Gastric Pathology Research Articles

Modification of the Gastric Mucosal Microbiota by a Strain-Specific Helicobacter pylori Oncoprotein and Carcinogenic Histologic Phenotype.

Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma; however, most infected individuals never develop this malignancy. Strain-specific microbial factors, such as the oncoprotein CagA, as well as environmental conditions, such as iron deficiency, augment cancer risk. Importantly, dysbiosis of the gastric microbiota is also associated with gastric cancer. To investigate the combinatorial effects of these determinants in an in vivo model of gastric cancer, Mongolian gerbils were infected with the carcinogenic cag+H. pylori strain 7.13 or a 7.13 cagA isogenic mutant, and microbial DNA extracted from gastric tissue was analyzed by 16S rRNA sequencing. Infection with H. pylori significantly increased gastric inflammation and injury, decreased α-diversity, and altered microbial community structure in a cagA-dependent manner. The effect of iron deficiency on gastric microbial communities was also investigated within the context of infection. H. pylori-induced injury was augmented under conditions of iron deficiency, but despite differences in gastric pathology, there were no significant differences in α- or β-diversity, phyla, or operational taxonomic unit (OTU) abundance among infected gerbils maintained on iron-replete or iron-depleted diets. However, when microbial composition was stratified based solely on the severity of histologic injury, significant differences in α- and β-diversity were present among gerbils harboring premalignant or malignant lesions compared to gerbils with gastritis alone. This study demonstrates that H. pylori decreases gastric microbial diversity and community structure in a cagA-dependent manner and that as carcinogenesis progresses, there are corresponding alterations in community structure that parallel the severity of disease.IMPORTANCE Microbial communities are essential for the maintenance of human health, and when these communities are altered, hosts can become susceptible to inflammation and disease. Dysbiosis contributes to gastrointestinal cancers, and specific bacterial species are associated with this phenotype. This study uses a robust and reproducible animal model to demonstrate that H. pylori infection induces gastric dysbiosis in a cagA-dependent manner and further that dysbiosis and altered microbial community structure parallel the severity of H. pylori-induced gastric injury. Ultimately, such models of H. pylori infection and cancer that can effectively evaluate multiple determinants simultaneously may yield effective strategies for manipulating the gastric microbiota to prevent the development of gastric cancer.

The Enterochromaffin-like [ECL] Cell-Central in Gastric Physiology and Pathology.

Background: Studies on the regulation of gastric and pancreatic secretion began more than 100 years ago. Secretin was the first hormone postulated to exist, initiating the field of endocrinology. Gastrin produced in the antral mucosa was the second postulated hormone, and together with histamine and acetylcholine, represent the three major gastric acid secretagogues known since 1920. For a long time, the mast cell was the only recognized histamine-producing cell in the oxyntic mucosa and, in the mid-1980s, the ECL cell was recognized as the cell producing histamine, taking part in the regulation of gastric acid secretion. Methods: This review is based upon literature research and personal knowledge. Results: The ECL cell carries the gastrin receptor, and gastrin regulates its function (histamine release) as well as proliferation. Long-term hypergastrinemia results in gastric neoplasia of variable malignancies, implying that gastric hypoacidity resulting in increased gastrin release will induce gastric neoplasia, including gastric cancer. Conclusions: The trophic effect of gastrin on the ECL cell has implications to the treatment with inhibitors of acid secretion.

Cut-off value verification for 13C-urease breath test using infrared (IR) spectrometer in the diagnosis of helicobacter pylori infection

Campylobacter and Helicobacter are curved Gram-negative rods and gastrointestinal-producing agents. Campylobacter is one of the most frequent foodborne pathogens, producing self-limited diarrhea in most of the patients, although it can cause more serious symptoms and neurological complications in immunosuppressed patients. Microbiological diagnosis is only carried out in severe cases, culture being the reference method that also makes it possible to study possible resistance to commonly used antibiotics, since an increase has been observed in recent years. Helicobacter pylori is part of the gastrointestinal mucosa of half the world's population. It is related to various gastric pathologies and increases the risk of developing peptic ulcer and gastric cancer. For its diagnosis there are invasive and non-invasive methods, with their respective advantages and limitations. H. pylori eradication therapy is considered one of the pillars in the gastric cancer elimination strategy, therefore it is recommended in all symptomatic patients. In recent years, resistance to first-line antibiotics has increased, so a study of their sensitivity must be carried out using molecular methods.

