mechanisms that regulate T-helper lymphocyte 1 (Th1) commitment in Helicobacter pylori-infected human gastric mucosa. The levels of gamma interferon (IFN-γ), interleukin-4 (IL-4), and IL-12 in total extracts of gastric biopsies taken from H. pylori-infected and uninfected patients were determined by an enzyme-linked immunosorbent assay. The levels of signal transducer and activator of transcription 4 (STAT4), STAT6, and T-box expressed in T cells (T-bet) in total proteins extracted from gastric biopsies were determined by Western blotting. Finally, the effect of a neutralizing IL-12 antibody on expression of Th1 transcription factors and the levels of IFN-γ in organ cultures of H. pylori-infected biopsies was examined. Increased levels of IFN-γ and IL-12 were found in gastric biopsy samples of H. pylori-infected patients compared to the levels in uninfected patients. In addition, H. pylori-infected biopsies exhibited high levels of expression of phosphorylated STAT4 and T-bet. Higher levels of IFN-γ and expression of Th1 transcription factors were associated with greater infiltration of mononuclear cells in the gastric mucosa. By contrast, production of IL-4 and expression of phosphorylated STAT6 were not associated with the intensity of mononuclear cell infiltration. In ex vivo organ cultures of H. pylori-infected biopsies, neutralization of endogenous IL-12 down-regulated the expression of phosphorylated STAT4 and T-bet and reduced IFN-γ production. Our data indicated that IL-12 contributes to the Th1 cell commitment in H. pylori-infected human gastric mucosa.

scholarly journals Influence of duodenogastric reflux in the gastric mucosa histological changes of rats infected with Helicobacter pylori

2016 ◽  
Vol 43 (4) ◽  
pp. 235-242 ◽  
Author(s):  
JOSÉ CARLOS RIBEIRO DE ARAUJO ◽  
JORGE JOSÉ DE CARVALHO ◽  
HUMBERTO OLIVEIRA SERRA
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Partial Gastrectomy ◽  
Duodenogastric Reflux ◽  
Histological Changes ◽  
Positive Correlation ◽  
Male Wistar Rats ◽  
H Pylori ◽  
The One

ABSTRACT Objective: to evaluate the influence of Duodenal reflux in histological changes of the gastric mucosa of rats infected with Helicobacter pylori submitted to pyloroplasty. Methods: after two weeks of acclimation, we infected 30 male Wistar rats with Helicobacter pylori. We randomly divided them into three groups: one submitted to pyloroplasty, another to partial gastrectomy and the third, only infected, was not operated. After six months of surgery, euthanasia was carried out. Gastric fragments were studied by light microscopy to count the number of H. pylori, and to observe the histological changes (gastritis, metaplasia, dysplasia and neoplasia). We confirmed these changes by immunohistochemistry using the molecular markers PCNA and TGF-beta. Results: the animals submitted to pyloroplasty had higher percentage of colonization by H. pylori (median=58.5; gastrectomy=16.5; control=14.5). There was a positive correlation between the amount of H. pylori and the occurrence of chronic gastritis present in the antral fragments. Neoplasia occurred in 40% of rats from the group submitted to pyloroplasty. The staining with PCNA and TGF-ß confirmed the histopathological changes visualized by optical microscopy. Conclusions: the antral region was the one with the highest concentration of H. pylori, regardless of the group. There was a positive correlation between the appearance of benign disorders (chronic gastritis, metaplasia, dysplasia) and cancer in mice infected with H. pylori submitted to pyloroplasty.

scholarly journals Comparative analysis of two-dimensional electrophoresis maps (2-DE) of Helicobacter pylori from Brazilian patients with chronic gastritis and duodenal ulcer: a preliminary report

2006 ◽  
Vol 48 (3) ◽  
pp. 175-177 ◽  
Author(s):  
Diego R.B. Pereira ◽  
Daniel Martins ◽  
Flavia V. Winck ◽  
Marcus B. Smolka ◽  
Nancy F. Nishimura ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Comparative Analysis ◽  
Chronic Gastritis ◽  
Protein Identification ◽  
Two Dimensional ◽  
Two Dimensional Gel Electrophoresis ◽  
Duodenal Ulcers ◽  
Pathogenic Factors ◽  
Gastric Biopsies ◽  
H Pylori

Helicobacter pylori is a bacterium recognized as the major cause of peptic ulcer and chronic gastritis. Recently, a proteome-based approach was developed to investigate pathogenic factors related to H. pylori. In this preliminary study, H. pylori strains were isolated from gastric biopsies of patients with chronic gastritis and duodenal ulcers. A partial proteomic analysis of H. pylori strains was performed by bacterial lyses and proteins were separated by two-dimensional gel electrophoresis (2-DE). A comparative analysis was performed to verify a differential protein expression between these two 2-DE maps. These data should be useful to clarify the role of different proteins related to bacterial pathogenesis. This study will be completed using a larger number of samples and protein identification of H. pylori by MALDI-TOF mass spectrometry.

