Helicobacter Pylori Colonization Research Articles

The Efficacy of Pre-Treatment Proton Pump Inhibitors in the Eradication of Helicobacter pylori

Objective: Proton pump inhibitors significantly reduce Helicobacter pylori colonization and provide recovery in its activity and inflammation. We investigated; the effects of eradication initiated 28 days after proton pump inhibitor treatment and eradication initiated simultaneously with proton pump inhibitor treatment, on treatment success rates of Helicobacter pylori. Material and Methods: The study took place at our tertiary care hospital, where 42 patients in the study group were given oral lansoprazole treatment for 28 days followed by eradication treatment and 41 patients in the control group were given both treatments simultaneously. Eradication success was monitored using Helicobacter pylori polyclonal antigen stool tests. Results: A total of 83 participants, aged between 8 and 18 years, tested positive for Helicobacter pylori. The mean age of the participants was 15.14 ± 2.01 years. The Helicobacter pylori cure rate was found to be 92.9% in the study group and 92.7% in the control group. There were no significant differences observed between the two groups in terms of eradicating Helicobacter pylori (p=0.976). Conclusion: We found no significant differences in Helicobacter pylori treatment success rates with modified proton pump inhibitor usage in children.

Consumption of non-antibacterial drugs may have negative impact on Helicobacter pylori colonization in the stomach

BackgroundNineteen non-antibacterials were examined to show that their consumption for treatment of other diseases may inhibit Helicobacter pylori. Four antibiotics were used for comparison. Materials and methodsAgar dilution method was used to examine the susceptibility of 20 H. pylori isolates to 4 antibiotics; metronidazole (MTZ), clarithromycin (CLR), amoxicillin (AMX), tetracycline (TET) and 19 non-antibacterials; proton pump inhibitors (PPIs), H2-blockers, bismuth subsalicylate (BSS), antifungals, statins, acetaminophen (ACE), aspirin (ASA), B-vitamins (B-Vits; Vit B1, Vit B6 and Vit Bcomplex) and vitamin C (Vit C). Blood agar plates were prepared with different concentrations of drugs and spot-inoculated with bacterial suspensions. Plates were incubated at 37 °C under microaerobic conditions and examined after 3–5 days. The isolate #20 that was mucoid and resistant to 19 drugs, including MTZ and SMV was tested against combined MTZ (8 μg/mL) and SMV (100 μg/mL). Results were analyzed statistically. ResultsMinimum inhibitory concentrations (MICs, μg/mL) of drugs and the frequency of susceptible H. pylori were determined as MTZ (8, 80%), CLR (2, 90%), AMX (1, 100%), TET (0.5, 70%), PPIs (8–128, 80%), H2-blockers (2000–8000, 75–80%), BSS (15, 85%), antifungals (64–256, 30–80%), statins (100–250, 35–90%), ACE (40, 75%), ASA (800, 75%), B-Vits (5000–20000, 80–100%) and Vit C (2048, 85%). Susceptibility of H. pylori isolates to 16 out of 19 non-antimicrobials (75–100%) was almost similar to those of antibiotics (70–100%) (P-value >0.05). The highest susceptibility rate (100%) belonged to Vit B1, Vit B6 and AMX. Out of 20 H. pylori isolates, 17 (85%) were susceptible to ≥13 non-antimicrobials and 3 (15%) were susceptible to < 13 (P-value <0.05). Mucoid H. pylori showed susceptibility to combination of MTZ and SMV. ConclusionsMost of non-antibacterials inhibited H. pylori isolates, similar to antibiotics but their MICs exceeded those of antibiotics and their plasma concentrations. At low plasma concentration, non-antimicrobials may act as weak antibacterials, antibiotic adjuvants and immunostimulators.