Discussions on Changes in Gastric Lymph Drainage in Malignant Gastric Pathology in Terms of Intraoperative Lymphography

Discussions on Changes in Gastric Lymph Drainage in Malignant Gastric Pathology in Terms of Intraoperative Lymphography

Increased LIGHT expression and activation of non-canonical NF-\u03baB are observed in gastric lesions of MyD88-deficient mice upon Helicobacter felis infection

Helicobacter pylori infection induces a number of pro-inflammatory signaling pathways contributing to gastric inflammation and carcinogenesis. Among those, NF-κB signaling plays a pivotal role during infection and malignant transformation of the gastric epithelium. However, deficiency of the adaptor molecule myeloid differentiation primary response 88 (MyD88), which signals through NF-κB, led to an accelerated development of gastric pathology upon H. felis infection, but the mechanisms leading to this phenotype remained elusive. Non-canonical NF-κB signaling was shown to aggravate H. pylori-induced gastric inflammation via activation of the lymphotoxin β receptor (LTβR). In the present study, we explored whether the exacerbated pathology observed in MyD88-deficient (Myd88−/−) mice was associated with aberrant activation of non-canonical NF-κB. Our results indicate that, in the absence of MyD88, H. felis infection enhances the activation of non-canonical NF-κB that is associated with increase in Cxcl9 and Icam1 gene expression and CD3+ lymphocyte recruitment. In addition, activation of signal transducer and activator of transcription 3 (STAT3) signaling was higher in Myd88−/− compared to wild type (WT) mice, indicating a link between MyD88 deficiency and STAT3 activation in response to H. felis infection. Thereby, MyD88 deficiency results in accelerated and aggravated gastric pathology induced by Helicobacter through activation of non-canonical NF-κB.

Potential Role of Biofilm Formation in the Development of Digestive Tract Cancer With Special Reference to Helicobacter pylori Infection.

Bacteria are highly social organisms that communicate via signaling molecules and can assume a multicellular lifestyle to build biofilm communities. Until recently, complications from biofilm-associated infection have been primarily ascribed to increased bacterial resistance to antibiotics and host immune evasion, leading to persistent infection. In this theory and hypothesis article we present a relatively new argument that biofilm formation has potential etiological role in the development of digestive tract cancer. First, we summarize recent new findings suggesting the potential link between bacterial biofilm and various types of cancer to build the foundation of our hypothesis. To date, evidence has been particularly convincing for colorectal cancer and its precursor, i.e., polyps, pointing to several key individual bacterial species, such as Bacteroides fragilis, Fusobacterium nucleatum, and Streptococcus gallolyticus subsp. Gallolyticus. Then, we further extend this hypothesis to one of the most common bacterial infection in humans, Helicobacter pylori (Hp), which is considered a major cause of gastric cancer. Thus far, there has been no direct evidence linking in vivo Hp gastric biofilm formation to gastric carcinogenesis. Yet, we synthesize the information to support an argument that biofilm associated-Hp is potentially more carcinogenic, summarizing biological characteristics of biofilm-associated bacteria. We also discuss mechanistic pathways as to how Hp or other biofilm-associated bacteria control biofilm formation and highlight recent findings on Hp genes that influence biofilm formation, which may lead to strain variability in biofilm formation. This knowledge may open a possibility of developing targeted intervention. We conclude, however, that this field is still in its infancy. To test the hypothesis rigorously and to link it ultimately to gastric pathologies (e.g., premalignant lesions and cancer), studies are needed to learn more about Hp biofilms, such as compositions and biological properties of extracellular polymeric substance (EPS), presence of non-Hp microbiome and geographical distribution of biofilms in relation to gastric gland types and structures. Identification of specific Hp strains with enhanced biofilm formation would be helpful not only for screening patients at high risk for sequelae from Hp infection, but also for development of new antibiotics to avoid resistance, regardless of its association with gastric cancer.