scholarly journals State of lipid peroxidation and antioxidant defense in chronic gastritis associated with Helicobacter pylori-infection in middle-aged males

2020 ◽  
Vol 10 (4) ◽  
pp. 741-746
Author(s):  
O. V. Smirnova ◽  
A. A. Sinyakov ◽  
N. M. Titova
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Antioxidant Defense ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Metabolism Enzymes ◽  
H Pylori

Helicobacter pylori is the most widespread human pathogen, with prevalence reaching up to 20—40% and 80— 90% of adult infection in developed and developing countries, respectively. Many authors consider this infection as a major factor in the development of gastric cancer. In case of H. pylori infection, free homogeneous oxidation is augmented, that elevates the blood amount of POL products. Hyperproduction of reactive oxygen species stimulates free radical POL, accompanied by membrane destruction, damage to proteins, lipids, and DNA. Thus, the destruction of the intracellular and cell outer membranes occurs resulting in cell death. In diseases associated with H. pylori infection, there is a dysregulation of the lipid peroxidation system — antioxidant defense contributing to inconsistency in the regeneration phases triggering disease progression. The aim of our work was to study indicators of POL (diene conjugates, malonic dialdehyde) and antioxidant protection (AOP) (superoxide dismutase enzymes, catalase) in chronic gastritis and chronic atrophic gastritis associated with H. pylori infection. In patients with CG associated with H. pylori as well as CAG and CAG associated with H. pylori they were featured with increased amount of primary (↑DC) and end TBA-active products of lipid peroxidation (↑MDA), whereas activity of superoxide dismutase was decreased, additionally highlighted with reduced catalase activity (↑CAT) in CAG and CAG associated with H. pylori. H. pylori just triggers the mechanisms of ROS generation in host cells. The energy of redox reactions is used by the microorganism to carry out its physiological functions and serves as a factor in its own pathogenicity, the ROS generated in such reactions can have a damaging effect on the structure of gastric mucosa. In addition, examining H. pylori genome has shown that it bears the genes encoding oxidative metabolism enzymes, such as SOD, catalase, nitroreductase, flavodoxin oxidoreductase. Long-term persistence of H. pylori in the gastric mucosa paralleled with its increased biomass accounts for it being the main source of ROS production able to augment lipid peroxidation and cause damage to the membrane structures and DNA of gastric epithelium cells.

scholarly journals Efficacy of immunohistochemical staining in detecting Helicobacter pylori in Saudi patients with minimal and atypical infection

2021 ◽  
Vol 65 (3) ◽  
Author(s):  
Mohammed Akeel ◽  
Ahmed Elhafey ◽  
Atef Shehata ◽  
Erwa Elmakki ◽  
Thanaa Aboshouk ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Direct Detection ◽  
Giemsa Staining ◽  
Pcr Analysis ◽  
Qrt Pcr ◽  
Urease Test ◽  
Gastric Biopsies ◽  
Polymerase Chain ◽  
H Pylori

Gastric Helicobacter pylori infection is diagnosed based on histopathological evaluation of gastric mucosal biopsies, urease test, urea breath test, H. pylori culturing, or direct detection using polymerase chain reaction (PCR). This study aimed to evaluate the efficacy of immunohistochemical (IHC) staining in detecting H. pylori in gastric biopsies from patients with chronic gastritis and minimal or atypical infection. Gastric biopsies from 50 patients with chronic gastritis were subjected to routine haematoxylin and eosin (H&E), modified Giemsa, and IHC staining. The results of staining were compared with those of quantitative real-time PCR (qRT-PCR). The qRT-PCR analysis identified 32 (64%) H. pylori-positive cases, whereas IHC, H&E, and modified Giemsa staining identified 29 (58%), 27 (54%), and 21 (42%) positive cases. The sensitivity of IHC staining (87.50%) was higher than that of H&E (59.38%) and modified Giemsa (43.75%) staining. The specificity of H&E, modified Giemsa, and IHC staining was 55.56%, 61.11%, and 94.44%, respectively. IHC staining exhibited the highest diagnostic accuracy (90%), followed by H&E (58%) and modified Giemsa (50%) staining. Active gastritis, intestinal metaplasia, and lymphoid follicles were detected in 32 (64%), 4 (8%), and 22 (44%) cases, respectively, and all of these cases were H. pylori positive. In contrast to routine H&E and modified Giemsa staining, IHC allows for the accurate H. pylori detection in cases with minimal or atypical infection. Moreover, IHC can be an alternative diagnostic method to qRT-PCR for detection of H. pylori in such cases.

CHRONIC GASTRITIS AND OLD AGE: A PROBLEM OR NOT?