Impact of Helicobacter pylori colonization density and depth on gastritis severity

Background and objectivesHelicobacter pylori (H. pylori) infection is the most common etiology of chronic gastric. H. pylori gastritis would gradually evolve into gastric atrophy, intestinal metaplasia, dysplasia and malignant lesions. Herein, this study aimed to investigate the potential impact of H. pylori colonization density and depth on the severity of histological parameters of gastritis.MethodsA prospective monocentric study was conducted from December 2019 to July 2022, enrolling patients with confirmed chronic H. pylori infection via histopathological evaluation. H. pylori colonization status was detected by immunohistochemical staining, pathological changes of gastric specimens were detected by hematoxylin eosin staining. Epidemiological, endoscopic and histopathological data were collected.ResultsA total of 1120 patients with a mean age of 45.8 years were included. Regardless of the previous history of H. pylori eradication treatment, significant correlations were observed between the density and depth of H. pylori colonization and the intensity of gastritis activity (all P < 0.05). Patients with the lowest level of H. pylori colonization density and depth exhibited the highest level of mild activity. In whole participants and anti-H. pylori treatment-naive participants, H. pylori colonization density and depth were markedly correlated with the severity of chronic gastritis and gastric atrophy (all P < 0.05). H. pylori colonization density (P = 0.001) and depth (P = 0.047) were significantly associated with ulcer formation in patients naive to any anti-H. pylori treatment. No significant associations were observed between the density and depth of H. pylori colonization and other histopathological findings including lymphadenia, lymphoid follicle formation and dysplasia.ConclusionsAs the density and depth of H. pylori colonization increased, so did the activity and severity of gastritis, along with an elevated risk of ulcer formation.

Assessment of helicobacter pylori colonization in patients with duodenogastric reflux: A retrospective study

Assessment of helicobacter pylori colonization in patients with duodenogastric reflux: A retrospective study

Lactobacillus acidophilus NCFM and Lactiplantibacillus plantarum Lp-115 inhibit Helicobacter pylori colonization and gastric inflammation in a murine model.

To determine the role of Lactobacillus strains and their combinations in inhibiting the colonization of H. pylori and gastric mucosa inflammation. Human gastric adenocarcinoma AGS cells were incubated with H. pylori and six probiotic strains (Lactobacillus acidophilus NCFM, L. acidophilus La-14, Lactiplantibacillus plantarum Lp-115, Lacticaseibacillus paracasei Lpc-37, Lacticaseibacillus rhamnosus Lr-32, and L. rhamnosus GG) and the adhesion ability of H. pylori in different combinations was evaluated by fluorescence microscopy and urease activity assay. Male C57BL/6 mice were randomly divided into five groups (uninfected, H. pylori, H. pylori+NCFM, H. pylori+Lp-115, and H. pylori+NCFM+Lp-115) and treated with two lactobacilli strains (NCFM and Lp-115) for six weeks. H. pylori colonization and tissue inflammation statuses were determined by rapid urease test, Hematoxylin-Eosin (HE) staining, immunohistochemistry, and qRT-PCR and ELISA. L. acidophilus NCFM, L. acidophilus La-14, L. plantarum Lp-115, L. paracasei Lpc-37, L. rhamnosus Lr-32, and L. rhamnosus GG reduced H. pylori adhesion and inflammation caused by H. pylori infection in AGS cells and mice. Among all probiotics L. acidophilus NCFM and L. plantarum, Lp-115 showed significant effects on the H. pylori eradication and reduction of inflammation in-vitro and in-vivo. Compared with the H. pylori infection group, the mRNA and protein expression levels of IL-8 and TNF-α in the six Lactobacillus intervention groups were significantly reduced. The changes in the urease activity (ureA and ureB) for 1-7h in each group showed that L. acidophilus NCFM, L. acidophilus La-14, L. plantarum Lp-115, and L. rhamnosus GG effectively reduced the colonization of H. pylori. We observed a higher ratio of lymphocyte and plasma cell infiltration into the lamina propria of the gastric mucosa and neutrophil infiltration in H. pylori+NCFM+Lp-115 mice. The infiltration of inflammatory cells in lamina propria of the gastric mucosa was reduced in the H. pylori+NCFM+Lp-115 group. Additionally, the expression of IFN-γ was decreased significantly in the NCFM and Lp-115 treated C57BL/6 mice. L. acidophilus NCFM and L. plantarum Lp-115 can reduce the adhesion of H. pylori and inhibit the gastric inflammatory response caused by H. pylori infection.

