scholarly journals THE INFECTION WITH HELICOBACTER PYLORI FAVORS THE PRESENCE OF GIARDIA LAMBLIA IN THE GASTRIC MUCOSA – CASE PRESENTATION

2016 ◽  
Vol 19 (3) ◽  
pp. 78-82
Author(s):  
Meliț Lorena Elena ◽  
◽  
Cristina Oana Mărginean ◽  
Simona Mocan ◽  
Nicoleta Suciu ◽  
...  

Helicobacter pylori and Giardia lamblia are common worldwide. Helicobacter pylori is a favoring factor for the presence of Giardia lamblia in the stomach due to the neutralization of the gastric pH through the secretion of urease. We present the case of a 5-year-old child, with intermittent gastro-intestinal symptoms in the recent personal pathological history, admitted in the Pediatrics Clinic 1 Târgu Mureș for abdominal pain, nausea, loss of appetite and hematemesis. The superior digestive endoscopy revealed multiple hemorrhagic lesions of the gastric mucosa, and the pathological exam of the antral gastric mucosa identified the coexistence of Helicobacter pylori and Giardia lamblia. The evolution of the patient was favorable under the eradication therapy of the infection with Helicobacter pylori and the antiparasitic drugs, the control endoscopy revealing a gastric mucosa without macroscopically obvious modifications, and the pathological re-evaluation pointed out regenerative modifications of the gastric mucosa. The particularity of the case is represented by the identification of the parasite Giardia lamblia in the gastric mucosa, a physiologically acid environment, alkalinized by the urease secreted by Helicobacter pylori, therefore providing favorable conditions for the development of this parasite in a 5-year-old child, from a favorable socio-economic environment, with intermittent gastrointestinal symptoms in his recent personal pathological history.

2012 ◽  
Vol 228 (3) ◽  
pp. 223-227 ◽  
Author(s):  
Naoki Asano ◽  
Katsunori Iijima ◽  
Shiho Terai ◽  
Xiaoyi Jin ◽  
Nobuyuki Ara ◽  
...  

2021 ◽  
pp. 80-89
Author(s):  
R. T. Fazlyakhmetov ◽  
R. R. Safiullin ◽  
A. V. Ustinov

Introduction. Many key questions regarding the etiology, pathogenesis, clinical manifestations and treatment of chronic gastritis remain open. So, despite the success of chronic gastritis pharmacotherapy, much attention is paid to non-drug methods of therapy, in particular, osteopathy. However, evidences of the osteopathic methods effectiveness for the chronic gastritis treatment, obtained by objective instrumental methods, are insufficiently presented in the modern literature.The goal of research — to study the results of osteopathic correction inclusion in the complex therapy of patients with chronic gastritis.Materials and methods. The study involved 50 patients with chronic gastritis, divided by simple randomization into a control group (25 people) and a main group (25 people). The participants in the control group received standard eradication therapy according to a three-component scheme. The participants of the main group additionally received osteopathic correction. In both groups, at the beginning and at the end of the study, there were performed fibroesophagogastroduodenoscopy with targeted biopsy to assess the gastric mucosa state, Helicobacter pylori identification, and intragastric pH-metry to assess gastric juice acidity.Results. According to the study results, a statistically significant (p<0,05) decrease in edema and hyperemia of gastric mucosa was found in the control and main groups. There was a statistically significant (p<0,001) decrease in gastric aciditywith osteopathic accompaniment, compared with unaccompanied drug treatment. In both groups, there was a statistically significant (p<0,05) decrease in the incidence of Helicobacter pylori carriage. Conclusion. Based on the obtained results, it can be assumed that an integrated approach using osteopathic correction in the treatment of chronic gastritis may be more effective than the standard course of treatment.


Author(s):  
Heung Up Kim

It is well known that <i>Helicobacter pylori (H. pylori)</i> can cause peptic ulcer, mucosa-associated lymphoid tissue lymphoma, atrophic gastritis, intestinal metaplasia, and ultimately, gastric cancer. Various studies have proven that <i>H. pylori</i>, which attaches to the gastric mucosa, is the cause of gastric cancer and can be eradicated using appropriate antibiotics. Since 2013, Japan has been carrying out national-led eradication treatment of <i>H. pylori</i> for the whole population. However, as drug exposure increases, the resistance rate to some antibiotics increases, and the pattern of antibiotic resistance varies from region to region. Therefore, the development of individualized antimicrobial therapies has become important since antibiotic resistance to <i>H. pylori</i> eradication is a problem worldwide. To help overcome this, remedies such as selection of antibiotics through susceptibility testing, selection of empirical treatment combinations appropriate for the region, dual therapy with high doses of amoxicillin, and the use of rifabutin or sitafloxacin with low antibiotic resistance have been studied. Potassium-competitive acid blocker has been reported to be more potent in inhibiting acid secretion than proton pump inhibitor, and its role in <i>H. pylori</i> eradication is expected. Drug formulations and regimens that are easy to take are being developed to increase compliance. New treatments such as spraying antibiotics directly to the gastric mucosa are being developed and studied.


