The infection caused by Helicobacter pylori is the most common on the planet, affecting half of the global population. It is usually transmitted during childhood and persists for life if untreated. It is the primary cause of chronic gastritis, peptic ulcer, and gastric cancer. In young dyspeptic patients without alarm symptoms, the test-and-treat strategy (detection of H. pylori through a non-invasive test and subsequent eradication) is the preferred approach. The causal role of the infection in the development of gastric adenocarcinoma provides an opportunity to implement preventive strategies. The infection can be diagnosed through invasive methods (requiring endoscopy, such as the rapid urease test or histology) and non-invasive methods (such as the breath test or stool antigen test). The treatment for H. pylori combines a proton pump inhibitor with several antibiotics or bismuth salts.

At a population level, the European Society of Gastrointestinal Endoscopy (ESGE), the European Helicobacter and Microbiota Study Group (EHMSG), and the European Society of Pathology (ESP) suggest endoscopic screening for gastric cancer (and precancerous conditions) in high-risk regions (age-standardized rate [ASR] > 20 per 100 000 person-years) every 2 to 3 years or, if cost-effectiveness has been proven, in intermediate risk regions (ASR 10-20 per 100 000 person-years) every 5 years, but not in low-risk regions (ASR < 10).ESGE/EHMSG/ESP recommend that irrespective of country of origin, individual gastric risk assessment and stratification of precancerous conditions is recommended for first-time gastroscopy. ESGE/EHMSG/ESP suggest that gastric cancer screening or surveillance in asymptomatic individuals over 80 should be discontinued or not started, and that patients' comorbidities should be considered when treatment of superficial lesions is planned.ESGE/EHMSG/ESP recommend that a high quality endoscopy including the use of virtual chromoendoscopy (VCE), after proper training, is performed for screening, diagnosis, and staging of precancerous conditions (atrophy and intestinal metaplasia) and lesions (dysplasia or cancer), as well as after endoscopic therapy. VCE should be used to guide the sampling site for biopsies in the case of suspected neoplastic lesions as well as to guide biopsies for diagnosis and staging of gastric precancerous conditions, with random biopsies to be taken in the absence of endoscopically suspected changes. When there is a suspected early gastric neoplastic lesion, it should be properly described (location, size, Paris classification, vascular and mucosal pattern), photodocumented, and two targeted biopsies taken.ESGE/EHMSG/ESP do not recommend routine performance of endoscopic ultrasonography (EUS), computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET)-CT prior to endoscopic resection unless there are signs of deep submucosal invasion or if the lesion is not considered suitable for endoscopic resection.ESGE/EHMSG/ESP recommend endoscopic submucosal dissection (ESD) for differentiated gastric lesions clinically staged as dysplastic (low grade and high grade) or as intramucosal carcinoma (of any size if not ulcerated or ≤ 30 mm if ulcerated), with EMR being an alternative for Paris 0-IIa lesions of size ≤ 10 mm with low likelihood of malignancy.ESGE/EHMSG/ESP suggest that a decision about ESD can be considered for malignant lesions clinically staged as having minimal submucosal invasion if differentiated and ≤ 30 mm; or for malignant lesions clinically staged as intramucosal, undifferentiated and ≤ 20 mm; and in both cases with no ulcerative findings.ESGE/EHMSG/ESP recommends patient management based on the following histological risk after endoscopic resection: Curative/very low-risk resection (lymph node metastasis [LNM] risk < 0.5 %-1 %): en bloc R0 resection; dysplastic/pT1a, differentiated lesion, no lymphovascular invasion, independent of size if no ulceration and ≤ 30 mm if ulcerated. No further staging procedure or treatment is recommended.Curative/low-risk resection (LNM risk < 3 %): en bloc R0 resection; lesion with no lymphovascular invasion and: a) pT1b, invasion ≤ 500 µm, differentiated, size ≤ 30 mm; or b) pT1a, undifferentiated, size ≤ 20 mm and no ulceration. Staging should be completed, and further treatment is generally not necessary, but a multidisciplinary discussion is required. Local-risk resection (very low risk of LNM but increased risk of local persistence/recurrence): Piecemeal resection or tumor-positive horizontal margin of a lesion otherwise meeting curative/very low-risk criteria (or meeting low-risk criteria provided that there is no submucosal invasive tumor at the resection margin in the case of piecemeal resection or tumor-positive horizontal margin for pT1b lesions [invasion ≤ 500 µm; well-differentiated; size ≤ 30 mm, and VM0]). Endoscopic surveillance/re-treatment is recommended rather than other additional treatment. High-risk resection (noncurative): Any lesion with any of the following: (a) a positive vertical margin (if carcinoma) or lymphovascular invasion or deep submucosal invasion (> 500 µm from the muscularis mucosae); (b) poorly differentiated lesions if ulceration or size > 20 mm; (c) pT1b differentiated lesions with submucosal invasion ≤ 500 µm with size > 30 mm; or (d) intramucosal ulcerative lesion with size > 30 mm. Complete staging and strong consideration for additional treatments (surgery) in multidisciplinary discussion.ESGE/EHMSG/ESP suggest the use of validated endoscopic classifications of atrophy (e. g. Kimura-Takemoto) or intestinal metaplasia (e. g. endoscopic grading of gastric intestinal metaplasia [EGGIM]) to endoscopically stage precancerous conditions and stratify the risk for gastric cancer.ESGE/EHMSG/ESP recommend that biopsies should be taken from at least two topographic sites (2 biopsies from the antrum/incisura and 2 from the corpus, guided by VCE) in two separate, clearly labeled vials. Additional biopsy from the incisura is optional.ESGE/EHMSG/ESP recommend that patients with extensive endoscopic changes (Kimura C3 + or EGGIM 5 +) or advanced histological stages of atrophic gastritis (severe atrophic changes or intestinal metaplasia, or changes in both antrum and corpus, operative link on gastritis assessment/operative link on gastric intestinal metaplasia [OLGA/OLGIM] III/IV) should be followed up with high quality endoscopy every 3 years, irrespective of the individual's country of origin.ESGE/EHMSG/ESP recommend that no surveillance is proposed for patients with mild to moderate atrophy or intestinal metaplasia restricted to the antrum, in the absence of endoscopic signs of extensive lesions or other risk factors (family history, incomplete intestinal metaplasia, persistent H. pylori infection). This group constitutes most individuals found in clinical practice.ESGE/EHMSG/ESP recommend H. pylori eradication for patients with precancerous conditions and after endoscopic or surgical therapy.ESGE/EHMSG/ESP recommend that patients should be advised to stop smoking and low-dose daily aspirin use may be considered for the prevention of gastric cancer in selected individuals with high risk for cardiovascular events.