Mutated Rnf43 Aggravates Helicobacter Pylori-Induced Gastric Pathology.

The E3 ubiquitin ligase ring finger protein 43 (RNF43) is frequently mutated in gastric tumors and loss of RNF43 expression was suggested to be one of the key events during the transition from adenoma to gastric carcinoma. Functional studies on RNF43 have shown that it acts as a tumor suppressor by negatively regulating Wnt signaling. Interestingly, we observed that RNF43H292R/H295R mice bearing two point mutations in the ring domain displayed thickening of the mucosa at early age but did not develop neoplasia. In this study, we infected these mice for 6 months with Helicobacter pylori, which has been described as one of the major risk factors for gastric cancer. Mice bearing mutant RNF43H292R/H295R showed higher gastritis scores upon H. pylori infection compared to wild-type mice, accompanied by increased lymphocyte infiltration and Ifng levels. Furthermore, infected Rnf43 mutant mice developed atrophy, hyperplasia and MUC2 expressing metaplasia and displayed higher levels of the gastric stem cell marker CD44 and canonical NF-κB signaling. In summary, our results show that transactivating mutations in the tumor suppressor Rnf43 can worsen H. pylori induced pathology.

ARTICLE PARTIAL RETRACTION] PREVALENCE OF HELICOBACTER PYLORI INFECTION IN DYSPEPTIC PATIENTS AND ITS ASSOCIATION WITH CLINICAL RISK FACTORS FOR DEVELOPING GASTRIC ADENOCARCINOMA.

In Brazil, particularly in the underdeveloped localities, the prevalence of Helicobacter pylori (H. pylori) infections can range up to 90%. These rates are higher in older individuals and vary by country region. H. pylori infections are linked to the development of gastric pathologies, namely mild to moderate gastritis, gastroenteritis, peptic ulcer, intestinal metaplasia, and gastric cancer. In 1994, this organism was classified by the International Agency for Research on Cancer (IARC) as pertaining to the Group 1 carcinogen for gastric adenocarcinoma etiology. Gastric cancer represents a significant public health problem, being the fourth most common malignant tumor and the second largest cause of cancer-related deaths. To investigate the prevalence of H. pylori infection in dyspeptic patients and determine the link between clinical risk factors and gastric adenocarcinoma diagnosis. Polymerase chain reaction (PCR) analysis was employed for molecular diagnosis of gastric tissue biopsies collected from 113 dyspeptic patients at the University Hospital of Federal University of Goiás. Molecular analyses allowed the identification of H. pylori infections. Furthermore, histopathological examinations were performed to determine the clinical risks of developing gastric malignancies. The test results identified 69 individuals older than 44 years, from 75 (66.4%) positive H. pylori infection samples. The prevalence of gastric adenocarcinoma in this study was 1.3%. Among the infected patients, six (8.2%) had high risk, and 67 (91.8%) had a low risk of developing gastric cancer (P<0.05). This study shows a high prevalence of H. pylori infection and identifies its contribution to gastric inflammations, which in the long term are manifested in high-risk clinical factors for the development of gastric adenocarcinoma.