Potential therapeutic benefit of ursodeoxycholic acid in the management of non hepato-biliary upper gastrointestinal disorders.

To examine the potential therapeutic effects of ursodeoxycholic acid (UDCA) on diseases of the esophagus, stomach, and duodenum. A search was conducted using EBSCO, Medline, PubMed, Google Scholar and Web of Science as well as international guidelines using MESH terms for treatment of UDCA for diseases of the upper gastrointestinal disorders in adult humans without regard to publication language or date restrictions. A total of 256 articles and 22 guidelines were initially identified, and 221 were excluded. Final revision of 13 articles and 22 guidelines confirmed that UDCA is found to have a cytoprotective role in Barret's esophagus within esophageal disorders, improves abdominal pain in functional dyspepsia, and does not alter Helicobacter pylori colonization or inflammation. Conflicting results are noted regarding the role of UDCA in the duodenum as chemopreventive treatment for familial adenomatous polyposis, with polyps regressing and their growth characteristics improving with low doses (10-25mg/kg/day). On the contrary, no positive effect was noted upon the combination with Celecoxib and with doses of 1000-2000mg or 20-30mg/kg/d. Gastrointestinal side effects were predominantly reported. No side effects necessitated hospitalization or ICU admission. Ursodeoxycholic acid has a limited therapeutic role in functional dyspepsia. There is promising evidence that it may serve as a chemopreventive for Familial adenomatous polyposis and Barret's esophagus, although further research is needed to confirm these findings.PROSPERO No.: CRD 42021267689.

Helicobacter pylori kolonizasyon yoğunluğu çölyak hastalığının gelişmesinde önemli rol oynayabilir

Background and Aims: The aim of this study was to investigate the relationship between celiac disease and Helicobacter pylori infection and to compare the severity of celiac disease and Helicobacter pylori infection in adults according to the modified Marsh score.&#x0D; Materials and Methods: This study included 148 patients with celiac disease and 240 control patients without celiac disease who underwent endoscopy for various reasons in a tertiary hospital. Age, gender, endoscopy indications, descriptive characteristics, complaints, serological, endoscopic and histopathological findings of the patients were recorded and analyzed. Results: Helicobacter pylori colonization in the celiac disease patients was 43.9% and in control group was 57.5% (p = 0.009). Helicobacter pylori positivity rate was significantly lower in Marsh 2, 3A, 3B, 3C groups ( p = 0.04). Pearson correlation analysis revealed a significant but weak negative relationship between the severity of Helicobacter pylori and celiac disease (r = -.109, p = 0.031). When Marsh score was increasing, Helicobacter pylori grade decreased. Conclusion: The current study indicated that the incidence of Helicobacter pylori infection was lower in adults with celiac disease compared to control patients, and Helicobacter pylori colonization density was associated with milder duodenal lesions in celiac patients. Helicobacter pylori colonization may have a protective role in the development of celiac disease.

Delivering a toxic metal to the active site of urease.

Urease is a nickel (Ni) enzyme that is essential for the colonization of Helicobacter pylori in the human stomach. To solve the problem of delivering the toxic Ni ion to the active site without diffusing into the cytoplasm, cells have evolved metal carrier proteins, or metallochaperones, to deliver the toxic ions to specific protein complexes. Ni delivery requires urease to form an activation complex with the urease accessory proteins UreFD and UreG. Here, we determined the cryo-electron microscopy structures of H. pylori UreFD/urease and Klebsiella pneumoniae UreD/urease complexes at 2.3- and 2.7-angstrom resolutions, respectively. Combining structural, mutagenesis, and biochemical studies, we show that the formation of the activation complex opens a 100-angstrom-long tunnel, where the Ni ion is delivered through UreFD to the active site of urease.

