scholarly journals Pathophysiology of H. pylori

2021 ◽  
Author(s):  
Karam Dawood ◽  
Israa Mamdooh
Keyword(s):  
Oral Route ◽  
Inflammatory Cell Infiltrate ◽  
Antral Mucosa ◽  
Ulcer Disease ◽  
H Pylori ◽  
Hepatobiliary Tract ◽  
Acute And Chronic Inflammation ◽  
Upper Gastrointestinal ◽  
Test Result

Helicobacter species were known for long as a causative agent of gastritis. H. pylori associated gastritis is characterized by the presence of acute and chronic inflammation. Previously, it was believed that in H. pylori gastritis, fundic inflammation was less important than that of the antral mucosa. However, H. pylori and gastroesophageal reflux disease create, or arise concurrently, may also be caused by the anatomical role of the inflammatory cell infiltrate. The source of H. pylori is mostly unknown. H. pylori has a small host range and is present in people and some non-human primates nearly exclusively. In rare cases, the presence of pets may be a concern for H. pylori infection; hence, pets should be isolated. There is also no definitive proof for zoonotic H. pylori transmission. The direct transmission from person to person, either oral or fecal-oral route or both, is expected to lead to new infections. H. pylori colonization is not an infection itself, but it impacts the relative likelihood that multiple pathological conditions of the upper gastrointestinal tract and even the hepatobiliary tract will grow. Therefore, H. pylori examination alone is not relevant but can be done in order to ascertain the cause of a basic disorder, such as peptic ulcer disease or to avoid disease, for example in subjects with family gastric carcinoma. A positive test result will validate the procedure, and a negative test result can suggest that other etiological causes or prevention steps needs to be examined. Gastritis is divided into acute and chronic. Several virulence factors play a role in the disease such as cag PAI (Pathogenicity Island) and VacA vacuolating cytotoxin. Different adhesins and their receptors aid in H. pylori colonization and invasion. Based on analogy with other mucosal infections, it was initially assumed that a protective immune response against H. pylori would predominantly be mediated by antibodies. Subsequent experiments have indicated that the relevance of the humoral system for protective immunity is only marginal. Antibodies can effectively prevent infection and reduce colonization in animal models.

scholarly journals Incidence of Duodenal Ulcers and Gastric Ulcers in a Western Population: Back to Where It Started

2009 ◽  
Vol 23 (9) ◽  
pp. 604-608 ◽  
Author(s):  
Marcel JM Groenen ◽  
Ernst J Kuipers ◽  
Bettina E Hansen ◽  
Rob J Th Ouwendijk
Keyword(s):  
Gastric Ulcers ◽  
Bleeding Complications ◽  
Upper Gastrointestinal Endoscopy ◽  
Peptic Ulcers ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Treatment Regimens ◽  
H Pylori ◽  
Upper Gastrointestinal ◽  
Over Time

BACKGROUND/OBJECTIVES: As recently as 40 years ago, a decline in the incidence of peptic ulcers was observed. The discovery of Helicobacter pylori had a further major impact on the incidence of ulcer disease. Our aim was to evaluate the trends in the incidence and bleeding complications of ulcer disease in the Netherlands.METHODS: From a computerized endoscopy database of a district hospital, the data of all patients who underwent upper gastrointestinal endoscopy from 1996 to 2005 were analyzed. The incidence of duodenal and gastric ulcers, with and without complications, were compared over time.RESULTS: Overall, 20,006 upper gastrointestinal endoscopies were performed. Duodenal ulcers were diagnosed in 696 (3.5%) cases, with signs of bleeding in 158 (22.7%). Forty-five (6.5%) of these ulcers were classified as Forrest I and 113 (16.2%) as Forrest II. Gastric ulcers were diagnosed in 487 cases (2.4%), with signs of bleeding in 60 (12.3%). A Forrest 1 designation was diagnosed in 19 patients (3.9%) and Forrest 2 in 41 patients (8.4%). The incidence of gastric ulcers was stable over time, while the incidence of duodenal ulcers declined.CONCLUSIONS: The incidence of duodenal ulcer disease in the Dutch population is steadily decreasing over time. Test and treatment regimens for H pylori have possibly contributed to this decline. With a further decline in the prevalence of H pylori, the incidence of gastric ulcers is likely to exceed the incidence of duodenal ulcers in the very near future, revisiting a similar situation that was present at the beginning of the previous century.

scholarly journals Correlation of Clinical, Endoscopic, and Pathological Findings among Suspected Peptic Ulcer Disease Patients in Abuja, Nigeria

