• Helicobacter pylori
• digestive tract diseases
• infection rate
• risk factor

• Adult
• Aged
• Female
• Humans
• Male
• Middle Aged
• China/epidemiology
• Cross-Sectional Studies
• Digestive System Diseases/epidemiology
• Digestive System Diseases/microbiology
• East Asian People
• Helicobacter Infections/complications
• Helicobacter Infections/epidemiology
• Helicobacter pylori
• Risk Factors

• Colorectal cancer
• Colorectal polyp
• Helicobacter pylori
• Risk factor

• Helicobacter pylori
• clarithromycin-containing triple therapy
• colorectal cancer
• epidemiology
• standardized incidence ratio

• National Natural Science Foundation of China

• colorectal polyps
• health examination
• low bone mineral density
• metabolic syndrome

• Aged
• Bone Diseases, Metabolic
• Colonic Polyps/epidemiology
• Colonoscopy
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/pathology
• Cross-Sectional Studies
• Duodenal Ulcer/complications
• Esophagitis, Peptic
• Humans
• Metabolic Syndrome/complications
• Metabolic Syndrome/epidemiology
• Middle Aged
• Retrospective Studies
• Risk Factors

It has been suggested that Helicobacter pylori (H. pylori) infection is associated with hypergastrinemia and proliferation of colorectal mucosa via direct stimulation, dysbiosis of the gut microbiome, and changes in the gut microbiome, all of which may lead to the formation of colorectal polyps. However, the consensus remains lacking regarding whether H. pylori infection is independently associated with colorectal polyps and whether the association differs according to histological type of colorectal polyps. To summarize the current evidence regarding the relationship between H. pylori infection and colorectal polyps, we conducted a meta-analysis of related observational studies according to the histological types of colorectal polyps.

Observational studies investigating the association between H. pylori infection and colorectal polyps using multivariate analyses were included by search of PubMed, Embase, and Web of Science. A random-effects model was adopted to combine the results.

Seventeen studies that include 322,395 participants were analyzed. It was shown that H. pylori infection was independently associated with overall colorectal polyps (odds ratio [OR]: 1.67, 95% CI: 1.24–2.24, p < 0.001; I² = 73%). According to the histological type of colorectal polyps, H. pylori infection was independently associated with adenomatous polyps (APs; OR: 1.71, 95% CI: 1.47–1.99, p < 0.001; I² = 86%), advanced APs (OR: 2.06, 95% CI: 1.56–2.73, p < 0.001; I² = 0%), and hyperplastic polyps (HPs; OR: 1.54, 95% CI: 1.02–2.30, p = 0.04; I² = 78%). Evidence based on only one study showed that H. pylori infection was not associated with sessile serrated polyps (SSPs; OR: 1.00, 95% CI: 0.93–1.07, p = 0.99).

Current evidence from case-control and cross-sectional studies suggested that H. pylori infection was independently associated with colorectal APs, advanced APs, and HPs, but not with SSPs. These findings suggested H. pylori infection may be a possible risk factor of colorectal polyp, which is important for the prevention of colorectal polyp in the adult population.

• colorectal adenoma
• diabetes prevalence
• helicobacter pylori

• Adenoma/epidemiology
• Adenoma/microbiology
• Adult
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/etiology
• Colorectal Neoplasms/microbiology
• Diabetes Mellitus/epidemiology
• Helicobacter Infections/complications
• Helicobacter Infections/epidemiology
• Helicobacter pylori/pathogenicity
• Humans
• Prevalence
• Risk Factors

• MMH-110-34 Mackay Memorial Hospital
• MOST-109-2314-B-195-007 Ministry of Science and Technology, Taiwan

• Adenomas
• Atrophy
• Colorectal
• Gastritis
• Health-check
• Helicobacter pylori