Antibiotic Resistance Among Helicobacter pylori Strains Isolated from Patients with Gastric Pathologies Towards Metronidazole, Clarithromycin, and Ciprofloxacin

Background: The extent of antibiotic resistance among Helicobacter pylori strains influences current clinical therapeutic regimens in each region. Objectives: This cross-sectional study aimed to determine the resistance property and minimum inhibitory concentration (MIC50-90) of Helicobacter pylori strains toward metronidazole, clarithromycin, and ciprofloxacin in patients with distinct gastric histopathological changes in Tehran, Iran. Methods: This study was conducted on 170 patients suffering from gastric complications in three hospitals in Tehran from October 2014 until March 2015. Two separate biopsy samples were collected from each patient and used for pathological and microbiological examinations. Antimicrobial susceptibility tests were performed by agar dilution method according to the CLSI guidelines. The MIC values and susceptibility to varying concentrations of metronidazole (4 to 64 µg/mL), ciprofloxacin (0.5 to 16 µg/mL), and clarithromycin (0.25 to 16 µg/mL) were determined based on EUCAST recommendations. Results: Our results indicated the infection with H. pylori in a frequency of 32% (55/170) among the study patients (female, 51% and male, 49%). Endoscopic findings indicated that 42% of the patients suffered from peptic ulcers, 33% from duodenal ulcers, and 25% with a non-ulcer disease. Pathological findings indicated 58% of the patients had chronic gastritis, 33% had active chronic gastritis, and 9% suffered from intestinal metaplasia. In terms of antibiotic susceptibility, nearly 76.3%, 49%, and 45.5% of the strains were resistant to metronidazole, clarithromycin, and ciprofloxacin, respectively. The MIC values at which the growth of 50% and 90% of the strains was inhibited (MIC50-90) were 32 - 64 µg/mL for metronidazole, 0.5 - 16 µg/mL for clarithromycin, and 2 - 16 µg/mL for ciprofloxacin. Conclusions: The overall resistance levels were relatively high among the study patients. Accordingly, the administration of other anti-Helicobacter drugs, as well as more appropriate therapeutic regimens based on laboratory results, is recommended in patients with a history of treatment failure.

Tryptophan usage by Helicobacter pylori differs among strains

Because of its association with severe gastric pathologies, including gastric cancer, Helicobacter pylori has been subject of research for more than 30 years. Its capacity to adapt and survive in the human stomach can be attributed to its genetic flexibility. Its natural competence and its capacity to turn genes on and off allows H. pylori to adapt rapidly to the changing conditions of its host. Because of its genetic variability, it is difficult to establish the uniqueness of each strain obtained from a human host. The methods considered to-date to deliver the best result for differentiation of strains are Rapid Amplification of Polymorphic DNA (RAPD), Multilocus Sequence Typing (MLST) and Whole Genome Sequencing (WGS) analysis. While RAPD analysis is cost-effective, it requires a stable genome for its reliability. MLST and WGS are optimal for strain identification, however, they require analysis of data at the bioinformatics level. Using the StainFree method, which modifies tryptophan residues on proteins using 2, 2, 2, - trichloroethanol (TCE), we observed a strain specific pattern of tryptophan in 1D acrylamide gels. In order to establish the effectiveness of tryptophan fingerprinting for strain identification, we compared the graphic analysis of tryptophan-labelled bands in the gel images with MLST results. Based on this, we find that tryptophan banding patterns can be used as an alternative method for the differentiation of H. pylori strains. Furthermore, investigating the origin for these differences, we found that H. pylori strains alters the number and/or position of tryptophan present in several proteins at the genetic code level, with most exchanges taking place in membrane- and cation-binding proteins, which could be part of a novel response of H. pylori to host adaptation.

Weight Loss After Bariatric Surgery Predicts an Improvement in the Non-alcoholic Fatty Liver Disease (NAFLD) Fibrosis Score.