Gastric intestinal metaplasia (GIM) is a pathological process where gastric mucosal epithelial cells are replaced by intestinal-type cells, serving as a precursor lesion for gastric cancer. This transformation involves various genetic and environmental factors, affecting key genes and signaling pathways. Recent research has revealed complex mechanisms, including changes in gene expression, abnormal signaling pathway activation, and altered cell behavior. This review summarizes the latest research on GIM, discussing its pathogenesis, current treatment strategies, and potential efficacy of emerging approaches like gene editing, microbiome interventions, and integrative medicine. By exploring these strategies, we aim to provide more effective treatments for GIM and reduce gastric cancer incidence. The review also highlights the importance of interdisciplinary studies in understanding GIM mechanisms and improving treatment strategies.

The problem of gastric cancer (GC) prevention remains relevant for a long time. Various methods of population serological screening of atrophic gastritis and precancerous changes in the gastric mucosa have been created at present. Modern endoscopic and morphological methods of verification of the diagnosis of precancerous diseases and changes in the gastric mucosa have been introduced into the practice of gastroenterologists and oncologists. GC risk stratification systems allow the formation of risk groups that require population screening. Practical hints for population serological screening of atrophic gastritis, endoscopic and morphological verification of precancerous changes and diseases of the stomach recommend using it: When developing state programs for the prevention of stomach cancer; when implementing preventive measures for stomach cancer by doctors of all specialties; the authors also offer the possibility of use by anyone over the age of 40, provided that they seek methodological help from their doctor; in the work of health schools in any medical and preventive institutions. The use of an assessment system of certain risk factor signatures with prognostic value would add significant assistance to preventive measures against GC.

Precancerous lesions of gastric cancer (PLGC) represent a critical pathological stage in the development of intestinal gastric cancer. Early detection and diagnosis are key to reducing the incidence of gastric cancer. Substantial advancements have been made in PLGC research in recent years, making it necessary to provide updated reviews using bibliometric methods. We hypothesize that this review will identify emerging trends, key research areas, and gaps in PLGC research, providing insights that could guide future studies and enhance prevention strategies.

