Role Of Helicobacter Pylori Infection Research Articles

Non-alcoholic fatty liver disease and Helicobacter pylori infection: is there a relationship? Review

The article outlines the relevance of finding a connection between non‑alcoholic fatty liver disease (NAFLD) and Helicobacter pylori infection. The presented data of the majority of studies indicate the presence of Helicobacter pylori infection as a risk factor for the development of NAFLD. In addition, a number of researchers point to the possibility of the influence of Helicobacter pylori on important pathogenetic chains of NAFLD: insulin resistance, the state of the intestinal microbiota, the level of such hormones as ghrelin, leptin, adiponectin, and also that the effect of Helicobacter pylori (H. pylori) toxins can cause direct damage to the liver and that Helicobacter pylori invasion of the small intestine mucosa can increase the permeability of the latter, disrupting the functioning of the gut—liver axis. The article emphasizes the relationship between H. pylori infection and an unfavorable metabolic profile: dyslipidemia, body mass index, blood pressure, fasting blood glucose, and insulin resistance. In addition, research data on the novelty of higher levels of aspartate and alanine aminotransferase in Helicobacter‑positive patients compared to Helicobacter‑negative patients, in the absence of differences in liver fibrosis, are given. Separately, the research data are given, which indicate that the successful eradication of Helicobacter infection does not have a significant effect on liver steatosis, but probably reduces the severity of insulin resistance. Also, the authors draw attention to the fact that in a number of studies, the connection of H. pylori with NAFLD was not found, and no significant differences were found in the levels of high and low‑density lipoprotein cholesterol in people with Helicobacter infection compared to Helicobacter‑negative ones. The authors conclude that today there is no clear understanding of the role of Helicobacter pylori infection in the NAFLD pathogenesis, which requires further research because, after all, most researchers testify in favor of the fact that H. pylori infection can be one of the risk factors, contributing to the emergence and progression of NAFLD, and eradication of H. pylori may be important in the treatment of this disease.

Role of Helicobacter pylori Infection in Pathogenesis, Evolution, and Complication of Atherosclerotic Plaque.

The therapeutic management of atherosclerosis focuses almost exclusively on the reduction of plasma cholesterol levels. An important role in the genesis and evolution of atherosclerosis is played by chronic inflammation in promoting thrombosis phenomena after atheroma rupture. This review aims to take stock of the knowledge so far accumulated on the role of endemic HP infection in atherosclerosis. The studies produced so far have demonstrated a causal relationship between Helicobacter pylori (HP) and CVD. In a previous study, we demonstrated in HP-positive patients that thrombin and plasma fragment 1 + 2 production was proportionally related to tumor necrosis factor-alpha levels and that eradication of the infection resulted in a reduction of inflammation. At the end of our review, we can state that HP slightly affects the risk of CVD, particularly if the infection is associated with cytotoxic damage, and HP screening could have a clinically significant role in patients with a high risk of CVD. Considering the high prevalence of HP infection, an infection screening could be of great clinical utility in patients at high risk of CVD.

The Role of Helicobacter Pylori Infection in the Development of Gastric Cancer - Review of the Literature.

Helicobacter pylori (H. pylori), classified as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC), is linked to gastric cancer. The progression from atrophy to metaplasia, dysplasia, and carcinoma constitutes the pathway for intestinal-type gastric carcinoma development. H. pylori infection significantly increases gastric cancer risk, particularly in individuals with atrophic gastritis. Virulence factors like CagA and VacA disrupt host signaling pathways, contributing to chronic inflammation and carcinogenesis. Pro-inflammatory cytokines and dysregulated tumor suppressor genes further fuel this process. Eradicating H. pylori reduces gastric cancer incidence, especially in patients with atrophic gastritis and/or intestinal metaplasia. However, it may not prevent cancer in those with advanced pre-neoplastic lesions. Early detection and management of H. pylori infection are crucial in mitigating gastric cancer risk, offering significant benefits.