Non-alcoholic fatty liver disease (NAFLD) is present in up to 90% of bariatric surgery patients. Previous literature has demonstrated an improvement in liver steatosis and fibrosis in post-bariatric surgery patients. Our study aims to investigate if bariatric surgery results in an improvement in NAFLD fibrosis scores, and if this correlates with weight loss. A retrospective study was conducted on all patients who underwent bariatric surgery from 2010 to 2016 in our institution. Patients who had a redo bariatric surgery or concomitant gastric pathologies were excluded. Indications for bariatric surgery followed the Asia-Pacific Metabolic and Bariatric Surgery Society guidelines. There were 192 patients in this study, with the majority being females (n = 120, 63%). Mean age was 42.7 ± 10.2years old. Pre-operative mean weight and body mass index (BMI) were 113 ± 27.9kg and 41.6 ± 7.98kg/m2 respectively. The mean pre-operative NAFLD fibrosis score was - 1.27. Six-month and 1-year follow-up post-surgery demonstrated a decrease in mean weight to 90.6 and 85.9kg and a decrease in mean BMI to 33.8 and 31.6kg/m2. Mean NAFLD scores improved from - 1.27 to - 1.56 to - 2.00. The correlation between weight loss and NAFLD fibrosis score improvement was statistically significant at the first post-operative year (r-coefficient = 0.36, p value ≤ 0.001). Bariatric surgery results in weight reduction as well as an improvement in the NAFLD fibrosis score. The degree of weight loss predicts the extent of improvement in NAFLD fibrosis scores. More long-term studies need to be conducted to assess if this effect is permanent.

Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of Hpylori Infection.

Background & AimsEpithelial cells are joined by tight junctions (TJs) to form a cell sheet. In the stomach, epithelial cell sheet forms an essential barrier against gastric material, including gastric acid. Although the decreased expression of stomach-type claudin-18 (stCldn18), a TJ protein, is generally observed in human gastritis and gastric cancer, its pathological roles are not fully understood. We previously reported that mice lacking stCldn18 (stCldn18-/-) exhibit gastric acid leakage through TJs, which induces active gastritis at a young age. Here, we examined the gastric pathologies in mice after long-term stCldn18 deficiency.MethodsThe gastric pathologies in stCldn18-/- mice were sequentially analyzed from youth to old age, and compared to those in humans. To examine the relationship between stCldn18 deficiency-induced gastric pathologies and Wnt-dependent tumorigenesis, we generated Wnt1-overexpressing stCldn18-/- mice.ResultsStCldn18-/- mice developed chronic active gastritis at middle age, with expression of the chemoattractant CCL28. At old age, 20-30% of these mice developed gastric tumors with CXCL5 expression, indicative of EMT. In this process, spasmolytic polypeptide-expressing metaplasia (SPEM) cells appeared. Increased expressions of CD44-variants, TLR2, and CXCL5 indicated age-dependent changes in cell characteristics. Some features of the stCldn18-/- mouse gastric tumorigenesis resembled H pylori-infection-related human carcinogenesis. The gastric tumorigenesis was accelerated in Wnt1-overexpressing stCldn18-/- mice, indicating that Wnt is involved in the stCldn18-/- mouse gastric tumorigenesis.ConclusionsStCldn18 deficiency induced gastric tumorigenesis in mice without H pylori infection. Our findings revealed that several signaling networks, including the cytokine-, stemness-, and Wnt-signaling pathways, may be activated under the stCldn18-deficiency-induced chronic active gastritis to accelerate the gastric tumorigenesis.

Helicobacter pylori infection coexisting with intestinal metaplasia is not associated with colorectal neoplasms.

IntroductionColorectal cancer is one of the most common cancers and is a major cause of morbidity and mortality in the world and our country. Studies have indicated that there might be a relationship between Helicobacter pylori (Hp) and colorectal neoplasia (CN), although others have not found any relationship.AimTo determine whether there is a potential relationship between Hp and CN in our patients.Material and methodsA total of 314 patients, aged 16–86 years, who underwent gastroscopy and colonoscopy at our department between 2015 and 2017 were evaluated retrospectively. The age, gender, endoscopy results, presence of Hp, complete blood count (CBC), vitamin B12, folic acid, C-reactive protein (CRP), and sedimentation levels of the patients were examined.ResultsCBC, ferritin, vitamin B12, and CRP measurements did not show statistical significance in terms of the presence of Hp (p > 0.05). Folate values of Hp-positive patients were significantly lower than Hp-negative patients (p = 0.007; p < 0.01). No significant relationship was detected between Hp and colon cancer (p > 0.05). Adenomatous polyps were not related to Hp (p > 0.05). Correlation between intestinal metaplasia (IM) and adenomatous polyps was insignificant. There was no statistically significant difference between colon and gastric pathology results.ConclusionsIn our study, no significant relationship was noted between Hp and CN. A few studies have been conducted in our country, and our results are consistent with some of these studies while it is contradictory to others. Large populational multicentre studies are needed in order to identify the relationship between Hp and CN.