25-hydroxyvitamin D levels in children of different ages and with varying degrees of Helicobacter pylori infection and immunological features.

Helicobacter pylori (HP) is a major cause of upper digestive tract diseases. However, the relationship between HP infection and 25-hydroxyvitamin D [25(OH)D] levels in children has not been fully elucidated. This study investigated the levels of 25(OH)D in children of different ages and with varying degrees of HP infection and immunological features as well as the correlations between 25(OH)D levels in children infected with HP and their ages and degrees of infection. Ninety-four children who underwent upper digestive endoscopy were divided into an HP-positive group without peptic ulcers (Group A), an HP-positive group with peptic ulcers (Group B) and an HP-negative control group (Group C). The serum levels of 25(OH)D and immunoglobulin and the percentages of lymphocyte subsets were determined. HP colonization, the degree of inflammation, and the degree of activity were further evaluated by HE staining and immunohistochemical staining in gastric mucosal biopsy. The 25(OH)D level of the HP-positive groups (50.93 ± 16.51 nmol/L) was significantly lower than that of the HP-negative group (62.89 ± 19.18 nmol/L). The 25(OH)D level of Group B (47.79 ± 14.79 nmol/L) was lower than that of Group A (51.53 ± 17.05 nmol/L) and was significantly lower than that of Group C (62.89 ± 19.18 nmol/L). The 25(OH)D level decreased with increasing age, and there was a significant difference between Group C subjects who were ≤5 years old and those who were aged 6-9 years and ≥10 years. The 25(OH)D level was negatively correlated with HP colonization (r = -0.411, P < 0.01) and the degree of inflammation (r = -0.456, P < 0.01). The percentages of lymphocyte subsets and immunoglobulin levels among Groups A, B and C were not significantly different. The 25(OH)D level was negatively correlated with HP colonization and the degree of inflammation. As the age of the children increased, the level of 25(OH)D decreased, and the susceptibility to HP infection increased.

Detection of Helicobacter Pylori in Nasal Polyps: An Epidemiological Study

Many studies have described the detection of Helicobacter pylori (HP) in the nasal polyps; however, although gastroesophageal reflux has been associated with chronic rhinosinusitis and nasal polyps development, the role of HP remains unclear. Our aim was to describe the prevalence of HP detection in nasal polyps and its association with gastric HP infection and gastroesophageal reflux dsease (GERD). The prospective study involved 36 patients with nasal polyps, who underwent to endoscopic surgery removal of nasal polyps. Before surgical procedure all patients were tested for gastric HP infection by 13 C-urea breath test, while tissue samples from nasal polyps were tested for HP detection, using rapid urease test (CLO test) and histological examination with Giemsa stain. All patients were asked about GERD-related symptoms. HP in nasal polyps was detected in 9 out of 36 patients (25%) using histological examination with Giemsa stain, while the detection rate of HP was 30.5% (11/36) using CLO test. Furthermore, 28 out of 36 patients (77.7%) had gastric HP infection. All patients with HP colonization in nasal polyps had gastric HP infection and all patients with HP in nasal polyps reported symptoms related to GERD. HP was detected in approximately one out of three patients in nasal polyps, while all patients with HP detection in nasal polyps had concurrently gastric HP infection and reported GERD-related symptoms, suggesting a gastro-nasal route of HP.

Metagenomic and single-cell RNA-Seq survey of the Helicobacter pylori-infected stomach in asymptomatic individuals.