The role of Helicobacter pylori infection in the development and course of allergic diseases in children with gastroesophageal reflux disease

Objective — to improve the prevention and treatment of esophageal lesions in children based on the study of Helicobacter pylori infection in pediatric patients with allergic diseases.
 Materials and methods. Examination involved 256 children aged 6 to 18 years, from them 118 children without allergic pathology were included in the control group. The diagnosis was verified according to the unified clinical protocols of primary and secondary medical care. H. pylori was determined with biopsy urease test or histologically. Video esophagogastroduodenoscopy with endoscopic determination of pH was used to assess the condition of mucosa of the upper gastrointestinal parts. The results were processed using the methods of non‑parametric statistics.
 Results. Helicobacter pylori infection occurred more often in children with atopic dermatitis (32%), less often and equally often (24%) at bronchial asthma and allergic rhinitis and in 16% of patients with a combination of allergic diseases. Only 2 (1.4%) patients had H. pylori‑associated chronic urticaria, which was related to the specificity of the hospital department. Helicobacter infection was observed more often in patients with allergic rhinitis and atopic dermatitis without atopic changes. When comparing the Helicobacter association in children with allergic diseases depending on age, a significant difference was established in the group of children aged 6—12 years with allergic rhinitis and mainly with atopy. Endoscopic changes in the esophageal mucosa and esophageal motility disorders in association with Helicobacter pylori more often diagnosed in patients with atopic dermatitis (10.3%), less often and equally often in patients with bronchial asthma and allergic rhinitis (7.7%), the lowest frequency of Helicobacter pylori infection was found in patients with combined allergic pathology (5.1%) and no association in patients with urticaria. Endoscopic signs of esophageal inflammation were more often detected in patients with atopic dermatitis who had Helicobacter pylori infection and esophageal motility disorders. Most often, inflammatory changes in esophageal mucosa were found in patients with allergies developed in the presence of motor disorders, the risk of their development increased in case of Helicobacter infection. It has not been proven that the presence of atopy affected the development of inflammation in the esophagus.
 Conclusions. Among allergic diseases, Helicobacter pylori infection was more often revealed in patients with atopic dermatitis (32%), allergic rhinitis (24%) and bronchial asthma (24%) without statistical significance. A significant difference in H. pylori contamination depending on age was found only in patients with allergic rhinitis (H. pylori was determined more often in elementary school age), in the rest of the patients and in the control group, no significant differences were found. Endoscopic lesions of the esophagus were more often detected in atopic dermatitis, in particular esophagitis (in 17.9%), it was Helicobacter‑associated in 10.3% of cases and was combined with moderate motor disorders in 10.3% of observations. Allergic rhinitis (15.4%) was also associated with Helicobacter pylori infection (7.7%) and was accompanied by motility disorders in 15.4% of cases. Motor disorders, which were registered both in patients with allergic diseases and in patients without allergies, played an important role in the esophagus inflammation and formation of gastroesophageal reflux disease.

RELATIONSHIP BETWEEN DISEASES OF ORAL MUCOSA AND GASTROINTESTINAL TRACT

A large number of scientific publications are devoted to diseases of the oral mucosa. This is due to their significant variety, prevalence, complexity of diagnosis and treatment, and medical and social significance as a determinant of precancerous diseases with subsequent malignant transformation. The data of professional studies show that most lesions of the oral mucosa are multifactorial and arise along with pathologies of various organs and systems, in particular, immune, cardiovascular, nervous, endocrine, and quite often, with diseases of the gastrointestinal tract. The purpose of this study was a retrospective analysis of professional literary sources devoted to a medically and socially relevant issue, the relationship between diseases of the oral mucosa and pathologies of the gastrointestinal tract. Bibliosemantic and analytical methods were used in the study. The analysis of data from the specialized literature shows the variety of diseases of the mucous membrane of the oral cavity and their close relationship with general somatic pathology. Clinical observations have revealed a significant correlation between chronic diseases such as gastritis, peptic ulcer disease (in the stomach and duodenum), chronic colitis, and enterocolitis, and various lesions of the oral mucous membrane. The severity of these lesions is dependent on the specific form and duration of the underlying gastrointestinal condition. Scientists attribute this relationship to the similarities in morphological structure, shared functions, common blood supply, and innervation. Professional sources substantiate the role of Helicobacter pylori infection and dysbiosis in the development and progression of oral mucosal lesions. The treatment of oral mucous membrane diseases places a significant emphasis on etiotropic therapy. However, when this approach is not feasible, pathogenetic or symptomatic treatment options are utilized.