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Onyedika Godfrey Okoye ◽  
Oluwole Olayemi Olaomi ◽  
Alexander M.E. Nwofor ◽  
Paul Jibrin ◽  
Cephas Shallangwa Batta ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Gastrointestinal Endoscopy ◽  
Upper Gastrointestinal Endoscopy ◽  
Pathological Findings ◽  
Histological Findings ◽  
National Hospital ◽  
Ulcer Disease ◽  
Endoscopic Findings ◽  
H Pylori ◽  
Upper Gastrointestinal

Background. Peptic ulcer disease (PUD) remains one of the most prevalent gastrointestinal diseases and has been linked to Helicobacter pylori (H. pylori) infection. This condition may be suspected on clinical grounds, but diagnosis is established using upper gastrointestinal endoscopy. Aims. To determine the correlation between the endoscopic and pathological findings among suspected PUD patients who have been referred for diagnostic upper gastrointestinal endoscopy in National Hospital Abuja. Methods. This is a hospital-based prospective study conducted among suspected PUD patients at National Hospital Abuja over a one-year period. Clinical, endoscopic, and histological findings were ascertained and documented. Data obtained were analyzed using SPSS version 21.0. Tests of significance were done using the chi-square test and Student t -test at 95% confidence intervals. Results. One hundred and thirty-two patients were included in the study. The ages ranged from 15 to 87 years, mean age 43.30 ± 11.94 years. Seventy-seven (58.3%) patients had abnormal endoscopic findings, of whom 37 (28.0%) had PUD. Prevalence of H. pylori infection was 42.2% and was found in 81.1% of PUD patients. H. pylori was significantly associated with confirmed PUD ( p < 0.001 ) and abnormal endoscopic findings ( p < 0.001 ). No association was found between normal endoscopic findings and histological findings ( p = 0.924 ). Conclusion. There is a poor correlation between clinical and endoscopic diagnoses of PUD. H. pylori was found to be significantly associated with PUD and abnormal endoscopic findings. Endoscopic facilities should therefore be made available and accessible for proper PUD diagnosis. Empirical treatment of H. pylori in patients with diagnosed PUD is strongly recommended.

Peptic Ulcer Disease

2014 ◽  
pp. 710-718
Author(s):  
Tyler M. Berzin ◽  
Kenneth R. Falchuk
Keyword(s):  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
The United States ◽  
Dietary Factors ◽  
Pathogenic Agent ◽  
Ulcer Disease ◽  
History Of ◽  
Ulcer Complications ◽  
H Pylori

Peptic ulcer disease (PUD) involves the stomach or duodenum and is a significant cause of morbidity and mortality both in the United States and worldwide, with a lifetime prevalence estimated at 5–15%. For a good part of the 20th century PUD was felt to be a condition related to stress and dietary factors. More recently, our understanding of PUD has been advanced by research into the role of gastric acid secretion and the benefits of various classes of antisecretory medications and, perhaps most importantly, in 1984, by Warren and Marshall, who identified Helicobacter pylori (H. pylori) as a pathogenic agent in this disease. Proton pump inhibitor (PPI) therapy and H. pylori eradication regimens have altered the natural history of what once was a chronic disease, and they have also reduced peptic ulcer complications, limiting the need for surgery.

scholarly journals Role of Helicobacter pylori in Upper Gastrointestinal Bleeding Among Ischemic Stroke Hospitalizations: A Nationwide Study of Outcomes

2019 ◽  
Vol 1 (3) ◽  
pp. 358-371
Author(s):  
Urvish K. Patel ◽  
Mihir Dave ◽  
Anusha Lekshminarayanan ◽  
Nidhi Patel ◽  
Abhishek Lunagariya ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Ischemic Stroke ◽  
Risk Stratification ◽  
Gastrointestinal Bleeding ◽  
Health Care Cost ◽  
Upper Gastrointestinal Bleeding ◽  
Increased Risk ◽  
H Pylori ◽  
Upper Gastrointestinal