• Adenoma/diagnosis
• Adenoma/epidemiology
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/epidemiology
• Cross-Sectional Studies
• Gastritis, Atrophic/diagnosis
• Gastritis, Atrophic/epidemiology
• Helicobacter Infections/complications
• Helicobacter Infections/diagnosis
• Helicobacter Infections/epidemiology
• Helicobacter pylori
• Humans
• Retrospective Studies
• Risk Factors

Intestinal flora is an important component in the human body, which have been reported to be involved in the occurrence and development of colorectal cancer (CRC). Indeed, changes in the intestinal flora in CRC patients compared to those in control subjects have been reported. Several bacterial species have been shown to exhibit the pro-inflammatory and pro-carcinogenic properties, which could consequently have an impact on colorectal carcinogenesis. In this review, we summarize the current knowledge on the potential links between the intestinal microbiota and CRC. We illustrated the mechanisms by which intestinal flora imbalance affects CRC, mainly focusing on inflammation, microbial metabolites, and specific bacteria species. In addition, we discuss how a diet exhibits a strong impact on microbial composition and provides risks for developing CRC. Finally, we describe the potential future directions that are based on intestinal microbiota manipulation for CRC diagnosis and treatment.

• colorectal cancer
• diet
• inflammation
• intestinal flora
• microbial metabolites

• colorectal cancer
• helicobacter pylori
• heterogeneity
• meta-analysis
• subgroup analysis
• systematic review

• Adult
• Aged
• Colorectal Neoplasms/microbiology
• Female
• Helicobacter Infections/complications
• Helicobacter Infections/microbiology
• Helicobacter pylori
• Humans
• Male
• Middle Aged
• Odds Ratio
• Risk Factors

H. pylori infection may play a role in the development of colorectal cancers (CRC). We aimed to examine the association between H. pylori infection and the risk of CRC by anatomical locations.

We conducted a case-control study on 91 incidence cases of CRC and 224 hospital controls. CRC was determined by histopathological examinations. H. pylori IgG antibody in serum was tested. We collected data on the diet, nutrition, and lifestyle by the validated semi-quantitative food frequency and demographic lifestyle questionnaire. The odds ratio and 95% confidence interval (OR (95%CI) were estimated for CRC and its subgroups.

Overall 54.95% of CRC cases and 42.41% of the controls were H. pylori-seropositive, OR (95%CI): 1.56 (0.88, 2.74), p for trend=0.115. Positive dose-response association in quartiles, highest vs lowest, was observed for total CRC, OR (95%CI): 2.14 (1.00, 4.58), p for trend=0.049, for proximal colon, OR (95%CI): 1.52 (0.37, 6.25), p for trend=0.571), and for distal colon and rectum cancers combined, OR (95%CI): 2.38 (1.03, 5.50), p for trend=0.039.

There is a positive association between H. pylori and colorectal cancers, especially distal colon and rectum cancers combined, but additional research is needed to determine the underlying mechanism of chronic H. pylori infection-induced CRC in humans.

• Case-control study
• H. pylori
• colorectal cancer

• Helicobacter pylori
• Atrophic gastritis
• Colorectal cancer
• Gastrointestinal neoplasms
• Intestinal metaplasia
• Polyps

To investigate whether Helicobacter pylori (H. pylori) infection increases the risk of colorectal adenomatous polyp (CAP) in the context of age and gender.

A total of 563 study subjects (male/female, 368/195) from Beijing, China, with higher nursing level who underwent colonoscopy were retrospectively collected. H. pylori and CAP were detected by carbon-13 urea breath test and colorectal colonoscopy. The correlations between the number, size, distribution, and pathological grade of CAP and H. pylori infection were analyzed. The population was further stratified by age and gender in order to examine the risk of H. pylori and CAP in the context of these variables. The influence of H. pylori on the risk of CAP was assessed by logistic regression model.