To comprehensively review the current state of research on PLGC, examining development trends and research hotspots.

We conducted a bibliometric analysis of PLGC-related studies published between 2004 and 2023 using the Web of Science Core Collection database. We employed Software, including VOSviewer, CiteSpace, R software, and SCImago Graphica, to map scientific networks and visualize knowledge trends in terms of publication volume, countries/regions, institutions, journals, authors, and keywords.

A total of 4097 articles were included, and overall publication volume showed an increasing trend. Over the past two decades, China published the most articles, followed by the United States, Japan, South Korea, and Italy. Among the top 10 contributors, the United States ranked highest in institutions, authors, and citations and demonstrated the strongest international collaboration. Research keywords in this field were clustered into three main categories: Risk factors, pathogenesis, and diagnosis and treatment. Pathogenesis and molecular biomarkers remain key areas of focus. Future research should explore the mechanisms of gut microbiota, immune microenvironment, metabolic reprogramming, and epigenetics. Advanced technologies, including single-cell sequencing, spatially resolved analysis, multi-omics approaches, artificial intelligence, and machine learning, will likely accelerate in-depth investigations of PLGC.

PLGC research has rapidly developed in recent years, gaining considerable attention. This bibliometric analysis reveals research state and emerging trends over the past 20 years, providing insights for future studies.

Recent studies have shown a noticeable increase in global Helicobacter pylori (H. pylori) resistance, with clarithromycin resistance surpassing 15% in various areas. However, inadequate epidemiological monitoring, especially in developing countries, and the absence of uniform testing methods lead to discrepancies between regions and a possible underestimation of resistance levels. The complexity of treating H. pylori is driven by its highly dynamic genome, which is prone to frequent mutations contributing to phenotypical resistance. The usual course of action in empirical treatment involves using a combination of various drugs simultaneously, leading to significant resistance selection pressure and potential side effects. The emergence of H. pylori strains resistant to multiple drugs is closely tied to failures in first-line treatment, highlighting the need to prevent further resistance by using optimal initial empirical therapy or regimens guided by antibiotic susceptibility testing, requiring a collection of mixed samples and multiple isolates for accurate assessment. The emergence of new treatments like potassium-competitive acid blockers offers a hopeful approach to decrease antimicrobial usage while still ensuring effectiveness in comparison to traditional therapies with proton pump inhibitors. Additionally, the use of probiotics is under investigation to identify specific strains and formulations that may mitigate therapy-associated adverse effects.

As a critical juncture in the pathological continuum from gastritis to gastric cancer, precancerous lesions of gastric cancer (PLGC) are increasingly prevalent, significantly undermining the health of the global population. The primary constituents of bile, specifically bile acids (BAs), disrupt the equilibrium of gastric hormone secretion and compromise the structural integrity of the gastric mucosa, thereby facilitating gastric oncogenesis. Moreover, gut microbiota modulate host physiological and pathological processes through immune response regulation, metabolic pathway interference, and direct interaction with gastric tumor cells. Extensive research has elucidated that the metabolic dysregulation of BAs and gut microbiota, in concert with the resultant impairment of the gastric mucosa, are central to the pathogenesis of PLGC. In anticipation of future clinical preventive and therapeutic strategies, this review collates recent insights into the roles of BAs and gut bacteria in PLGC, examining their interplay and significance in the pathogenic mechanism of PLGC.

Observational studies suggest that Helicobacter pylori (H. pylori) is associated with an increased risk of gastric cancer, yet the effect of H. pylori eradication on gastric cancer risk in patients with intestinal metaplasia (IM) or dysplasia remains controversial. The purpose of this study was to summarize the evidence from randomized controlled trials (RCTs) investigating H. pylori eradication on gastric cancer risk in patients with IM or dysplasia to determine the evidence base.

PubMed, Embase, Cochrane Library, Web of science and China National Knowledge Internet database were searched for RCTs published through May 2024 in adults with IM or dysplasia comparing the risk of gastric cancer following H. pylori eradication versus no eradication therapy. Relative risk (RR) with its 95% confidence interval (CI) using random-effects model were employed for the effect estimate. Sensitivity, meta-regression, and subgroup analyses were also calculated.

