Gastric cancer is associated with high morbidity and mortality worldwide. To reduce the socioeconomic burden related to gastric cancer, it is very important to identify and manage high risk group for gastric cancer. In this review, we describe the general risk factors for gastric cancer and define high risk group for gastric cancer. We discuss strategies for the effective management of patients for the prevention and early detection of gastric cancer. Atrophic gastritis (AG) and intestinal metaplasia (IM) are the most significant risk factors for gastric cancer. Therefore, the accurate selection of individuals with AG and IM may be a key strategy for the prevention and/or early detection of gastric cancer. Although endoscopic evaluation using enhanced technologies such as narrow band imaging-magnification, the serum pepsinogen test, Helicobacter pylori serology, and trefoil factor 3 have been evaluated, a gold standard method to accurately select individuals with AG and IM has not emerged. In terms of managing patients at high risk of gastric cancer, it remains uncertain whether H. pylori eradication reverses and/or prevents the progression of AG and IM. Although endoscopic surveillance in high risk patients is expected to be beneficial, further prospective studies in large populations are needed to determine the optimal surveillance interval.
Gastroscopy ; Helicobacter Infections/complications/diagnosis ; Humans ; Risk Factors ; Socioeconomic Factors ; Stomach Neoplasms/*diagnosis/etiology/prevention & control/therapy

BACKGROUND/AIMS: The Helicobacter pylori (H. pylori) eradication rate of standard triple therapy is unsatisfactory in Korea, and sequential therapy (SQT) has been suggested to be a practical first-line alternative regimen. The aim of this prospective study was to document changes in annual eradication rates of SQT. METHODS: A total of 983 H. pylori-positive subjects were enrolled from 2010 to 2018 and their data were subjected to intention-to-treat (ITT) and per-protocol (PP) analysis. All subjects received 10-day sequential therapy consisting of 40 mg esomeprazole and 1 g amoxicillin b.i.d for 5 days followed by 40 mg esomeprazole b.i.d, 500 mg clarithromycin b.i.d and 500 mg metronidazole t.i.d for 5 days. The 13C-urea breath test, rapid urease test (CLO test®), and histology were used to confirm eradication. Compliance and side effects were also investigated. RESULTS: ITT and PP eradication rates of SQT were 69.9% (687 of 983) and 87.1% (657 of 754), respectively. The annual eradication rate of ITT remained consistent over the 8-year study period (p for trend=0.167), whereas PP analysis showed the eradication rate increased (p for trend=0.042). The overall adverse event rate for SQT was 41.7% (410 subjects). CONCLUSIONS: Despite high antibiotic resistance rates in Korea, the eradication rate of SQT did not decrease over the 8-year study period.
Amoxicillin ; Breath Tests ; Clarithromycin ; Compliance ; Drug Resistance, Microbial ; Esomeprazole ; Helicobacter pylori ; Helicobacter ; Intention to Treat Analysis ; Korea ; Metronidazole ; Prospective Studies ; Urease

Although genetic background is known to contribute to colon carcinogenesis, the exact etiology of the disease remains elusive. The organ’s extensive interaction with microbes necessitated research on the role of microbiota on development of colon cancer. In this review, we summarized the defense mechanism of colon from foreign organism, and germ-free animal models that have been employed to elucidate microbial effect. We also comprehensively discussed the metabolic property of microbiota such as butyrate production, facilitation of heme toxicity, bile acid transformation, and nitrate reduction that has been shown to contribute to the development of the tumor. Finally, up-to-date subjects such as the effect of age and gender on microbiota are briefly discussed.
Bile ; Bile Acids and Salts ; Butyrates ; Butyric Acid ; Carcinogenesis ; Colon ; Colonic Neoplasms ; Genetic Background ; Heme ; Microbiota ; Models, Animal

Although there are many guidelines recommending Helicobacter pylori (H. pylori) eradication therapy for atrophic gastritis (AG) and intestinal metaplasia (IM), there have been contradictory reports regarding the reversibility of precancerous lesions such as AG and IM after eradication of H. pylori. There have been many reports that have shown AG seems to improve upon eradication of H. pylori to some extent. In contrast, IM has been regarded as ‘the point of no return’ according to previous reports. However, as recent studies have suggested the improvement of intestinal metaplasia as well, early eradication therapy for reversible histological status is important and necessary for the prevention of gastric cancer. In this review, we focused on the progress of gastritis resulting in AG and IM mainly by H. pylori, the relationship of AG and IM with gastric cancer, the subtype of IM, and the reversibility of AG and IM by eradication of H. pylori. Finally, we introduced the recent extension of indications for H. pylori eradication with coverage by medical insurance, which was published by the Korean Ministry of Health and Welfare in January 2018.
Gastritis ; Gastritis, Atrophic* ; Helicobacter pylori* ; Helicobacter* ; Insurance ; Metaplasia* ; Stomach Neoplasms

There has been an accumulation of data regarding the chemopreventive effects of Helicobacter pylori (H. pylori) eradication. However, it remains unclear how H. pylori infection causes gastric cancer (GC) and how H. pylori eradication can prevent GC. Atrophic gastritis (AG) and intestinal metaplasia (IM) are known as precancerous lesions which mainly lead to intestinal-type GC but to some extent, can also lead to diffuse-type GC. The most important mechanism of AG/IM is H. pylori-induced chronic gastritis. Thus, the reversibility of AG and IM by H. pylori eradication therapy is very important in the prevention of GC. There have been many studies providing data supporting the improvement of AG by the eradication of H. pylori to some extent. In contrast, IM has been regarded as “the point of no return.” However, more recent studies have implied the improvement of IM after eradication, suggesting the importance of early eradication therapy in reversible histological status. In this review, we focused on the reversibility of AG and IM by H. pylori eradication and tried to investigate the predicting factors for the improvement of AG and IM including age, sex, smoking, and diet, as well as H. pylori infection.