Helicobacter pylori colonization of the gastric niche can persist for years in asymptomatic individuals. To deeply characterize the host-microbiota environment in H. pylori-infected (HPI) stomachs, we collected human gastric tissues and performed metagenomic sequencing, single-cell RNA-Seq (scRNA-Seq), flow cytometry, and fluorescent microscopy. HPI asymptomatic individuals had dramatic changes in the composition of gastric microbiome and immune cells compared with noninfected individuals. Metagenomic analysis uncovered pathway alterations related to metabolism and immune response. scRNA-Seq and flow cytometry data revealed that, in contrast to murine stomachs, ILC2s are virtually absent in the human gastric mucosa, whereas ILC3s are the dominant population. Specifically, proportion of NKp44+ ILC3s out of total ILCs were highly increased in the gastric mucosa of asymptomatic HPI individuals, and correlated with the abundance of selected microbial taxa. In addition, CD11c+ myeloid cells and activated CD4+ T cells and B cells were expanded in HPI individuals. B cells of HPI individuals acquired an activated phenotype and progressed into a highly proliferating germinal-center stage and plasmablast maturation, which correlated with the presence of tertiary lymphoid structures within the gastric lamina propria. Our study provides a comprehensive atlas of the gastric mucosa-associated microbiome and immune cell landscape when comparing asymptomatic HPI and uninfected individuals.

Biodegradable Guar-Gum-Based Super-Porous Matrices for Gastroretentive Controlled Drug Release in the Treatment of Helicobacter pylori: A Proof of Concept.

An increase in resistance to key antibiotics has made the need for novel treatments for the gastric colonization of Helicobacter pylori (H. pylori) a matter of the utmost urgency. Recent studies tackling this topic have focused either on the discovery of new compounds to ameliorate therapeutic regimes (such as vonoprazan) or the synthesis of gastroretentive drug delivery systems (GRDDSs) to improve the pharmacokinetics of oral formulations. The use of semi-interpenetrating polymer networks (semi-IPNs) that can act as super-porous hydrogels for this purpose is proposed in the present work, specifically those displaying low ecological footprint, easy synthesis, self-floating properties, high encapsulation efficiency for drugs such as amoxicillin (AMOX), great mucoadhesiveness, and optimal mechanical strength when exposed to stomach-like fluids. To achieve such systems, biodegradable synthetic copolymers containing acid-labile monomers were prepared and interpenetrated with guar gum (GG) in a one-pot polymerization process based on thiol-ene click reactions. The resulting matrices were characterized by SEM, GPC, TGA, NMR, and rheology studies, and the acidic hydrolysis of the acid-sensitive polymers was also studied. Results confirm that some of the obtained matrices are expected to perform optimally as GRDDSs for the sustained release of active pharmaceutical ingredients at the gastrointestinal level, being a priori facilitated by its disaggregation. Therefore, the optimal performance of these systems is assessed by varying the molar ratio of the labile monomer in the matrices.

Does enteral nutrition through a percutaneous endoscopic gastrostomy, attenuate Helicobacter pylori colonization?: is it worth mentioning?

In patients who experience difficulties in oral feeding, alimentary intake can be supported by creating direct access into the stomach through a percutaneous endoscopic gastrostomy. The present study purposed to compare naïve and exchanged percutaneous endoscopic gastrostomy tubes in terms of Helicobacter pylori infection and other clinical characteristics. A total of 96 cases who underwent naïve or exchanged percutaneous endoscopic gastrostomy procedures with various indications were incorporated into the study. The patients' demographic data, such as age and gender, etiology of percutaneous endoscopic gastrostomy, anti-HBs status, Helicobacter pylori status, the presence of atrophy and intestinal metaplasia, biochemical parameters, and lipid profiles, had been analyzed. In addition, the anti-HCV and anti-HIV statuses had also been evaluated. The most common indication for percutaneous endoscopic gastrostomy placement was dementia in 26 (27.08%) cases (p=0.033). The presence of Helicobacter pylori positivity was significantly lower in the exchange group compared to the naïve group (p=0.022). Total protein, albumin, and lymphocyte levels were significantly higher in the exchange group compared to the naïve group (both p=0.001), and the mean calcium, hemoglobin, and hematocrit levels were statistically significantly higher in the exchange group (p<0.001). Preliminary outcomes of the present study revealed that enteral nutrition attenuates the incidence of Helicobacter pylori infection. Considering the acute-phase reactant, the significantly lower ferritin values in the exchange group suggest that there is no active inflammatory process in the patients and that immunity is sufficient.