Sixteen RCTs involving 15,027 patients with IM or dysplasia met the inclusion criteria. In a pooled analysis, H. pylori eradication resulted in a 45% reduction in RR for gastric cancer risk relative to no eradication (RR: 0.55; 95% CI: 0.46-0.67; p < 0.001). H. pylori eradication significantly reduced the risk of gastric cancer in patients with dysplasia (RR: 0.51; 95% CI: 0.32-0.82; p = 0.005), and IM (RR: 0.61; 95% CI: 0.40-0.93; p = 0.022). Further, if the study conducted in countries other than those in Asia, sample size <500, percentage of male <50.0%, follow-up duration <5.0 years, and low study quality, then there was no significant association between H. pylori eradication and a decreased risk of gastric cancer.

H. pylori eradication is protective against gastric cancer in patients with IM or dysplasia.

INPLASY202530010, https://inplasy.com/.

This study aims to assess the serum levels of pepsinogen (PG)I, PG II, and gastrin (G17) in patients with gastric intestinal metaplasia (GIM) and evaluate their correlation with demographic characteristics.

A total of 247 normal controls (NC) and 240 patients diagnosed with GIM were enrolled in this study. All participants underwent a gastroscopy procedure followed by pathological examination for diagnosis confirmation. The expression level of PGI, PG II, and G 17 was detected by fluorescence immunochromatography and Hp infection was detected by 13-carbon breath test. The demographic characteristics of the subjects were obtained through questionnaires.

Compared to the NC group, the GIM group showed a reduction in PG II expression level [10.71(6.40,16.89) VS 9.21(6.14,14.55), p = 0.010]. GIM patients had a higher prevalence of previous Hp eradication history (14.98% VS 23.75%, p = 0.014). The low PG II group exhibited a higher incidence rate of GIM compared to the high PG II group (54.10% VS 44.44%, p = 0 0.020). In the Hp-negative(Hp-) group, there was a decrease in both PGI and PG II expression levels when compared to the Hp-positive(Hp+) group [146.73 ± 78.53 VS 125.61 ± 68.75 and 10.19(7.27, 16.58) VS 7.36(5.62,12.53), p = 0.036 and p < 0.001]. Among patients without Hp eradication history, those with low PG II levels had a higher proportion of individuals with a history of Hp eradication than those with high PG II levels (29.31% VS 3.13%, p = 0.003). Additionally, within the subgroup that underwent Hp eradication, there was a decrease in PG II expression level compared to the subgroup without Hp eradication (6.16(5.13, 7.52) VS 8.73(5.67, 13.35), p = 0.041).

The prevalence of GIM was significantly associated with low levels of PG II. There was a significant association between HP eradication history and the prevalence of GIM. Hp eradication history resulted in reduced expression levels of PG II in Hp- GIM patients.

The purpose of this study was to construct a nomogram to identify patients at high risk of gastric precancerous lesions (GPLs). This identification will facilitate early diagnosis and treatment and ultimately reduce the incidence and mortality of gastric cancer.

In this single-center retrospective cohort study, 563 participants were divided into a gastric precancerous lesion (GPL) group (n=322) and a non-atrophic gastritis (NAG) group (n=241) based on gastroscopy and pathology results. Laboratory data and demographic data were collected. A derivation cohort (n=395) was used to identify the factors associated with GPLs to develop a predictive model. Then, internal validation was performed (n=168). We used the area under the receiver operating characteristic curve (AUC) to determine the discriminative ability of the predictive model; we constructed a calibration plot to evaluate the accuracy of the predictive model; and we performed decision curve analysis (DCA) to assess the clinical practicability predictive model.

Four -predictors (i.e., age, body mass index, smoking status, and -triglycerides) were included in the predictive model. The AUC values of this predictive model were 0.715 (95% CI: 0.665-0.765) and 0.717 (95% CI: 0.640-0.795) in the derivation and internal validation cohorts, respectively. These values indicated that the predictive model had good discrimination ability. The calibration plots and DCA suggested that the predictive model had good accuracy and clinical net benefit. The Hosmer-Lemeshow test results in the derivation and validation cohorts for this predictive model were 0.774 and 0.468, respectively.