Immune Cell Signaling by Helicobacter pylori: Impact on Gastric Pathology.

Helicobacter pylori represents a highly successful colonizer of the human stomach. Infections with this Gram-negative bacterium can persist lifelong, and although in the majority of cases colonization is asymptomatic, it can trigger pathologies ranging from chronic gastritis and peptic ulceration to gastric cancer. The interaction of the bacteria with the human host modulates immune responses in different ways to enable bacterial survival and persistence. H. pylori uses various pathogenicity-associated factors such as VacA, NapA, CGT, GGT, lipopolysaccharide, peptidoglycan, heptose 1,7-bisphosphate, ADP-heptose, cholesterol glucosides, urease and a type IV secretion system for controlling immune signaling and cellular functions. It appears that H. pylori manipulates multiple extracellular immune receptors such as integrin-β2 (CD18), EGFR, CD74, CD300E, DC-SIGN, MINCLE, TRPM2, T-cell and Toll-like receptors as well as a number of intracellular receptors including NLRP3, NOD1, NOD2, TIFA and ALPK1. Consequently, downstream signaling pathways are hijacked, inducing tolerogenic dendritic cells, inhibiting effector T cell responses and changing the gastrointestinal microbiota. Here, we discuss in detail the interplay of bacterial factors with multiple immuno-regulatory cells and summarize the main immune evasion and persistence strategies employed by H. pylori.

Impact of Helicobacter pylori Virulence Factors on the Host Immune Response and Gastric Pathology.

Helicobacter pylori chronically infects nearly half the world's population, yet most of those infected remain asymptomatic throughout their lifetime. The outcome of infection-peptic ulcer disease or gastric cancer versus asymptomatic colonization-is a product of host genetics, environmental influences, and differences in bacterial virulence factors. Here, we review the current understanding of the cag pathogenicity island (cagPAI), the vacuolating cytotoxin (VacA), and a large family of outer membrane proteins (OMPs), which are among the best understood H. pylori virulence determinants that contribute to disease. Each of these virulence factors is characterized by allelic and phenotypic diversity that is apparent within and across individuals, as well as over time, and modulates inflammation. From the bacterial perspective, inflammation is probably a necessary evil because it promotes nutrient acquisition, but at the cost of reduction in bacterial load and therefore decreases the chance of transmission to a new host. The general picture that emerges is one of a chronic bacterial infection that is dependent on both inducing and carefully regulating the host inflammatory response. A better understanding of these regulatory mechanisms may have implications for the control of chronic inflammatory diseases that are increasingly common causes of human morbidity and mortality.

Ultrasound in functional GI disorders

There are great advantages using ultrasound generating high temporal resolution enabling detailed imaging of dynamic sequences and local contractility with involvement of various GI wall layers, even compared to CT, MR, SPECT and PET imaging. The aim of this presentation is to show how advanced imaging can disclose organic and functional behaviour of the GI tract, often adding information about contractility, intestinal content and propulsion, meal distribution and accommodation of the stomach. Ultrasound of the stomach was initially performed to detect and investigate organic diseases of the gastric wall. Subsequently, different methods were developed to study functional aspects of gastric pathology. Ultrasound can be used to evaluate antral contractility, gastric emptying, transpyloric flow, gastric configuration, intragastric distribution of meals, gastric accommodation and strain of the gastric wall. Advanced methods for 3D ultrasound imaging and tissue Doppler (Strain Rate Imaging) have also been developed to study configuration and motility of the stomach. Furthermore, anaesthesiologists are now using ultrasound to estimate gastric content prior to surgery to assess risk of aspiration during the procedure. Moreover, adding contrast agents or elastography to the examination may further increase diagnostic yield. Ultrasound of the duodenum, jejunum, ileum and colon may also provide important clinical information about motility in diseases like coeliac, crohns, and GUCY-2C mutations.