Introduction: Helicobacter pylori (H. pylori) is a well-recognized risk factor for upper gastrointestinal bleeding (UGIB). The exposure to tissue plasminogen activator (tPA), anti-platelets, and anticoagulants increases the risk of UGIB in acute ischemic stroke (AIS) patients, the risk stratification of H. pylori infection is not known. In this retrospective cross-sectional study, we aimed to evaluate the relationship between H. pylori and GIB in patients hospitalized with AIS. Methods: In the nationwide data, hospitalization for AIS was identified by primary diagnosis using International Classification of Diseases, clinical modification (ICD-9-CM) codes. Subgroup of patients with GIB and H. pylori were identified in AIS cohort. A stepwise multivariable logistic regression model was fitted to evaluate the outcome of upper GIB and role of H. Pylori in UGIB. Results: Overall 4,224,924 AIS hospitalizations were identified, out of which 18,629 (0.44%) had UGIB and 3122 (0.07%) had H. pylori. The prevalence of H. pylori-induced UGIB among UGIB in AIS was 3.05%. The prevalence of UGIB was markedly elevated among the H. pylori infection group (18.23% vs. 0.43%; p < 0.0001) compared to the non-H. pylori group. In multivariable regression analysis, H. pylori was associated with markedly elevated odds of UGIB (aOR:27.75; 95%CI: 21.07–36.55; p < 0.0001). Conclusion: H. pylori infection had increased risk-adjusted occurrence of UGIB amongst the AIS hospitalized patients. H. pylori testing may improve risk stratification for UGIB and lower the health care cost burden in stroke hospitalization.

scholarly journals Optimization Strategies Aimed to Increase the Efficacy of Helicobacter pylori Eradication Therapies with Quinolones

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 5084
Author(s):  
Javier P. Gisbert
Keyword(s):  
Gastroduodenal Ulcer ◽  
Eradication Therapy ◽  
Ulcer Disease ◽  
Simple Alternative ◽  
Third Line ◽  
H Pylori ◽  
Triple Regimen ◽  
Meta Analyses ◽  
Cure Rates

H. pylori infection is the main cause of gastritis, gastroduodenal ulcer disease, and gastric cancer. Fluoroquinolones such as levofloxacin, or more recently moxifloxacin or sitafloxacin, are efficacious alternatives to standard antibiotics for H. pylori eradication. The aim of the present review is to summarize the role of quinolone-based eradication therapies, mainly focusing on the optimization strategies aimed to increase their efficacy. Several meta-analyses have shown that, after failure of a first-line eradication treatment, a levofloxacin-containing rescue regimen is at least equally effective, and better tolerated, than the generally recommended bismuth quadruple regimen. Compliance with the levofloxacin regimens is excellent, and the safety profile is favourable. Higher cure rates have been reported with longer treatments (>10–14 days), and 500 mg levofloxacin daily is the recommended dose. Adding bismuth to the standard triple regimen (PPI-amoxicillin-levofloxacin) has been associated with encouraging results. Unfortunately, resistance to quinolones is easily acquired and is increasing in most countries, being associated with a decrease in the eradication rate of H. pylori. In summary, a quinolone (mainly levofloxacin)-containing regimen is an encouraging second-line (or even third-line) strategy, and a safe and simple alternative to bismuth quadruple therapy in patients whose previous H. pylori eradication therapy has failed.

scholarly journals The role of acid inhibition in Helicobacter pylori eradication

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 1747 ◽  
Author(s):  
David R. Scott ◽  
George Sachs ◽  
Elizabeth A. Marcus
Keyword(s):  
Helicobacter Pylori ◽  
Urease Activity ◽  
Eradication Therapy ◽  
Acid Inhibition ◽  
Acid Suppression ◽  
Helicobacter Pylori Eradication ◽  
Ulcer Disease ◽  
Chronic Active Gastritis ◽  
H Pylori

Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid.

scholarly journals Is the presence ofHelicobacter pyloriin the Dental Plaque of Patients with Chronic Periodontitis a Risk Factor for Gastric Infection?

2009 ◽  
Vol 23 (3) ◽  
pp. 177-179 ◽  
Author(s):  
Mohammed Al Asqah ◽  
Nawaf Al Hamoudi ◽  
Sukumaran Anil ◽  
Abdulrahman Al jebreen ◽  
Waleed Khalid Al-hamoudi
Keyword(s):  
Risk Factor ◽  
Chronic Periodontitis ◽  
Dental Plaque ◽  
Group Versus ◽  
Periodontal Pocket ◽  
Upper Gastrointestinal Endoscopy ◽  
Peptic Ulcers ◽  
H Pylori ◽  
Upper Gastrointestinal ◽  
Test Result