2020 ◽  
pp. 30-39
Author(s):  
Zh.G. Simonova ◽  
M.N. Prikhod'ko ◽  
E.M. Shul'gina
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Elderly Patients ◽  
Old Age ◽  
Chronic Gastritis ◽  
Morphological Changes ◽  
Eradication Therapy ◽  
Prospective Clinical Study ◽  
H Pylori ◽  
Endoscopic Picture

The objective of the paper is to study the clinical and functional characteristics of chronic H. pylori-associated gastritis in the elderly patients. Materials and Methods. A group of elderly patients (n=116) (aged 69.5±3.2) with chronic H. pylori-associated gastritis was formed during a prospective clinical study. All patients underwent esophagogastroduodenoscopy with biopsy. OLGA staging system was used for histological assessment. The dyspeptic index (DI) was used to measure dyspepsia. The patients were followed up for 48 weeks. Results. Dyspepsia was found only in 41.3 % of patients, while 58.7 % of patients had asymptomatic disease progression. Atrophic changes in the gastric mucosa were found in 30.1 % of the trial subjects. The efficacy of the eradication therapy was 88.7 %. During the study, the endoscopic picture of the gastroduodenal zone improved. There was no progression of atrophic and metaplastic changes in the gastric mucosa. Conclusion. Thus, in elderly patients, chronic H. pylori-associated gastritis is often asymptomatic. Eradication of H. pylori infection promotes disease remission and prevents morphological changes in the gastric mucosa. Keywords: chronic gastritis, Helicobacter pylori, atrophic gastritis, dyspepsia, old age, eradication therapy. Цель – изучить клинико-функциональные особенности течения хронического H. pylori-ассоциированного гастрита у лиц пожилого возраста. Материалы и методы. В процессе проспективного клинического исследования была сформирована группа больных (n=116) пожилого возраста (69,5±3,2 года) с хроническим H. pylori-ассоциированным гастритом. Всем больным была выполнена эзофагогастродуоденоскопия с биопсией. Для гистологической оценки применяли классификацию OLGA. Для оценки диспепсического синдрома использовали диспепсический индекс (ДИ). Длительность наблюдения больных составила 48 нед. Результаты. Наличие диспепсического синдрома было установлено у 41,3 % больных, 58,7 % пациентов имели бессимптомное течение заболевания. У 30,1 % обследуемых выявлены атрофические изменения слизистой оболочки желудка. Эффективность проведенной эрадикационной терапии составила 88,7 %. В процессе исследования установлено улучшение эндоскопической картины гастродуоденальной зоны. Отмечено отсутствие прогрессирования атрофических и метапластических изменений слизистой оболочки желудка. Выводы. У больных пожилого возраста течение хронического H. pylori-ассоциированного гастрита чаще имеет бессимптомный характер. Эрадикация инфекции H. pylori способствует ремиссии заболевания и предотвращает морфологические преобразования слизистой оболочки желудка. Ключевые слова: хронический гастрит, Helicobacter pylori, атрофический гастрит, синдром диспепсии, пожилой возраст, эрадикационная терапия.

scholarly journals Long-Term Infection of Mongolian Gerbils with Helicobacter pylori: Microbiological, Histopathological, and Serological Analyses

2005 ◽  
Vol 12 (2) ◽  
pp. 347-353 ◽  
Author(s):  
Shigehito Nakagawa ◽  
Takako Osaki ◽  
Yasunori Fujioka ◽  
Hiroyuki Yamaguchi ◽  
Shigeru Kamiya
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Real Time ◽  
Mononuclear Cells ◽  
Bacterial Colonization ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mongolian Gerbils ◽  
Rt Pcr ◽  
H Pylori

ABSTRACT The effects of long-term infection with Helicobacter pylori on the gastric mucosa of Mongolian gerbils were examined. Colonization by H. pylori was evaluated by both microaerobic cultivation and real-time reverse transcriptase PCR (RT-PCR). Persistent infection with H. pylori in gastric mucosa was detected by real-time RT-PCR during 6 months after infection, but no H. pylori was isolated 4 months after infection by cultivation. Infiltration with neutrophils and mononuclear cells was observed from 2 months after infection. Both intestinal metaplasia and gastric atrophy were also detected from 2 months after infection. The results by enzyme-linked immunosorbent assay indicated that antibody titers against whole H. pylori antigens, H. pylori heat shock protein 60 (HSP60), and Escherichia coli GroEL were significantly higher in the infected gerbils than in noninfected gerbils. After long-term infection with H. pylori for 18 months, marked atrophy of gastric mucosa and multiple cysts in the submucosa were observed in the glandular stomach of the infected gerbils. In addition, squamous cell papilloma with hyperkeratosis was observed in cardia of all the infected gerbils. These results indicate that evaluation of bacterial colonization during long-term infection can be done by real-time RT-PCR and that mucosal damage might be induced by host immune response against whole H. pylori antigen.

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