Helicobacter pylori-related gastric corpus pathological changes in obese patients referred for laparoscopic sleeve gastrectomy

Background Obesity is a serious health problem worldwide and laparoscopic sleeve gastrectomy (LSG) is a therapeutic option in obese patients. Helicobacter pylori infection increases the risk for gastric pathology and plays a role in limiting access to bariatric surgery. This study aimed to evaluate prevalence of different histopathologic changes in LSG, including H. pylori and non-H. pylori gastritis in the gastrectomy specimens and risk factors associated.Materials and methods Sleeve gastrectomy specimens (542 patients) were examined histopathologically for detection of different histopathologic changes and presence of H. pylori, which was confirmed with Giemsa stain. Assessment of association of different risk factors with frequent histopathologic changes was done. Lastly, we examined the agreement of histopathology and serology methods for H. pylori diagnosis.Results The results demonstrated a relatively high H. pylori infection (38.7%), and it was significantly associated with chronic active gastritis, chronic superficial gastritis, and follicular gastritis (P<0.001). The serological diagnosis has sensitivity of 64.4% and specificity of 79.6%.Conclusion Routine histopathological biopsies with LSG are useful in detection of different histopathological changes, including H. pylori infection, which may affect the prognosis of the surgery. Biopsy is still to be preferred to serology as a detection method for H. pylori infection.

Epidemiology, Diagnosis and Risk Factors of Helicobacter pylori Infection.

Helicobacter pylori is a human-specific pathogen, which leads to gastric pathologies including gastric cancer. It is a highly unique bacterium considered as a carcinogenic agent. H. pylori remains a major human health problem, responsible for ~90% of the gastric cancer cases. Approximately four billion individuals have been detected for H. pylori infection worldwide in 2015. At the turn of the twenty-first century, the prevalence of H. pylori has been declining in highly industrialized countries of the Western world, whereas prevalence has plateaued at a high level in developing and newly industrialized countries. However, the infection status remains high in immigrants coming from countries with high prevalence of H. pylori infection. H. pylori can be diagnosed both by invasive and non-invasive methods. Urea breath test and stool antigens detection are among the most commonly used non-invasive ones. Although the way H. pylori is transmitted remains still not fully clear, the level of contamination is strongly dependent on the familial and environmental context, with a drastic impact of living conditions with poor hygiene and sanitation. However, familial socioeconomic status is the main risk factor for H. pylori infection among children. In addition, food and water source have a high impact on the prevalence of H. pylori infection worldwide. This chapter highlights the latest knowledge in the epidemiology of H. pylori infection, its diagnosis and critical risk factors responsible for its high prevalence in some populations and geographic areas.

Demonstration of the Capabilities of Transabdominal Ultrasonography in Assessment of Structures and Functional Disorders of Locally Advanced Gastric Cancer of Diverse Localization