2019 ◽  
Vol 9 (3-4) ◽  
pp. 523-530
Author(s):  
L. B. Drygina ◽  
V. N. Ellenidi ◽  
N. A. Bardysheva ◽  
M. M. Bogoslovskiy

Effective eradication of Helicobacter pylori infection is an important means to reduce the risk of precancerous changes in the gastric mucosa and prevention of gastric cancer. A search for non-invasive diagnostic tools for Helicobacter pylori infection, evaluation of the effectiveness of eradication remains of high importance.The aim of the study was to assess an informative value of detecting pepsinogen I and II as well as serum antibodies to Helicobacter pylori while assessing an efficacy of treated chronic Helicobacter gastritis and identifying preneoplastic changes in the stomach mucosa. There enrolled 113 male patients with chronic gastritis aged 41 to 76, average age- (56.7±0.7) years. Examination of patients was carried out at admission to the clinic, as well as at 2 and 12 months after administering a standard eradication therapy. It was found that Helicobacter pylori infection was detected in 101 (89.4%) patients. Groups of patients with effective eradication therapy were noted. A time-dependent level of antibodies to Helicobacter pylori, as well as measured concentration of pepsinogen I and II after the onset of eradication treatment were determined. Which were analyzed in connection with the results of histology examination of gastric mucosa biopsy specimens and expression of oncoproteins Ki-67, Bcl-2, c-erbB-2, p16 in the gastric mucosa depending on efficacy of eradication therapy. It is shown that effective eradication therapy was characterized by significantly decreased serum level of IgG antibodies to Helicobacter pylori 2 months after the onset of treatment. Moreover, a significantly decreased pepsinogen II and serum IgG antibodies to Helicobacter pylori during eradication therapy were accompanied by a significant decrease in Ki-67 expression in the gastric epithelium. Decreased concentration of pepsinogen II within the first year after Helicobacter pylori eradication therapy was due to a greater decrease in activity of inflammatory changes in the gastric mucosa than to dynamic changes in gastric atrophy and metaplasia. An inverse relation between the serum level of pepsinogen I and atrophy as well as intestinal metaplasia within the gastric mucosa were found.