Role of Helicobacter Pylori Infection and Nonsteroidal Anti-Inflammatory Drug Use in Bleeding Peptic Ulcers

Most peptic ulcers and their complications are caused by Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs). Objective: To characterize the bleeding peptic ulcers features. Methods: This prospective study was carried out on 124 cases in the Department of Gastroenterology, Lady Reading Hospital in collaboration with Pharmacology Unit of Khyber Medical University, Peshawar from July 2018 to June 2020. All the patients were categorized into four groups: Positive H. pylori and no NSAID history (Group I), Positive H. pylori and NSAID use (Group-II), Negative H. pylori and NSAID user (Group-III), and Negative H. pylori and no NSAID history (Group-IV). Data analysis was carried out in SPSS version 26. Results: Of the total 124 cases, the prevalence of positive and negative H. pylori infection was 77.4% (n=96) and 22.6% (n=28) respectively. The number of patients in group I, II, III, and IV patients were 80 (64.5%), 16 (12.9%), 17 (13.7%), and 11 (8.9%) respectively. The incidence of NSAID users were 33 (26.6%) patients, out of which 18 used on daily basis and 15 on demand. Those in groups I and IV were substantially younger than groups II and III and they had less comorbid disorders than patients in group I. Conclusion: The present study concluded that about 26.6% of patients with bleeding ulcers took NSAIDs, meaning that low-dose aspirin will cause bleeding ulcers as will NSAID use on-demand.

The active form of Helicobacter pylori vacuolating cytotoxin induces decay-accelerating factor CD55 in association with intestinal metaplasia in the human gastric mucosa.

High‐level expression of decay‐accelerating factor, CD55, has previously been found in human gastric cancer (GC) and intestinal metaplasia (IM) tissues. Therapeutic effects of CD55 inhibition in cancer have been reported. However, the role of Helicobacter pylori infection and virulence factors in the induction of CD55 and its association with histological changes of the human gastric mucosa remain incompletely understood. We hypothesised that CD55 would be increased during infection with more virulent strains of H. pylori, and with more marked gastric mucosal pathology. RT‐qPCR and immunohistochemical analyses of gastric biopsy samples from 42 H. pylori‐infected and 42 uninfected patients revealed that CD55 mRNA and protein were significantly higher in the gastric antrum of H. pylori‐infected patients, and this was associated with the presence of IM, but not atrophy, or inflammation. Increased gastric CD55 and IM were both linked with colonisation by vacA i1‐type strains independently of cagA status, and in vitro studies using isogenic mutants of vacA confirmed the ability of VacA to induce CD55 and sCD55 in gastric epithelial cell lines. siRNA experiments to investigate the function of H. pylori‐induced CD55 showed that CD55 knockdown in gastric epithelial cells partially reduced IL‐8 secretion in response to H. pylori, but this was not due to modulation of bacterial adhesion or cytotoxicity. Finally, plasma samples taken from the same patients were analysed for the soluble form of CD55 (sCD55) by ELISA. sCD55 levels were not influenced by IM and did not correlate with gastric CD55 mRNA levels. These results suggest a new link between active vacA i1‐type H. pylori, IM, and CD55, and identify CD55 as a molecule of potential interest in the management of IM as well as GC treatment. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Modern views on the mechanisms of pathogenesis and tactics of management of patients with overlap of irritable bowel syndrome and functional dyspepsia. Review