315 participants were diagnosed with CAP, and 207 participants were classified as healthy controls. The prevalence of H. pylori in the CAP group was significantly higher than that in the healthy control group (119/315, 37.8% versus 44/207, 21.3%) (p < 0.001). The proportion of H. pylori positive plus CAP in participants <50 years old was significantly higher than that in participants >50 years old (87/250; 34.8% versus 32/65; 49.2%) (p < 0.001). The proportion of H. pylori positive plus CAP in participants <50 years old was significantly higher than that in participants >50 years old (87/250; 34.8% versus 32/65; 49.2%) (p < 0.001). The proportion of H. pylori positive plus CAP in participants <50 years old was significantly higher than that in participants >50 years old (87/250; 34.8% versus 32/65; 49.2%) (p < 0.001). The proportion of H. pylori positive plus CAP in participants <50 years old was significantly higher than that in participants >50 years old (87/250; 34.8% versus 32/65; 49.2%) (

H. pylori is a major risk factor for CAP. Further studies are needed to assess the effects of H. pylori treatment or persistent infection on the occurrence or recurrence of CAP.

Helicobacter pylori may reportedly be associated with extragastric malignancy beyond gastric cancer. The present study aimed to evaluate the association between H. pylori infection and colorectal neoplasia through a systematic review and meta-analysis.

A great number of researches over the last years are allocated to know cancer reasons, prevention and treatment strategies. Bacterial infections are one of the promoting factors in cancer development. The present study was carried out to study effects of heat-killed bacteria on cancer cell lines MCF7 and HT-29. To this purpose, four bacterial strains including Salmonella typhi, Staphylococcus epidermidis, Escherichia coli and Pseudomonas aeruginosa were assayed. Thermal inactivation method was used to kill the bacteria and preserve the bacterial surface proteins unchangeable. The concentrations of 0.01, 0.1, 0.5 and 1 mg/ml of inactivated bacteria were prepared to evaluate the effects of heat-inactivated bacterial solutions on MCF7 and HT-29 cell lines. MTT assay was used to measure the cell viability of cancer cells treated with different concentration of inactivated bacterial solutions.The MTT assay results after 48 hours showed that the heat-killed bacterial solutions were able to induce the proliferation of both cancer cell lines. In addition, the most cell viability in MCF-7 cell line was seen in samples treated with S. epidermidis, while in HT29 cells, the most one was seen in S. typhi treated samples. It was concluded that bacterial infections are cancer-deteriorating agents, and any species of bacteria is specific to certain cancerous tissue.

• Breast cancer
• Chronic infections
• Colon cancer
• Heat inactivation
• Inflammatory responses
• MTT-assay

• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/microbiology
• Disease Susceptibility
• Helicobacter Infections/complications
• Helicobacter Infections/microbiology
• Helicobacter pylori/pathogenicity
• Humans
• Prevalence
• Risk Factors

• R01 CA190428 NCI NIH HHS

• Helicobacter pylori
• advanced colorectal neoplasia
• age
• smoking

Helicobacter pylori is a major risk factor for atrophic gastritis (AG) and gastric cancer. The correlation between H. pylori, AG and colorectal neoplasm (CRN) has only been examined in a limited number of studies, and findings have been inconclusive. We aimed to investigate the association between H. pylori infection status, AG and advanced CRN.

This cross-sectional study investigated the relationship between the presence of serum anti-H. pylori IgG antibodies, AG, and advanced CRN in 6,351 consecutive asymptomatic subjects who underwent a screening colonoscopy.

A total of 316 participants (5.0%) had advanced CRN. H. pylori seropositivity was 61.3%. In a univariate analysis, the presence of H. pylori infection was associated with advanced CRN (odds ratio [OR], 1.49; 95% confidence interval [CI], 1.17 to 1.91; p=0.001). H. pylori infection was associated with an increased risk of advanced CRN after adjusting for clinically relevant confounders (OR, 1.34; 95% CI, 1.04 to 1.72; p=0.023). H. pylori-related AG was significantly associated with the risk of advanced CRN (OR, 1.40; 95% CI, 1.03 to 1.91; p=0.030), whereas H. pylori infection without AG was not.