Author(s):  
Е.Е. Дубская ◽  
Т.Е. Афанасенкова ◽  
С.М. Баженов

Ведущим этиологическим фактором хронического гастрита является инфекция Helicobacter pylori. Герпесвирусная инфекция может принимать участие в развитии и поддержании воспалительного процесса в слизистой оболочке желудка. Особое место среди герпесвирусов занимает вирус Эпштейна–Барр, которым инфицировано 95% населения. Целью работы было определить персистенцию вируса Эпштейна–Барр в слизистой оболочке желудка у больных хроническим Helicobacter pylori-индуцированным гастритом с эрозиями желудка и влияние на течение заболевания в зависимости от проводимой терапии. Под наблюдением находились 84 больных хроническим Helicobacter pylori-индуцированным гастритом с эрозиями желудка. У всех больных при первичном обращении кроме Нelicobacter pylori в слизистой оболочке желудка определялся вирус Эпштейна–Барр. Длительность заболевания составила от 1 до 10 лет. В зависимости от проводимой терапии пациенты с хроническим Helicobacter pylori-индуцированным гастритом с эрозиями желудка были разделены на 2 группы, между которыми через 1 год после первичного обращения проводилось сравнение частоты встречаемости вируса Эпштейна–Барр в слизистой оболочке желудка. Выявление Helicobacter pylori проводилось тремя методами: дыхательным уреазным тестом, цитологическим исследованием мазков и методом полимеразной цепной реакции биоптата. У пациентов с хроническим Helicobacter pylori-индуцированным гастритом с эрозиями желудка при выявлении герпесвирусной инфекции в слизистой оболочке желудка применение меглюмина акридонацетата в четырехкомпонентной эрадикационной терапии позволяет достоверно уменьшить количество вирусов Эпштейна–Барр. Сравнительная оценка полученных данных по наличию Helicobacter pylori в слизистой оболочке желудка у пациентов двух групп наблюдения свидетельствует о хорошем уровне эрадикационной терапии: в 1-й группе наблюдения эрадикация составила 91,3%, а во 2-й группе наблюдения – 89,5%. Микст-инфекция (Helicobacter pylori и вирус Эпштейна–Барр) в слизистой оболочке желудка является фактором, осложняющим процесс лечения пациентов. The leading etiological factor of chronic gastritis is Helicobacter pylori infection. Herpesvirus infection can take part in the development and maintenance of the inflammatory process in the gastric mucosa. A special place among herpesviruses is occupied by the Epstein–Barr virus, 95% of the population is infected with it. The aim was to determine the persistence of the Epstein–Barr virus in the gastric mucosa in patients with chronic Helicobacter pylori-induced gastritis with gastric erosions and to determine the effect on the course of the disease, depending on the therapy. 84 patients with chronic Helicobacter pylori-induced gastritis with gastric erosions were under observation. The Epstein–Barr virus was detected in the gastric mucosa in all patients at the initial treatment except for Helicobacter pylori. The duration of the disease was from 1 to 10 years. Depending on the treatment of chronic Helicobacter pylori-induced gastritis with gastric erosions, patients were divided into 2 groups, between them, 1 year after the initial treatment, the frequency of occurrence of Epstein–Barr virus in the gastric mucosa was compared. The detection of Helicobacter pylori was carried out by three methods: respiratoryurease test, cytological examination of smears and the method of polymerase chain reaction of the biopsy. In patients with chronic Helicobacter pylori-induced gastritis with gastric erosions, when detecting a herpesvirus infection in the gastric mucosa, the use of meglumine acridonacetate in four-component eradication therapy can significantly reduce the number of Epstein–Barr viruses. A comparative assessment of the data obtained on the presence of Helicobacter pylori in the gastric mucosa in patients of two observation groups indicates a good level of eradication therapy: in the 1st observation group, eradication was 91,3%, and in the 2nd observation group – 89,5%. Mixed infection (Helicobacter pylori and Epstein–Barr virus) in the gastric mucosa is a factor that complicates the treatment process of patients.


2020 ◽  
Vol 115 (1) ◽  
pp. S19-S19
Author(s):  
Yuka Hirashita ◽  
Masahide Fukuda ◽  
Yasuhiro Wada ◽  
Kensuke Fukuda ◽  
Kazuhisa Okamoto ◽  
...  

2021 ◽  
Author(s):  
Yuka Hirashita ◽  
Masahide Fukuda ◽  
Masaaki Kodama ◽  
Yoshiyuki Tsukamoto ◽  
Tadayoshi Okimoto ◽  
...  

Abstract Background Although eradication therapy for chronic Helicobacter pylori reduces the risk of gastric cancer (GC), its effectiveness is incomplete. Therefore, it is critically important to identify those patients who remain at high risk after H. pylori eradication therapy. Accumulation of protein methylation is strongly implicated in cancer, and a recent study showed that dimethylation of eEF1A lysine 55 (eEF1AK55me2) promotes carcinogenesis in vivo. We aimed to investigate the relationship between eEF1A dimethylation and H. pylori status in gastric mucosa and to reveal potential downstream molecules of eEF1A dimethylation in H. pylori-eradicated mucosa. Methods Records of 115 patients (11 H. pylori-negative, 29 H. pylori-positive, 75 post-eradication patients) who underwent upper gastrointestinal endoscopy were retrospectively reviewed. The eEF1A dimethyl level was evaluated in each functional cell type of gastric mucosa by immunofluorescent staining. We also investigated the relationship between eEF1AK55me2 downregulation by CRISPR/Cas9-mediated deletion of Mettl13, which is known as a dimethyltransferase of eEF1AK55me2. Results The level of eEF1A dimethylation significantly increased in the surface and basal areas of H. pylori-positive mucosa compared with -negative mucosa (surface, p=0.0031; basal, p<0.0001). The eEF1A dimethyl levels in the surface area were significantly reduced by eradication therapy (p=0.005), but those in the basal area were maintained even after eradication therapy. Multivariate analysis revealed that high dimethylation of eEF1A in the basal area of the mucosa was the independent factor related to GC incidence (odds ratio=3.6611, 95% confidence interval=1.0350–12.949, p=0.0441). We also showed the relationship between eEF1A dimethylation and expressions of reprogramming factors Oct4 and Nanog by immunohistochemistry and in vitro genome editing experiments. Conclusions The results indicated that H. pylori infection potently induced eEF1A dimethylation in gastric mucosa. The accumulation of dimethyl-eEF1A in the basal area of the mucosa might contribute to GC risk via regulation of reprograming factors in H. pylori-eradicated gastric mucosa.


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