Such widespread functional gastrointestinal disorders as irritable bowel syndrome (IBS) and functional dyspepsia (FD), although not represented by any obvious structural lesions of the gastrointestinal tract, but they seriously affect quality of life of many patients. According to epidemiological data, 26.7 — 48.7 % of IBS patients and 20.0 — 42.1 % of patients with FD have a crossover of symptoms, also known as overlap IBS/FD syndrome. Overlap syndrome usually leads to more serious clinical manifestations, deterioration of quality of life and complications. Chronic low‑intensity post‑infectious inflammation or non‑infectious microinflammation and the immune response play an important role in the pathogenesis of both IBS and FD, leading to visceral hypersensitivity, dysfunction of «brain‑gut» axis and intestinal mucosal barrier, which are usually the cause of IBS or FD. However, whether inflammation has the same mechanism in the syndrome of the overlap of IBS and FD (IBS/FD) remains unclear. The presented review considers the latest advances in the study of inflammatory mechanisms in IBS/FD and proposes new treatment tactics. Current data on the role of gastrointestinal infection, secondary chronic inflammation and immune response, intestinal mucosal barrier damage associated with gastrointestinal infection, effects of gastrointestinal infections on the enteric nervous system and the «gut‑brain» axis, possible role of Helicobacter pylori infection at the overlap of IBS/FD are discussed. The role of non‑infectious inflammation, in particular, bacterial overgrowth syndrome, food allergy, psychological or mental stress in the pathogenesis of IBS, FD and IBS/FD overlapping is also considered. The modern tactics of treatment and management of such patients, which is based on the impact on inflammatory mechanisms also are presented.

Impact of Helicobacter pylori infection on fluid duodenal microbial community structure and microbial metabolic pathways

BackgroundThe bioactivities of commensal duodenal microbiota greatly influence the biofunction of hosts. We investigated the role of Helicobacter pylori infection in extra-gastroduodenal diseases by determining the impact of H. pylori infection on the duodenal microbiota. We sequenced 16 S rRNA genes in samples aspirated from the descending duodenum of 47 (male, 20; female, 27) individuals who were screened for gastric cancer. Samples were analysed using 16 S rRNA gene amplicon sequencing, and the LEFSe and Kyoto Encyclopaedia of Genes and Genomes methods were used to determine whether the duodenal microflora and microbial biofunctions were affected using H. pylori infection.ResultsThirteen and 34 participants tested positive and negative for H. pylori, respectively. We identified 1,404 bacterial operational taxonomic units from 23 phyla and 253 genera. H. pylori infection changed the relative mean abundance of three phyla (Proteobacteria, Actinobacteria, and TM7) and ten genera (Neisseria, Rothia, TM7-3, Leptotrichia, Lachnospiraceae, Megasphaera, F16, Moryella, Filifactor, and Paludibacter). Microbiota features were significantly influenced in H. pylori-positive participants by 12 taxa mostly classified as Gammaproteobacteria. Microbial functional annotation revealed that H. pylori significantly affected 12 microbial metabolic pathways.ConclusionsH. pylori disrupted normal bacterial communities in the duodenum and changed the biofunctions of commensal microbiota primarily by upregulating specific metabolic pathways. Such upregulation may be involved in the onset of diseases associated with H. pylori infection.