H. pylori infection increased the risk of advanced CRN, especially when it was combined with AG. Strict colonoscopy screening and surveillance may be warranted in those with H. pylori-positive AG.

• Atrophy
• Gastritis
• Helicobacter pylori
• Neoplasms

Colorectal cancer, the fourth leading cause of cancer-related death worldwide, is a multifactorial disease involving genetic, environmental and lifestyle risk factors. In addition, increased evidence has established a role for the intestinal microbiota in the development of colorectal cancer. Indeed, changes in the intestinal microbiota composition in colorectal cancer patients compared to control subjects have been reported. Several bacterial species have been shown to exhibit the pro-inflammatory and pro-carcinogenic properties, which could consequently have an impact on colorectal carcinogenesis. This review will summarize the current knowledge about the potential links between the intestinal microbiota and colorectal cancer, with a focus on the pro-carcinogenic properties of bacterial microbiota such as induction of inflammation, the biosynthesis of genotoxins that interfere with cell cycle regulation and the production of toxic metabolites. Finally, we will describe the potential therapeutic strategies based on intestinal microbiota manipulation for colorectal cancer treatment.

• colorectal cancer
• genotoxins
• host-pathogen interaction
• inflammation
• intestinal microbiota

• Adaptive Immunity
• Bacteria/classification
• Bacteria/metabolism
• Bacteria/pathogenicity
• Carcinogenesis
• Cell Cycle/drug effects
• Cell Transformation, Neoplastic/immunology
• Cell Transformation, Neoplastic/metabolism
• Cell Transformation, Neoplastic/pathology
• Colorectal Neoplasms/immunology
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/microbiology
• Colorectal Neoplasms/pathology
• Food
• Gastrointestinal Microbiome/immunology
• Gastrointestinal Microbiome/physiology
• Host-Pathogen Interactions
• Humans
• Immunity, Innate
• Inflammation/immunology
• Inflammation/metabolism
• Inflammation/microbiology
• Mutagens/adverse effects
• Risk Factors

• Helicobacter pylori
• colorectal neoplasm
• insulin resistance
• metabolic syndrome

Background: Several studies have suggested that Helicobacter pylori (H. pylori) infection is a risk factor for colorectal cancer (CRC), while others have not confirmed this hypothesis. This work aimed to assess the relation of CRC with H. pylori seropositivity and with seropositivity to 16 H. pylori proteins, in the MultiCase-Control study, MCC-Spain.

Methods: MCC-Spain is a multicase-control study carried out in Spain from 2008 to 2013. In total, 2,140 histologically-confirmed incident CRC cases and 4,098 population-based controls were recruited. Controls were frequency-matched by sex, age, and province. Epidemiological data were collected through a questionnaire fulfilled by face-to-face interviews and a self-administered food-frequency questionnaire. Seroreactivities against 16 H. pylori proteins were determined in 1,488 cases and 2,495 controls using H. pylori multiplex serology. H. pylori seropositivity was defined as positivity to ≥4 proteins. Multivariable logistic regression mixed models were used to estimate odds ratios (OR) and 95% confidence intervals (CI).

Results:H. pylori seropositivity was not associated with increased CRC risk (OR = 0.91; 95% CI: 0.71–1.16). Among H. pylori seropositive subjects, seropositivity to Cagδ showed a lower CRC risk, and risk decreased with increasing number of proteins seropositive. Seropositivity to the most recognized virulence factors, CagA and VacA, was not associated with a higher CRC risk. No statistically significant heterogeneity was identified among tumor sites, although inverse relations were stronger for left colon cancer. An interaction with age and sex was found: H. pylori seropositivity was associated with a lower CRC risk in men younger than 65 and with a higher risk in older women.