Effect of gastric helicobacter pylori colonization in the development of erosive esophagitis in patients with hiatal hernia.

There may be various factors that determine gastroesophageal reflux disease (GERD) as a result of hiatal hernia (HH) (such as the size of the hernia, age, other host and environmental factors) and the presence of protective factors to explain the absence of reflux disease should not be ignored. Helicobacter pylori (Hp) infection can prevent the development of GERD or cause it. This study aimed to determine whether Hp colonized in the stomach and hernia affects the development of erosive esophagitis (EE) in patients with HH. In this case-controlled study, 111 patients with HH were eligible for the study. Study group with EE (n = 61, 55%) and control group without EE (n = 50, 45%) were formed. Groups were compared for gastric Hp and Hp in the hernia. While the frequency of Hp in the antrum was 55.7% in the group with EE, it was 30% in the control group (p = 0.01, OR: 2.94 in 95% CI 1.34-6.46). The rates in terms of HP frequency in the corpus were 43.6% and 32.1%, respectively, (p = 0.45). Hp colonization in HH was detected in 18 cases (29.50%) and 14 cases (28%), respectively, (p = 0.86). In regression analysis, antral Hp was found to be effective in the development of EE (p = 0.01). As a result of this study, we think that antral Hp may have a causative role in the development of reflux esophagitis, but the presence of Hp in HH does not have an effective role in reflux esophagitis formation.

Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling.

Helicobacter pylori colonization and persistence could precede gastric adenocarcinoma. Elucidating immune recognition strategies of H. pylori is therefore imperative to curb chronic persistence in the human host. Toll-like receptor 7 (TLR7) and TLR8 are widely known as viral single-stranded RNA (ssRNA) sensors yet less studied in the bacteria context. Here, we investigated the involvement of these receptors in the immunity to H. pylori. Human THP-1 monocytic cells were infected with H. pylori, and the expression levels of human Toll-like receptors (TLRs) were examined. The roles of TLR7 and TLR8 in response to H. pylori infection were further investigated using receptor antagonists. Among all TLR transcripts examined, TLR8 exhibited the most prominent upregulation, followed by TLR7 in the THP-1 cells infected with H. pylori J99 or SS1 strains. H. pylori infection-mediated IFN-α and IFN-β transactivation was significantly abrogated by the TLR7/8 (but not TLR7) antagonist. Additionally, TLR7/8 antagonist treatment reduced H. pylori infection-mediated phosphorylation of interferon regulatory factor 7 (IRF7). Our study suggests a novel role of TLR8 signaling in host immunity against H. pylori through sensing live bacteria to elicit the production of type I interferon.

S1407 Potential Therapeutic Benefit of Ursodeoxycholic Acid (UDCA) in the Management of Non-Hepato-Biliary Upper Gastrointestinal Disorders: A Systemic Review