The nomogram constructed herein demonstrated good performance in terms of predicting the risk of GPLs. This nomogram can be beneficial for the early detection of patients at high risk of GPLs, thus facilitating early treatment and ultimately reducing the incidence and mortality of gastric cancer.

Helicobacter pylori (H. pylori) is an established gastric carcinogen, also associated with an increased risk of colorectal cancer. Therefore, we suspected that H. pylori eradication lowers the risk of colorectal cancer.

We assessed if H. pylori eradication therapy is associated with a reduced risk of colorectal adenocarcinoma in a population-based nationwide cohort study. This study included all Swedish adults with at least one recorded H. pylori eradication episode between July 2005 and December 2012, based on the high-quality Swedish health registries. Colorectal adenocarcinoma risks were compared to the Swedish background population, presented as standardized incidence ratios (SIRs) and 95% confidence intervals (CIs), accounting for age, sex, calendar period, tumor location (left or right sided), stage, and number of eradication episodes, from 1 year after eradication and onward.

Among 80,381 individuals receiving H. pylori eradication therapy (average follow-up 4.1 years), 282 were diagnosed with colorectal cancer (97.2% adenocarcinoma). Overall, H. pylori eradication was associated with an elevated risk of colorectal adenocarcinoma (SIR 1.27, 95% CI: 1.12-1.43). The colorectal adenocarcinoma risk was increased 1-2 years after eradication (SIR 1.42, 95% CI: 1.17-1.72), then decreased 2-4 years (SIR 0.80, 95% CI: 0.65-0.98) and 4-6 years (SIR 0.76, 95% CI: 0.57-0.99), yet not ≥ 6 years (SIR 1.36, 95% CI: 0.78-2.21) after eradication compared to the general population. Overall, right-sided (SIR 1.47, 95% CI: 1.21-1.76) and left-sided (SIR 1.35, 95% CI: 1.09-1.67) colon adenocarcinomas risks were higher among eradicated individuals than the general population.

H. pylori eradication was not associated with a clear and consistent reduction of colorectal cancer in our Swedish cohort.

Gastric cancer is a major cause of cancer-related death worldwide, despite the reduction in its incidence. The disease is still burdened with a poor prognosis, particularly in Western countries. The main risk factor is the infection by Helicobacter pylori, classified as a class I carcinogen by the IARC, and It is well-known that primary prevention of gastric cancer can be achieved with the eradication of the infection. Moreover, non-invasive measurement of pepsinogens (PGI and PGI/PGII ratio) allows the identification of patients that should undergo upper gastrointestinal (GI) endoscopy. Gastric non-cardia adenocarcinoma is indeed preceded by a well-defined precancerous process that involves consecutive stages, described for the first time by Correa et al. more than 40 years ago, and patients with advance stages of gastric atrophy/intestinal metaplasia and with dysplastic changes should be followed-up periodically with upper GI endoscopies. Despite these effective screening and surveillance methods, national-level screening campaigns have been adopted only in few countries in eastern Asia (Japan and South Korea). In this review, we describe primary and secondary preventive measures for gastric cancer, discussing the need to introduce screening also in Western countries. Moreover, we propose a simple algorithm for screening that could be easily applied in clinical practice.

Helicobacter pylori (H. pylori) infection is a widespread global health issue with a varying prevalence influenced by geography, socioeconomic status, and demographics. In the U.S., the prevalence is lower, though certain groups, such as older adults and immigrants from high-prevalence regions, show higher rates. The decrease in infection rates in developed countries is due to improved sanitation, antibiotics, and healthcare, whereas developing countries continue to experience high rates due to poor living conditions. H. pylori infection can be asymptomatic or cause symptoms like dyspepsia, abdominal pain, bloating, nausea, and loss of appetite. Pathophysiologically, H. pylori contribute to conditions such as gastritis, peptic ulcers, and gastric cancer through mechanisms including urease production and the release of virulence factors, leading to chronic inflammation and an increased cancer risk. Diagnostic methods for H. pylori have progressed significantly. Non-invasive techniques, such as serological assays, stool antigen tests, and urea breath tests, are practical and sensitive. Invasive methods, including endoscopic biopsy and molecular diagnostics, are more definitive but resource intensive. Recent advancements in diagnostic technology, including matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), biosensor technology, and next-generation sequencing (NGS), promise improved speed, accuracy, and accessibility. These innovations are expected to enhance the detection and management of H. pylori, potentially reducing the global disease burden. This review aims to discuss these diagnostic modalities with a focus on further advances under investigation.