Helicobacter pylori cagA status and gastric mucosa-associated lymphoid tissue lymphoma: a systematic review and meta-analysis

BackgroundRecent studies have investigated the role of Helicobacter pylori infection in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. It is estimated that approximately 0.1% of people infected with H. pylori develop gastric MALT lymphoma. However, the role of the CagA antigen, the highest causative agent of H. pylori, in increasing the risk of gastric MALT lymphoma remains unclear and controversial. A systematic review and meta-analysis were conducted to evaluate the effect of cagA status on the development of gastric MALT lymphoma.MethodsAll articles evaluating the status of the cagA gene in the development of gastric MALT lymphoma were collected using systematic searches in online databases, including PubMed, Scopus, Embase, and Google Scholar, regardless of publication date. The association between cagA and gastric MALT lymphoma was assessed using the odds ratio (OR) summary. In addition, a random-effects model was used in cases with significant heterogeneity.ResultsA total of 10 studies met our inclusion criteria, among which 1860 patients participated. No association between cagA status and the development of MALT lymphoma (extranodal marginal zone B-cell lymphoma) was found in this study (OR 1.30; 0.906–1.866 with 95% CIs; I2: 45.83; Q-value: 12.92). Surprisingly, a meaningful association was observed between cagA status and diffuse large B-cell lymphoma (OR 6.43; 2.45–16.84 with 95% CIs). We also observed an inverse association between vacA and gastric MALT lymphoma risk (OR 0.92; 0.57–1.50 with 95% CIs).ConclusionsIt seems that the infection with cagA-positive H. pylori strains does not have a meaningful effect on the gastric MALT lymphoma formation, while translocated CagA antigen into the B cells plays a crucial role in the development of diffuse large B-cell lymphoma.

Gastric MALT lymphoma - from pathogenetic insights to consequent deescalation of therapy

Gastric MALT- (mucosa-associated-lymphoid-tissue) lymphoma represents the most frequent gastrointestinal lymphoma. For decades, surgery and later on radiation and chemotherapy were regarded as established therapy. Some 30 years ago, the pathogenetic role of Helicobacter pylori infection for the development of gastric MALT-lymphoma became evident. During the following years, the pathogenetic insights were consequently implemented into clinical medicine. This lead to a radical change of the therapeutic approach to these lymphoma. Nowadays, Helicobacter pylori eradication is the internationally established therapy of first choice. It is followed by lymphoma regression in most cases. The long-term prognosis of patients after exclusive eradication therapy is excellent, even if endoscopic and/or histological residuals persist and a watch-and-wait strategy is favored.The pathogenetic insights und their clinical application implicated a consequent deescalation of therapy of gastric MALT-lymphoma. This review summarizes the single steps of this development and gives a recommendation for the actual management of patients with gastric MALT lymphoma.

Study the Role of Helicobacter Pylori Infection in a Group of Iraqi Patients with Colorectal Cancer

Background Increased developed of colorectal tumor may be linked with Helicobacter pylori. However, theunderlying mechanisms were still uncertain.objective: Helicobacter pylori infection in the world, in particular in developing countries, is one of mostcommon chronic bacterial infections, This bacterium is responsible for many diseases such as gastritis,peptic ulcer, lymphoma and in some patients may lead to gastric cancer, it is in the world has known 2ndmajor cause of death from cancer. H.pylori infection may likely raise the risk of colorectal cancer, accordingto recently published studies. The aimed of this study to detected the role of H. pylori in colorectal cancer.Methods: Serum of 50 colorectal cancer and colorectal normal with positive H. pylori infection patientswere estimated by 14Urea breath test and 25 subjects with no any inflammatory disease as the control group.from each patient were collected Blood samples to investigated of H. pylori specific immunoglobulin G(IgG) and CagA IgG antibodies by using enzyme-linked immunosorbent assay (ELISA).Results: A total of 50 patients in this study 25 had colorectal cancer and 25 had colorectal normal with H.pylori infection (immunoglobulin G (IgG) P ? 0.01 and CagA IgG antibodies P < 0.01) were significantlymore prevalent in the patients with colorectal_ cancer and colorectal normal with Helicobacter pylori_infection compared with the healthy controls (P= 0.00019, P= 0.00022 respectively) The relation wasstatistically non-significant between the antibody seropositivity and gender but Highly significant with age.Conclusion: The findings indicate that Helicobacter pylori_ infection can be regarded as a contributinginfluence for progressive tumor in colorectal.