Conclusions: Our results suggest that neither H. pylori seropositivity, nor seropositivity to the virulence factor CagA are associated with a higher CRC risk. A possible effect modification by age and sex was identified.

• Helicobacter pylori
• bacterial infections
• chronic infection
• colorectal neoplasm
• multiplex serology
• non-infectious diseases

To explore the association between Helicobacter pylori (H. pylori) infection status, intestinal metaplasia (IM), and colorectal adenomas.

We retrospectively reviewed 1641 individuals aged ≥ 40 years who underwent physical examination, laboratory testing, ¹³C-urea breath testing, gastroscopy, colonoscopy, and an interview to ascertain baseline characteristics and general state of health. Histopathological results were obtained by gastric and colorectal biopsies.

The prevalence of H. pylori infection and adenomas was 51.5% (845/1641) and 18.1% (297/1641), respectively. H. pylori infection was significantly correlated with an increased risk of colorectal adenomas (crude OR = 1.535, 95%CI: 1.044-1.753, P = 0.022; adjusted OR = 1.359, 95%CI: 1.035-1.785, P = 0.028). Individuals with IM had an elevated risk of colorectal adenomas (crude OR = 1.664, 95%CI: 1.216-2.277, P = 0.001; adjusted OR = 1.381, 95%CI: 0.998-1.929, P = 0.059). Stratification based on H. pylori infection stage and IM revealed that IM accompanied by H. pylori infection was significantly associated with an increased risk of adenomas (crude OR = 2.109, 95%CI: 1.383-3.216, P = 0.001; adjusted OR = 1.765, 95%CI: 1.130-2.757, P = 0.012).

H. pylori-related IM is associated with a high risk of colorectal adenomas in Chinese individuals.

• Helicobacter pylori
• Chinese population
• Colorectal neoplasms
• Intestinal metaplasia
• Chronic gastritis

• Adult
• Aged
• Biopsy
• Breath Tests
• Colonoscopy
• Colorectal Neoplasms/pathology
• Gastric Mucosa/pathology
• Gastritis/pathology
• Gastroscopy
• Helicobacter Infections/complications
• Helicobacter pylori
• Humans
• Intestines/microbiology
• Intestines/pathology
• Metaplasia/complications
• Metaplasia/microbiology
• Metaplasia/pathology
• Middle Aged
• Prevalence
• Regression Analysis
• Retrospective Studies
• Risk Factors
• Stomach/pathology
• Treatment Outcome

• Adenoma
• Colonoscopy
• H. Pylori
• Risk factor

• biomarkers
• colorectal adenoma
• distal
• immunohistochemistry
• proximal
• β-catenin

• Colorectal cancer
• Gastric cancer
• Microsatellite instability
• p53

From the first isolation of Helicobacter pylori (H. pylori) from the gastric mucosa by Marshall and Warren in 1983, 33 years have passed. H. pylori has been found to be closely associated not only with chronic gastric diseases but also with multiple system diseases. Advances in research of H. pylori infection has led to a better understanding of the pathogenicity of H. pylori and the prevention and treatment of related disease. In 2015, Professor Zou's team developed oral recombinant H. pylori vaccine, which is promising in the prevention of H. pylori infection. Japan aims to reduce the risk of H. pylori infection in the whole population in 2014 to reduce the incidence of gastric cancer, which has caused widespread concern. H. pylori infection is a kind of infectious disease, and the infection rate in China is about 56%.Therefore, it is of great clinical importance to strengthen the research on bacteriology and pathogenesis of H. pylori, improve the prevention and treatment related diseases, and seek antibacterial regimens with better efficacy and lower drug resistance.

• Helicobacter pylori
• Pathogenicity
• Treatment options
• Protective effect
• Prevention

AIM: To explore the correlation between Helicobacter pylori (H. pylori)-associated gastric diseases and colorectal neoplasia.