Introduction: Ultrasound study of locally advanced gastric cancer that has spread to adjoining tissue and lymph nodes. This tumor can be associated with T2 to T4 stages of cancer. A “Locally advanced gastric cancer” is a tumor, which may be categorized as ‘resectable’ cancer when compared with M1 advanced cancer. Objective: The aim of this study was to evaluate the Capabilities of transabdominal ultrasonography in assessment of structures and functional disorders of the locally advanced gastric cancer of diverse localization Materials and Methods: A total of61 patients with locally advanced gastric cancer were analyzed of which 36 (59,0%) were males (mean age 62.7 years) and 25 (41,0%) were females (mean age 59.3 years). All patients were managed surgically and underwent preoperative X-ray, virtual gastroscopy techniques, multidetector computed tomography and transabdominal ultrasonography (USG). Histopathology results found, in 58 (95,1%) cases adenocarcinoma, in 3 (4,9%) – ring-cell carcinoma (cricoidal) gastric cancer was established. Stage T2 was diagnosed in 16 (26.2%) cases, T3 - in 41 (67.2%) cases, T4 - in 4 (6.6%) cases. The stomach tumor in 29 (47.5%) cases was localized mainly in the antrum, 27 (44.3%) – in the body, 5 (8.2%) in the cardia and fundus (Table 1). In 24 (39,3%) cases, pyloric stenos was diagnosed - of which in 6 (9,8%) it was compensated, in 18 (29,5%) - sub compensated. All patients underwent preoperative X-ray, virtual gastroscopy techniques, multidetector computed tomography and transabdominal ultrasonography (USG). Normal ultrasound features were observed in 35 patients without gastric pathology. Ultrasonography was carried out with the convex and micro convex transducers in the frequency range of 2-5 MHz and 4-7 MHz respectively in B and color Doppler modes. Results: The polypoid type of gastric cancer was detected in 3 (4,9±2,8%) cases, the ulcerative type – in 18 (29,5±5,8%), the infiltrative ulcerative type – in 27 (44,3±6,4%) and the diffuse infiltrative type – in 13 (21,3%±5,2%) cases respectively. In 24 (39,3%) cases, pyloric stenos was diagnosed - of which in 6 (9,8%) it was compensated, in 18 (29,5%) – sub compensated. The layers of the gastric wall were not differentiated in all patients with sub compensated pyloric stenos. The gastric wall thickness of the affected area was 10,2±2,9mm in the case compensated pyloric stenosis, the length was 27,1±6,2mm, the diameter of the pylorus was 8,3±0,8mm. Among patients with sub compensated pyloric stenos, the thickness of the gastric wall was 19,8±4,1mm, the length was 43,6±4,5mm, the pyloric diameter was 4,3±1,1mm. Among the 61 patients studied, pathological vascularization was detected in 42 (68.8%) cases. It was observed that, all 4 (6.5%) patients with gastric cancer were stage T4 and 38 (62.3%) were stage T3. Vascularization was weak in 13 cases, in 24 cases - moderate, and in 5 cases - enhanced. Metastases to the regional lymph nodes were diagnosed in 52 cases. Ultrasonographically, they were detected only in 37 (71.2%) cases. Conclusions: In the diagnosis of locally advanced gastric cancer, ultrasonography demonstrates good capabilities for determining the extent and depth of the affected area. Color doppler mode allows the study of vascularisation of a locally thickened area, as well as nearby enlarged lymph nodes, which is very important to ascertain the degree of malignancy of the hyperplastic process. ltrasonography can independently determine the degree of pyloric stenosis in patients with distal gastric cancer.

GASTRIC PATHOLOGY

Objectives: To determine the frequency &amp; histopathological type of gastric pathology in individuals presenting with epigastric pain. Period: Six months from July to Dec 2017. Study Design: Cross sectional study. Setting: Department of Gastroenterology, Liaquat National Hospital Institute for Postgraduate Medical Studies and Health Sciences, Karachi. Patients and Methods: The total of 333 patients had history of epigastric pain were included in this study. The specimen for mucosal biopsy was taken during endoscopy and sent to the clinical laboratory for histopathology examination for the classification. All the information was entered and saved on the annexed / proforma. Results: The mean ±SD of age for all thepatients was 41.31±7.89 years. Frequency of gastric pathology in patient presenting with epigastric pain was 51.35% (171/333) cases. There were 171 histopatholocal diagnoses, non-Noeplastic lesion was confirmed in 99.42% (170/177) and one case had Noeplastic lesion. Regarding the type of gastric pathology, 25.73 % (44/171) had gastric ulcer, 48.54 (83/171) was H. pylori gastric and 25.15% (43/171) had chronic gastritis. Conclusion: The study frequency of gastric pathology in patient presenting with epigastric pain was high.