Helicobacter pylori infection in the palm and sole of psoriatic patients

ObjectiveTo clarify the role of Helicobacter pylori infection in psoriatic patients with palm and sole affectionBackgroundPsoriasis is a chronic inflammatory disease that affects 2–3% of the population worldwide. H. pylori infection has been implicated in the pathogenesis of various skin diseases.Patients and methodsThis case–control study was conducted on 40 patients with psoriasis vulgaris and 40 age-matched and sex-matched healthy individuals. All patients were subjected to history taking and complete medical examination. Serum levels of anti-H. pylori immunoglobulin G were measured by enzyme-linked immunosorbent assay technique. Serum levels of anti-H. pylori immunoglobulin G were statistically analyzed in relation to psoriasis area and severity index score.ResultsH. pylori infection was more prevalent among patients who did not manifest palm and sole affection. However, 50% of palm-affected and sole-affected patients were positive for H. pylori infection (P = 0.02).ConclusionH. pylori may play a significant role in the development of palmoplantar psoriasis and may provide important clues to assist in the development of new therapeutic strategies for palmoplantar psoriatic patients through its eradication.

Role of Helicobacter Pylori Infection on Diabetic and Lipid Profile in Pre-diabetic Patients

Introduction:Helicobacter Pylori (H.pylori) infection is related to gastritis, peptic ulcers, gastric cancers and Mucosa Associated Lymphoid Tissue lymphomas (MALT). It is also associated with several extra-gastrointestinal pathologies owing to its association with increased production of proinflammatory cytokines, bacterial virulence factors and environmental factors. It may have an effect on onset of diabetes mellitus and alter lipid profile. Aim: To find the effect of H.pylori infection on diabetic and lipid profile in pre-diabetic patients. Materials and Methods: A single centre, cross-sectional study was conducted over a period from January 2019 to June 2020, on pre-diabetic patients (HbA1c 5.7-6.4%.). A total of 118 patients were recruited in the study and divided into two groups based on the H.pylori positive (group A) and negative (group B) results. HbA1c, Low Density Lipoprotein (LDL) and High Density Lipoprotein (HDL) were investigated at baseline, six months and 12 months and the results of the two groups were compared using student’s t-test. Supply Support Planning and Execution (SSPE) Software version 20.0 were used for analysis of the collected data. A p-value&lt;0.05 to be considered significant. Results: Of the 118 patients, 96 (mean age 48.3 years) completed the study. There 59 (61.5%) were males and 37 (38.5%) were females. A total of 54 (56%) of the study population tested positive for the H.pylori colonisation. The study showed that patients infected with H.pylori (group A) had comparative rapid increase in the HbA1c levels (p-value=0.048) when compared with the non-infective group (group B). The group A also had statistically significant increase in the LDL cholesterol levels (p-value=0.032) and decrease in HDL cholesterol levels (p-value=0.02) than group B. Conclusion: Infection with H.pylori is associated with increase in the level of HbA1c in pre-diabetics. It is also associated with increase in the LDL cholesterol levels and decrease in the HDL cholesterol levels. Eradication of the pathogen may help in preventing or delaying the progression of pre-diabetes and dyslipidemia. However, larger studies without any confounding factors are needed to establish the association between H.pyloriinfection and its effect on diabetic and lipid profile.

The Role of Helicobacter Pylori Infection in Idiopathic Thrombocytopenic Purpura in Children