METHODS: Patients included in this study underwent a colonoscopy and esophago-gastro-duodenoscopy (EGD) along with histopathological measurement between March 2012 and March 2015 at Qi-Lu Hospital of Shandong University, who also had results of H. pylori detection. A total of 233 cases were selected. Demographic data, H. pylori infection status (including results of rapid urease tests and gastric mucosa pathological examinations) and histopathological examination results of gastric and colorectal mucosa were gathered and analyzed. The statistical analysis focused on the prevalence of colorectal neoplasms among patients with various histopathological categories of the stomach. ORs and their 95%CI were calculated to describe the strengths of the associations.

RESULTS: The incidence rates of colorectal adenoma without high-grade intraepithelial neoplasia (HGIEN) (OR = 2.400, 95%CI: 0.969-5.941), adenoma with HGIEN (5.333, 1.025-27.758) and adenocarcinoma (1.455, 0.382-5.543) were all higher for patients with H. pylori-associated gastritis than for those in the control group. The incidence rate of colorectal adenoma with HGIEN (3.218, 0.767-13.509) was higher in patients with intestinal metaplasia than in the control group, while the incidence rates of adenoma without HGIEN (0.874, 0.414-1.845) and adenocarcinoma (0.376, 0.096-1.470) were lower in the intestinal metaplasia group than in the control group. The incidence rate of colorectal adenoma without HGIEN (3.111, 1.248-7.753) was significantly higher in the gastric intraepithelial neoplasia group than in the control group, while the rates of adenoma with HGIEN (1.481, 0.138-15.941) and adenocarcinoma (2.020, 0.561-7.272) were higher in the gastric intraepithelial neoplasia group. Incidence rates of colorectal adenoma without HGIEN (1.067, 0.264-4.314), adenoma with HGIEN (2.667, 0.231-30.800) and adenocarcinoma (2.182, 0.450-10.585) were all higher in the gastric adenocarcinoma group than in the control group.

CONCLUSION: H. pylori infection as well as H. pylori-associated gastric diseases are risk factors for colorectal neoplasia.

• Helicobacter pylori
• Helicobacter pylori-associated gastric diseases
• Colorectal neoplasia
• Endoscopy with pathological biopsy
• Chinese population

• Adenocarcinoma/diagnosis
• Adenocarcinoma/epidemiology
• Adenocarcinoma/microbiology
• Adenoma/diagnosis
• Adenoma/epidemiology
• Adenoma/microbiology
• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Biopsy
• Carcinoma in Situ/diagnosis
• Carcinoma in Situ/epidemiology
• Carcinoma in Situ/microbiology
• Chi-Square Distribution
• China/epidemiology
• Colonoscopy
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/microbiology
• Databases, Factual
• Female
• Gastric Mucosa/microbiology
• Gastric Mucosa/pathology
• Gastritis/diagnosis
• Gastritis/epidemiology
• Gastritis/microbiology
• Helicobacter Infections/diagnosis
• Helicobacter Infections/epidemiology
• Helicobacter Infections/microbiology
• Helicobacter pylori/isolation & purification
• Humans
• Incidence
• Male
• Middle Aged
• Odds Ratio
• Prevalence
• Retrospective Studies
• Risk Factors
• Young Adult

Ever since Helicobacter pylori (H. pylori) was recognized as an infectious cause of gastric cancer, there has been increasing interest in examining its potential role in colorectal carcinogenesis. Data from case-control and cross-sectional studies, mostly relying on hospital-based samples, and several meta-analyses have shown a positive statistical relationship between H. pylori infection and colorectal neoplasia. However, the possibility exists that the results have been influenced by bias, including the improper selection of patients and disparities with respect to potential confounders. While the evidence falls short of a definitive causal link, it appears that infection with H. pylori/H. pylori-related gastritis is associated with an increased, although modest, risk of colorectal adenoma and cancer. The pathogenic mechanisms responsible for this association remain uncertain. H. pylori has been detected in colorectal malignant tissues; however, the possibility that H. pylori is a direct activator of colonic carcinogenesis remains purely hypothetical. On the other hand, experimental data have indicated a series of potential oncogenic interactions between these bacteria and colorectal mucosa, including induction and perpetuation of inflammatory responses, alteration of gut microflora and release of toxins and/or hormonal mediators, such as gastrin, which may contribute to tumor formation.