BACKGROUND:Helicobacter pyloriis considered to be a pathogen responsible for gastritis and peptic ulcers, and a risk factor for gastric cancer. A periodontal pocket in the teeth of individuals with chronic periodontitis may function as a reservoir forH pylori.OBJECTIVE: The present study was undertaken to evaluate whether the presence ofH pyloriin the dental plaque of patients with and without periodontitis correlates with gastric involvement.METHODS: A total of 101 patients with dyspepsia were included in the present study. Subjects were divided into periodontitis and non-periodontitis groups. For the detection ofH pyloriin dental plaque, samples were collected from two teeth using a periodontal curette. Subgingival plaque was obtained by inserting two sterile paper points into periodontal pockets for 20 s. This was followed by an upper gastrointestinal endoscopy and antral biopsies.RESULTS: Sixty-five per cent of patients had dental plaque positive forH pyloriand more than 50% harboured the bacteria in their stomach. Periodontitis patients had a significantly higher percentage ofH pyloriin their dental plaque (79% versus 43%; P<0.05) and the stomach (60% versus 33%; P<0.05) than patients with no periodontitis. Additionally, 78% of patients from the periodontitis group versus only 30% from the nonperiodontitis group had a positive test result for the coexistence ofH pyloriin both dental plaque and the stomach.CONCLUSION: Patients with poor oral hygiene have a higher prevalence ofH pyloriin dental plaque and in the stomach. This finding suggests that the oral cavity may be a reservoir forH pylori,and potentially a source of transmission or reinfection.

scholarly journals Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

2021 ◽  
Author(s):  
Ghorbanali Rahimian ◽  
Milad Shahini Shams Abadi ◽  
Reza Ahmadi ◽  
Mohammedhadi Shafigh ◽  
Fatemeh Azadegan-Dehkordi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Treg Cells ◽  
Infected Group ◽  
Ulcer Disease ◽  
Tnf Α ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Helicobacter pylori (H. pylori) -induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori –associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells.Methods: Fifty-five patients with H. pylori –associated gastritis, 47 patients with H. pylori –associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments.Results: Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group.Conclusion: These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

scholarly journals Association of Helicobacter pylori infection with nodular antritis and follicular gastritis

2006 ◽  
Vol 63 (3) ◽  
pp. 313-315 ◽  
Author(s):  
Ratko Tomasevic ◽  
Gradimir Golubovic ◽  
Miroslav Kiurski ◽  
Dragana Stankovic ◽  
Radoje Doder ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Case Report ◽  
Chronic Gastritis ◽  
Upper Gastrointestinal Endoscopy ◽  
Antral Mucosa ◽  
Urease Test ◽  
Sydney System ◽  
H Pylori ◽  
The Relationship ◽  
Upper Gastrointestinal

Introduction. Helicobacter pylori (H. pylori) infection is known to be the must common cause of chronic gastritis having some endoscopic and pathologic characteristies as determinated by the Sydney System for Gastritis Classification. The aim of our case report was to point out the relationship between an endoscopic finding of nodular antritis and the presence of H. pylori infection and active chronic gastritis. Case report. Our patient underwent upper gastrointestinal endoscopy for dyspeptic complaints and was diagnosed as having nodular antritis, but also underwent urease test and hystopathologic examination of antral mucosa, to determine the presence and density of H. pylori infection and the presence and severity of gastritis. After a course of anti H. pylori treatment, dyspepsia improved and new biopsy specimens obtained two months and six months afterwards revealed no pathological findings. Conclusion. The case report supported the association of H. pylori infection of lymphoid follicles with nodular gastric mucosis.

scholarly journals The Human Gastric Pathogen Helicobacter pylori and Its Association with Gastric Cancer and Ulcer Disease

Ulcers ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-23 ◽  
Author(s):  
Bianca Bauer ◽  
Thomas F. Meyer
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Strain Differences ◽  
Protective Effects ◽  
Ulcer Disease ◽  
Prophylactic Measures ◽  
H Pylori

With the momentous discovery in the 1980's that a bacterium, Helicobacter pylori, can cause peptic ulcer disease and gastric cancer, antibiotic therapies and prophylactic measures have been successful, only in part, in reducing the global burden of these diseases. To date, ~700,000 deaths worldwide are still attributable annually to gastric cancer alone. Here, we review H. pylori's contribution to the epidemiology and histopathology of both gastric cancer and peptic ulcer disease. Furthermore, we examine the host-pathogen relationship and H. pylori biology in context of these diseases, focusing on strain differences, virulence factors (CagA and VacA), immune activation and the challenges posed by resistance to existing therapies. We consider also the important role of host-genetic variants, for example, in inflammatory response genes, in determining infection outcome and the role of H. pylori in other pathologies—some accepted, for example, MALT lymphoma, and others more controversial, for example, idiopathic thrombocytic purpura. More recently, intriguing suggestions that H. pylori has protective effects in GERD and autoimmune diseases, such as asthma, have gained momentum. Therefore, we consider the basis for these suggestions and discuss the potential impact for future therapeutic rationales.

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