Introduction: Ursodeoxycholic acid (UDCA) is a secondary bile acid with different therapeutic effects on the hepatobiliary tree. Little is known of the local effects of UDCA as a therapy of upper gastrointestinal tract disorders. These diseases that relate to acid peptic, inflammatory and premalignant etiologies in which gaps of the current treatment do exist. Our aim to search for UDCA therapeutic effect and review its role on the management effect of diseases of the esophagus, stomach and Duodenum if exist and describe its therapeutic potential. Methods: Search of Medline, PubMed, EBSO, Google Scholar, Web of Science and International guidelines using MESH terms describing therapy of UDCA for diseases of the upper gastrointestinal disorders in adult humans with no language or publication date restrictions. Results: A 256 articles and 22 guidelines initially identified, in whom 221 excluded, Final revision of 13 article and 22 guidelines showed that UDCA is found to have a cytoprotective role in Barret’s esophagus among esophageal disorders, it improves abdominal pain in functional dyspepsia and does not alter colonization of Helicobacter pylori and its inflammation. In the duodenum a conflicting result on the role of UDCA as chemoprevention for familial adenomatous polyposis, with regression of polyps and its growth characteristics with low doses used (10-25 mg/kg/day) alone. In contrary, no positive effect observed when combined with Celecoxib and with doses of 1000-2000 mg or 20-30 mg/kg/d. Side effects profile is predominantly related to Gastrointestinal side effects and no side effect attributed to morbidity or ICU admission. (Figure) (Table) Conclusion: UDCA has limited therapeutic role in few uncontrolled small studies for functional dyspepsia. Its chemopreventive role is promising for Familial adenomatous polyposis and Barret’s esophagus, await further studies to support these roles.Figure 1. Table 1. - Reported Side effects of UDCA use Type Events (n) Frequency Gastrointestinal • Abdominal Pain (1) 2.5 % • Anal and Perianal Pain (4) 10% • Heartburn (1) 2.5 % • Constipation (3) 7.5 % • Diarrhea (2) 5 % • Bloating (1) 2.5 % • Flatulence (1) 2.5 % • Nausea (1) 2.5 % • Vomiting (1) 2.5 % • Dyspepsia (3) 7.5 % • Terminal ileum Ulceration (1) 2.5 % • Elevated AST and GGT (1) 2.5 % Neurologic • Dizziness (1) 2.5 % • Mood alteration (1) 2.5 % • Neuropathy, Carpal tunnel syndrome (1) 2.5 % Renal • Lower urinary tract symptom, Prostatism (1) 2.5 % Skin • Hair loss (1) 2.5 % • Skin Rash (2) 5% Hematology • Anemia (1) 2.5 % • Leukopenia (1) 2.5 % Auditory • Otitis (1) 2.5 % Infection • Dental Infection (1) 2.5 % • Skin Infection (1) 2.5 % • Gastroenteritis (1) 2.5 % Lymphatics • Lower Limbs edema (2) 5% Metabolic • Hypokalemia (1) 2.5 % Constitutional • Fatigue (2) 5 % • Insomnia (1) 2.5 % Malignancy • Basal cell carcinoma, nose (1) 2.5 % Total Events (n) % 40

Diet and carcinogenesis of gastric cancer.

Several recent studies have corroborated a strong association between diet and gastric cancer risk; investigators have also identified dietary factors that protect against gastric cancer. This review summarizes the literature on this topic and guides future research directions. High-salt intake disrupts the gastric mucosal defense barrier, promoting Helicobacter pylori colonization and penetration of other carcinogenic compounds. Processed foods, processed meats, red meat, alcohol, foods with high dietary fat, and dietary cholesterol increase the risk of gastric carcinogenesis. On the other hand, increased consumption of fruits, vegetables, whole grains, nuts, and a low-salt diet may offer a protective effect. Despite decreases in gastric cancer incidence because of increased identification and treatment of H. pylori , gastric cancer remains one of the most common cancers worldwide with a high mortality rate. This disturbing statistic highlights the importance of reducing and eliminating other risk factors for gastric cancer. There is a strong body of evidence that alcohol, processed foods, high salt intake, high fat intake, and foods with animal products (meats, eggs, and dairy) increase the risk of gastric cancer. A diet that is high in whole grains, fruits, vegetables, nuts and is low in salt may reduce the risk of gastric cancer.

Host Cell Antimicrobial Responses against Helicobacter pylori Infection: From Biological Aspects to Therapeutic Strategies.

The colonization of Helicobacter pylori (H. pylori) in human gastric mucosa is highly associated with the occurrence of gastritis, peptic ulcer, and gastric cancer. Antibiotics, including amoxicillin, clarithromycin, furazolidone, levofloxacin, metronidazole, and tetracycline, are commonly used and considered the major treatment regimens for H. pylori eradication, which is, however, becoming less effective by the increasing prevalence of H pylori resistance. Thus, it is urgent to understand the molecular mechanisms of H. pylori pathogenesis and develop alternative therapeutic strategies. In this review, we focus on the virulence factors for H. pylori colonization and survival within host gastric mucosa and the host antimicrobial responses against H. pylori infection. Moreover, we describe the current treatments for H. pylori eradication and provide some insights into new therapeutic strategies for H. pylori infection.