• Helicobacter pylori
• Colorectal cancer
• Polyp
• Adenoma
• Gastrin

• Cell Transformation, Neoplastic/genetics
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/microbiology
• Gastritis/diagnosis
• Gastritis/microbiology
• Helicobacter Infections/complications
• Helicobacter Infections/diagnosis
• Helicobacter Infections/microbiology
• Helicobacter pylori/genetics
• Helicobacter pylori/pathogenicity
• Host-Pathogen Interactions
• Humans
• Oncogenes
• Precancerous Conditions/diagnosis
• Precancerous Conditions/genetics
• Precancerous Conditions/microbiology
• Risk Factors

Colorectal cancer is a common malignant tumor in the digestive system, and the early diagnosis of colorectal cancer has been the focus of its prevention and control. Colorectal intraepithelial neoplasia and adenoma are considered to be the most important precancerous lesions of colorectal cancer. In recent years, with the development of biological medicine, genetics,

and other disciplines, many studies have explored the relationship between intraepithelial neoplasia and adenoma and colorectal cancer, and some new research progress has been achieved to provide some guidance for the future clinical screening, regular follow-up and chemical prevention. However, it remains to be studied how colorectal intraepithelial neoplasia and adenoma form and evolve to colorectal cancer.

• Intraepithelial neoplasia
• Adenoma
• Genetics
• Screening
• Follow-up
• Prevention

• Hispanic
• colorectal adenoma
• colorectal cancer
• neoplasia

Helicobacter pylori (H. pylori) is an extremely common, yet underappreciated, pathogen that is able to alter host physiology and subvert the host immune response, allowing it to persist for the life of the host. H. pylori is the primary cause of peptic ulcers and gastric cancer. In the United States, the annual cost associated with peptic ulcer disease is estimated to be $6 billion and gastric cancer kills over 700000 people per year globally. The prevalence of H. pylori infection remains high (> 50%) in much of the world, although the infection rates are dropping in some developed nations. The drop in H. pylori prevalence could be a double-edged sword, reducing the incidence of gastric diseases while increasing the risk of allergies and esophageal diseases. The list of diseases potentially caused by H. pylori continues to grow; however, mechanistic explanations of how H. pylori could contribute to extragastric diseases lag far behind clinical studies. A number of host factors and H. pylori virulence factors act in concert to determine which individuals are at the highest risk of disease. These include bacterial cytotoxins and polymorphisms in host genes responsible for directing the immune response. This review discusses the latest advances in H. pylori pathogenesis, diagnosis, and treatment. Up-to-date information on correlations between H. pylori and extragastric diseases is also provided.

• Enterohepatic
• Pathogenesis
• Diagnosis
• Treatment
• Extragastric
• CagA
• Cancer
• Autoimmune
• Inflammation
• Virulence factor

• Animals
• Anti-Bacterial Agents/therapeutic use
• Drug Resistance, Viral
• Genetic Predisposition to Disease
• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Helicobacter Infections/epidemiology
• Helicobacter Infections/genetics
• Helicobacter Infections/microbiology
• Helicobacter pylori/drug effects
• Helicobacter pylori/genetics
• Helicobacter pylori/pathogenicity
• Host-Pathogen Interactions
• Humans
• Incidence
• Predictive Value of Tests
• Prevalence
• Risk Factors
• Stomach Diseases/diagnosis
• Stomach Diseases/drug therapy
• Stomach Diseases/microbiology
• Treatment Outcome
• Virulence