Background: Many studies had found obvious relation between helicobacter pylori infection and chronic idiopathic thrombocytopenic purpura; several studies have reported remission of immune thrombocytopenic purpura (ITP) after eradication of a coexistent Helicobacter pylori infection in adults, data in children are limited. Objective: To detect the association of H. pylori infection and idiopathic thrombocytopenic purpura in children and the effect of eradication of the infection on platelet count in these patients. Patients and methods: This study was conducted on 83 chronic idiopathic thrombocytopenic purpura children with age range from 3 to 13 years. They were 46 males 37 females. Also the study included 104 healthy individual with the same range of age. They were 58 males and 46 females as a control group. This was between October 2018 and September 2019 in the Pediatric Hematology and GIT Clinics or inpatients wards of Pediatric Department. Results: Clinical benefit occurred in 31 cases of the 83 chronic ITP (cITP) patients screened; nevertheless, we have a simple, inexpensive, non‐invasive screening method; the adverse events of eradication therapy are negligible, together with an affordable cost, all uncommon attributes among the specific treatments currently available for cITP; therefore it is worthwhile to test for and treat H. pylori infection. Conclusion: Our data showed a prevalence of H. pylori infection in cITP pediatrics that was similar to other studies. We found that successful H. pylori eradication induced platelet response in 37.3% of 83 cases included in our study.

The Role of Helicobacter Pylori Infection in Idiopathic Thrombocytopenic Purpura in Children

Background: Many studies had found obvious relation between helicobacter pylori infection and chronic idiopathic thrombocytopenic purpura; several studies have reported remission of immune thrombocytopenic purpura (ITP) after eradication of a coexistent Helicobacter pylori infection in adults, data in children are limited. Objective: To detect the association of H. pylori infection and idiopathic thrombocytopenic purpura in children and the effect of eradication of the infection on platelet count in these patients. Patients and methods: This study was conducted on 83 chronic idiopathic thrombocytopenic purpura children with age range from 3 to 13 years. They were 46 males 37 females. Also the study included 104 healthy individual with the same range of age. They were 58 males and 46 females as a control group. This was between October 2018 and September 2019 in the Pediatric Hematology and GIT Clinics or inpatients wards of Pediatric Department. Results: Clinical benefit occurred in 31 cases of the 83 chronic ITP (cITP) patients screened; nevertheless, we have a simple, inexpensive, non‐invasive screening method; the adverse events of eradication therapy are negligible, together with an affordable cost, all uncommon attributes among the specific treatments currently available for cITP; therefore it is worthwhile to test for and treat H. pylori infection. Conclusion: Our data showed a prevalence of H. pylori infection in cITP pediatrics that was similar to other studies. We found that successful H. pylori eradication induced platelet response in 37.3% of 83 cases included in our study.

Autoimmune gastritis.

Autoimmune gastritis (AIG) is an increasingly prevalent, organ-specific, immune-mediated disorder characterized by the destruction of gastric parietal cells, leading to the loss of intrinsic factor and reduced acid output. These alterations result in malabsorption of iron, vitamin B12 (pernicious anaemia) and potentially other micronutrients. For several years, most studies have focused on pernicious anaemia only, generating confusion between the two entities. In AIG, the gastric proton pump, H+/K+ ATPase, is the major autoantigen recognized by autoreactive T cells. The T cell-dependent activation of B cells stimulates the production of anti-parietal cell antibodies, the serological hallmark of AIG. The role of Helicobacter pylori infection in activating or favouring the autoimmune process is still uncertain. Early histopathological alterations allowing a more precise and prompt recognition have recently been described. AIG is burdened by a substantial diagnostic delay as it can present with varied clinical signs including, among others, gastrointestinal symptoms and neuropsychiatric manifestations. In advanced stages, AIG might progress to neuroendocrine tumours and gastric adenocarcinoma. Management includes early detection through a proactive case-finding strategy, micronutrient supplementation and endoscopic surveillance. This Primer comprehensively describes the most important insights regarding the epidemiology, pathophysiology, diagnosis and management of AIG, focusing on the most controversial, outstanding issues and future directions.

Association of helicobacter pylori with multiple sclerosis: Protective or risk factor?