Is Molecular Analysis Mandatory for Better Post-surgical Outcome in Sleeve Gastrectomy Specimens with Asymptomatic Helicobacter pylori Colonization? A Study from Pakistan

Background: Helicobacter pylori colonizes gastric tissue in obese patients and mostly remains undetected clinically, as histological and molecular analysis is seldom ordered in such cases. Objectives: This study aimed to detect the frequency of H. pylori using different techniques in sleeve gastrectomy specimens of obese patients with minimal or no symptoms suggestive of gastritis. Methods: This longitudinal study was carried out at Farooq Hospital Westwood Lahore, Morbid Anatomy and Histopathology Department and Resource Laboratory at the University of Health Sciences, Lahore, Pakistan, from February 2021 to September 2021. This study selected 80 cases who underwent sleeve gastrectomy within six months. Helicobacter pylori was detected by rapid urease test (RUT), modified Giemsa staining, and polymerase chain reaction (PCR) techniques. Results: Most patients (83.7%) were clinically asymptomatic, while 10% had mild and 6.3% had moderate to severe gastritis symptoms. Of the asymptomatic patients, 56.7% of biopsies showed chronic gastritis. Rapid urease test and modified Giemsa staining showed positive evidence for H. pylori in 47.3% of cases, whereas an additional 13.2% of biopsies that were negative on conventional methods showed the amplification of H. pylori DNA by PCR. Patients were discharged with proton-pump inhibitors therapy (40 mg/day) that showed no adverse post-surgical event over a follow-up of six months. Conclusions: Persistent obesity and other socioeconomic factors may lead to colonizing asymptomatic H. pylori infection. More sensitive techniques for detecting H. pylori may be employed in resource-constrained settings for better patient outcomes and to minimize the complications after sleeve gastrectomy.

Correlation between the intensity of Helicobacter pylori colonization and severity of gastritis: Results of a prospective study.

Helicobacter pylori infection is strongly associated with chronic gastritis and is probably the main course of chronic inflammation in the gastric mucosa. Gradually, H.pylori gastritis will result in gastric atrophy and intestinal metaplasia. Identifying the relationship between intensity of colonization and activity of gastritis helps the clinician in more effective treatment and post-treatment follow-ups. The aim of our work was to analyze the relationship between the density of H.pylori colonization of the gastric mucosa and the severity of histological parameters of gastritis (inflammation activity, gastric atrophy, and intestinal metaplasia). This was a prospective monocentric study conducted from January 2020 to December 2020, collecting patients naive to any anti-H.pylori treatment and having a chronic H.pylori infection documented by histological examination. Epidemiological, endoscopic, and anathomopathological data were collected. Ninety-seven patients with a mean age of 42.6 years [18-65 years] and a sex ratio of M/F=0.64 were included. The density of H.pylori colonization was mild (+) in 43.3% of patients, moderate (++) in 47.4% of patients, and significant (+++) in 9.3% of patients. Nearly, ten per cent of patients had no gastritis, 33% had mild gastritis, 50.5% had moderate gastritis, and 6.2% had severe gastritis. Gastric atrophy and intestinal metaplasia were found in 44.3% and 10.3% of our population, respectively. Patients with mild H.pylori colonization rates had the highest level of mild activity (59.5%). There was a statistically significant association between the severity of H.pylori infection and gastritis activity (p < .001). Gastric atrophy was significantly associated with the intensity of H.pylori colonization (p=.049). No significant relationship was found between the intensity of colonization and metaplasia (p=.08). Our study shows that there is a statistically significant association between the density of H.pylori and histopathological findings including gastritis activity and intestinal atrophy.