Increasing rates of antimicrobial resistance to clarithromycin and metronidazole present challenges in maintaining optimal eradication rates. Knowledge of local antibiotic resistance and consumption pattern is important in selecting a reliable regimen. In addition, adverse effect profiles of therapeutic regimens are important and must be addressed to enhance compliance rates. Various methods of enhancing the eradication rates of Helicobacter pylori (H. pylori) have been investigated, including changing combinations or durations of established drugs, adding adjuvant drugs, or development of new molecules or agents. Bismuth-containing quadruple, sequential, concomitant, and levofloxacin-based triple therapies are replacing the long-standing standard of the triple regimen. Despite the encouraging results of these regimens, individualized approaches like treatment after antibiotics resistance test or CYP2C19 genotyping would be the mainstream of future therapy. Because scientific, economic, and technical problems make these advance therapies unfit for widespread use, future development for H. pylori therapy should be directed to overcome individualized antibiotic resistance. Although various novel regimens and additive agents have indicated favorable outcomes, more studies or validations are needed to become a mainstream H. pylori therapy.

• Helicobacter pylori
• Antimicrobial drug resistance
• Clarithromycin
• Metronidazole
• Microbial sensitivity tests

• Animals
• Anti-Bacterial Agents/administration & dosage
• Biotransformation
• Cytochrome P-450 CYP2C19/genetics
• Cytochrome P-450 CYP2C19/metabolism
• Drug Administration Schedule
• Drug Resistance, Multiple, Bacterial
• Drug Therapy, Combination
• Genotype
• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Helicobacter Infections/microbiology
• Helicobacter pylori/drug effects
• Helicobacter pylori/growth & development
• Humans
• Microbial Sensitivity Tests
• Patient Selection
• Pharmacogenetics
• Phenotype
• Precision Medicine
• Predictive Value of Tests
• Proton Pump Inhibitors/administration & dosage
• Proton Pump Inhibitors/pharmacokinetics
• Treatment Outcome

• Colorectal neoplasms
• adenomatous polyps
• bacteria
• helicobacter pylori
• meta-analysis

To summarize the current views and insights on associations between Helicobacter pylori (H. pylori)-related chronic gastritis and colorectal neoplasm, we reviewed recent studies to clarify whether H. pylori infection/H. pylori-related chronic gastritis is associated with an elevated risk of colorectal neoplasm. Recent studies based on large databases with careful control for confounding variables have clearly demonstrated an increased risk of colorectal neoplasm associated with H. pylori infection. The correlation between H. pylori-related chronic atrophic gastritis (CAG) and colorectal neoplasm has only been examined in a limited number of studies. A recent large study using a national histopathological database, and our study based on the stage of H. pylori-related chronic gastritis as determined by serum levels of H. pylori antibody titer and pepsinogen, indicated that H. pylori-related CAG confers an increased risk of colorectal neoplasm, and more extensive atrophic gastritis will probably be associated with even higher risk of neoplasm. In addition, our study suggested that the activity of H. pylori-related chronic gastritis is correlated with colorectal neoplasm risk. H. pylori-related chronic gastritis could be involved in an increased risk of colorectal neoplasm that appears to be enhanced by the progression of gastric atrophy and the presence of active inflammation.

• Colorectal neoplasm
• Cancer risk
• Pepsinogen
• Helicobacter pylori antibody
• Atrophic gastritis

• Animals
• Chronic Disease
• Colonic Neoplasms/complications
• Colonic Neoplasms/microbiology
• Disease Progression
• Gastritis/complications
• Gastritis/microbiology
• Helicobacter Infections/microbiology
• Helicobacter pylori
• Humans
• Inflammation/microbiology
• Pepsinogen A/blood
• Risk Factors

• Helicobacter pylori
• colorectal adenoma
• colorectal cancer
• meta-analysis
• systematic review

• bacteria
• cancer risk.
• colon cancer
• colorectal cancer
• infection
• infectious agent
• virus