Background: Multiple sclerosis (MS) is a common autoimmune inflammatory disease in the central nervous system (CNS) without exact pathology. Environmental factors such as infections have a causal or protective role in MS. Helicobacter pylori (HP) is one of the infections in digestive diseases and previous studies reported controversial findings of this infection role in MS. So, we conducted this study to assess the frequency of HP infection in patients with MS in comparison to the healthy population. Methods: This cross-sectional study was undertaken between 2015 and 2019. 191 participants including 58 patients with clinically isolated syndrome (CIS), 57 patients with relapsing-remitting MS (RRMS), 39 patients with secondary progressive MS (SPMS), and 39 age- and sex-matched healthy controls (HCs) were tested for the presence of HP immunoglobulin G (IgG) and IgM antibodies (Abs) in their serum sample. Results: The frequency of HP IgG seropositivity in patients with SPMS was significantly higher than patients with CIS [Odds ratio (OR): 6.333, 95% confidence interval (CI): 2.522-15.906, P < 0.001], patients with RRMS (OR: 4.583, 95% CI: 1.842-11.407, P = 0.001), and HCs (OR: 8.485, 95% CI: 3.058-23.540, P < 0.001). We did not find a significant difference among other study groups regarding IgG seropositivity. No significant difference among groups regarding HP IgM seropositivity was evident. On univariate model, Expanded Disability Status Scale (EDSS) score (OR: 1.038, 95% CI: 1.038-1.460, P = 0.017) and SPMS (OR: 4.583, 95% CI: 1.842-11.407, P = 0.001) were predictor for HP IgG seropositivity. On multivariate model, only SPMS had higher risk for HP IgG seropositivity compared to RRMS (OR: 5.554, 95% CI: 1.327-23.253, P = 0.019). We did not find a significant association between clinical and demographic variables with HP IgM seropositivity. Conclusion: Based on our findings, progressive MS and HP infection may have association. Further longitudinal studies with large sample size are needed to determine the role of HP infection in MS.

Response to article of K. I. Grigoriev et al. “Peptic ulcer disease — historical dynamics: views on etiopathogenesis and treatment”, In Experimental and Clinical Gastroenterology. 2019;161(1): 155–165. (In Russ.) DOI: 10.31146/1682–8658-ecg-161–1–155–165

In this article is discussed the historical facts of the study of peptic ulcer during 190 years after its self-selection in an independent nosological form. The scientific facts and arguments refuting the leading role of Helicobacter pylori infection in its etiology and pathogenesis are given; the conclusion of the authors of this article about the inevitability of a new paradigm of peptic ulcer in the near future is supported.

ASSOCIATION OF DUODENAL EOSINOPHILIC INFILTRATE WITH HELICOBACTER PYLORI INFECTION, BUT NOT WITH FUNCTIONAL DYSPEPSIA.

The role of Helicobacter pylori infection on eosinophilic infiltration in duodenal mucosa is poorly studied. An increase in the number of eosinophils in duodenum has been associated with functional dyspepsia. To evaluate the influence of H. pylori infection on duodenal eosinophil count and the role of eosinophilic infiltrate of duodenum in functional dyspepsia. Positive and negative H. pylori individuals were included. Both functional dyspeptic patients according to Rome III criteria (cases) and individuals without gastrointestinal symptoms (controls) were enrolled. They were submitted to upper endoscopy and H. pylori infection was verified by gastric histopathology and urease test. Eosinophils in the duodenal mucosa were counted in five high-power fields, randomly selected on slides of endoscopic biopsies. Thirty-nine H. pylori positive (mean age 40.5 and 69.2% women) and 24 negative patients (mean age 37.3 and 75% women) were included. The influence of the infection was observed in the duodenal eosinophil count, which was higher in infected individuals: median 13.2 vs 8.1 in non-infected individuals (P=0.005). When we analyzed patients according to symptoms, cases - mean age 39.6; 71.4% women - and controls - mean age 38.7; 71.4% women - had similar duodenal eosinophil count: median 11.9 and 12.6 respectively (P=0.19). We did not demonstrate association of duodenal eosinophil count with functional dyspepsia but found association with H. pylori infection.