Precancerous lesions of gastric cancer (PLGC) represent a critical pathological stage in the transformation from normal gastric mucosa to gastric cancer (GC). The global incidence of PLGC has been rising over the past few decades, with a trend towards younger onset ages. Increasing evidence suggests that early prevention and treatment of PLGC can effectively reverse the malignant development of gastric mucosal epithelial cells. However, there is currently a lack of effective therapeutic drugs and methods. Recent years have witnessed substantial advancements in PLGC research, with the elucidation of novel regulatory mechanisms offering promising avenues for clinical intervention and drug development. This review aims to delineate potential targets for early prevention and diagnosis of GC while exploring innovative approaches to PLGC management. This article focuses on elucidating the regulatory mechanisms of the inflammatory microenvironment, bile acids (BA), glycolysis, autophagy, apoptosis, ferroptosis, and cellular senescence. We pay particular attention to potential therapeutic targets for PLGC, with the goal of providing insights and theoretical basis for clinical research on PLGC.

Both Helicobacter pylori (H. pylori) infection and metabolic syndrome (MetS) are highly prevalent worldwide. The emergence of relevant research suggesting a pathogenic linkage between H. pylori infection and MetS-related cardio-cerebrovascular diseases and neurodegenerative disorders, particularly through mechanisms involving brain pericyte deficiency, hyperhomocysteinemia, hyperfibrinogenemia, elevated lipoprotein-a, galectin-3 overexpression, atrial fibrillation, and gut dysbiosis, has raised stimulating questions regarding their pathophysiology and its translational implications for clinicians. An additional stimulating aspect refers to H. pylori and MetS-related activation of innate immune cells, mast cells (MC), which is an important, often early, event in systemic inflammatory pathologies and related brain disorders. Synoptically, MC degranulation may play a role in the pathogenesis of H. pylori and MetS-related obesity, adipokine effects, dyslipidemia, diabetes mellitus, insulin resistance, arterial hypertension, vascular dysfunction and arterial stiffness, an early indicator of atherosclerosis associated with cardio-cerebrovascular and neurodegenerative disorders. Meningeal MC can be activated by triggers including stress and toxins resulting in vascular changes and neurodegeneration. Likewise, H.pylori and MetS-related MC activation is linked with: (a) vasculitis and thromboembolic events that increase the risk of cardio-cerebrovascular and neurodegenerative disorders, and (b) gut dysbiosis-associated neurodegeneration, whereas modulation of gut microbiota and MC activation may promote neuroprotection. This narrative review investigates the intricate relationship between H. pylori infection, MetS, MC activation, and their collective impact on pathophysiological processes linked to neurodegeneration. Through a comprehensive search of current literature, we elucidate the mechanisms through which H. pylori and MetS contribute to MC activation, subsequently triggering cascades of inflammatory responses. This highlights the role of MC as key mediators in the pathogenesis of cardio-cerebrovascular and neurodegenerative disorders, emphasizing their involvement in neuroinflammation, vascular dysfunction and, ultimately, neuronal damage. Although further research is warranted, we provide a novel perspective on the pathophysiology and management of brain disorders by exploring potential therapeutic strategies targeting H. pylori eradication, MetS management, and modulation of MC to mitigate neurodegeneration risk while promoting neuroprotection.

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the gastric mucosa and is associated with various gastrointestinal disorders. H. pylori is a pervasive pathogen, infecting nearly 50% of the world's population, and presents a substantial concern due to its link with gastric cancer, ranking as the third most common cause of global cancer-related mortality. This review article provides an updated and comprehensive overview of the current understanding of H. pylori infection, focusing on its pathogenesis, diagnosis, and treatment strategies. The intricate mechanisms underlying its pathogenesis, including the virulence factors and host interactions, are discussed in detail. The diagnostic methods, ranging from the traditional techniques to the advanced molecular approaches, are explored, highlighting their strengths and limitations. The evolving landscape of treatment strategies, including antibiotic regimens and emerging therapeutic approaches, is thoroughly examined. Through a critical synthesis of the recent research findings, this article offers valuable insights into the contemporary knowledge of Helicobacter pylori infection, guiding both clinicians and researchers toward effective management and future directions in combating this global health challenge.