The distribution of gut microbiota varies according to age (childhood, puberty, pregnancy, menopause, and old age) and sex. Gut microbiota are known to contribute to gastrointestinal (GI) diseases such as irritable bowel syndrome, inflammatory bowel disease, and colon cancer; however, the exact etiology remains elusive. Recently, sex and gender differences in GI diseases and their relation to gut microbiota has been suggested. Furthermore, the metabolism of estrogen and androgen was reported to be related to the gut microbiome. As gut microbiome is involved in the excretion and circulation process of sex hormones, the concept of “microgenderome” indicating the role of sex hormone on the gut microbiota has been suggested. However, further research is needed for this concept to be universally accepted. In this review, we summarize sex- and gender-differences in gut microbiota and the interplay of microbiota and GI diseases, focusing on sex hormones. We also describe the metabolic role of the microbiota in this regard. Finally, current subjects, such as medication including probiotics, are briefly discussed.

The distribution of gut microbiota varies according to age (childhood, puberty, pregnancy, menopause, and old age) and sex. Gut microbiota are known to contribute to gastrointestinal (GI) diseases such as irritable bowel syndrome, inflammatory bowel disease, and colon cancer; however, the exact etiology remains elusive. Recently, sex and gender differences in GI diseases and their relation to gut microbiota has been suggested. Furthermore, the metabolism of estrogen and androgen was reported to be related to the gut microbiome. As gut microbiome is involved in the excretion and circulation process of sex hormones, the concept of “microgenderome” indicating the role of sex hormone on the gut microbiota has been suggested. However, further research is needed for this concept to be universally accepted. In this review, we summarize sex- and gender-differences in gut microbiota and the interplay of microbiota and GI diseases, focusing on sex hormones. We also describe the metabolic role of the microbiota in this regard. Finally, current subjects, such as medication including probiotics, are briefly discussed.

BACKGROUND/AIMS: Despite numerous studies on the relation of genetic polymorphisms with irritable bowel syndrome (IBS), the results still remain inconclusive. The aim of this study was to assess the possible association between SLC6A4 serotonin transporter gene linked polymorphic region (5-HTTLPR), ADRA2A -1291C>G, GNB3 825C>T, CCK1R intron 779T>C and TRPV1 945G>C polymorphisms and IBS based on Rome III criteria in Korea. METHODS: Study subjects were prospectively recruited from visitors to Seoul National University Bundang Hospital between July 2009 and January 2014. Ninety-nine IBS patients and 171 healthy controls were enrolled. Polymorphisms of above-mentioned 5 genes were genotyped. Serum serotonin from 101 participants was measured by ELISA and compared according to SLC6A4 5-HTTLPR polymorphisms and IBS subtypes. RESULTS: Regarding SLC6A4 5-HTTLPR polymorphism, L/L genotype was significantly associated with the total IBS, constipation predominant IBS (IBS-C) and mixture of diarrhea and constipation IBS (IBS-M) (adjusted OR: 4.35, 95% CI: 1.04-16.67; adjusted OR: 11.11, 95% CI: 1.69-50.00 and adjusted OR: 5.56, 95% CI: 1.05-33.33, respectively). Carrying ADRA2A -1291G allele was significantly associated with total IBS and diarrhea predominant IBS (adjusted OR: 3.37, 95% CI: 1.16-9.77 and adjusted OR: 5.64, 95% CI: 1.18-27.01, respectively). IBS-C patients showed reduced level of serum serotonin compared to controls and patients with diarrhea predominant IBS (50.2 ng/mL vs. 69.0 ng/mL and 92.9 ng/mL, P = 0.017 and P = 0.001, respectively). CONCLUSIONS: Genetic polymorphisms of SLC6A4 5-HTTLPR and ADRA2A -1291C>G could be one of the pathophysiological factors of IBS in Korea. Reduced serum serotonin shown in the IBS-C group suggested a role of serotonin in IBS, but large study is needed for confirming genotypic difference in serum serotonin level.
Alleles ; Constipation ; Diarrhea ; Enzyme-Linked Immunosorbent Assay ; Genotype ; Humans ; Introns ; Irritable Bowel Syndrome* ; Korea ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Prospective Studies ; Receptors, Adrenergic ; Seoul ; Serotonin ; Serotonin Plasma Membrane Transport Proteins*

Gastric cancer is associated with high morbidity and mortality rates worldwide. Identifying individuals at high risk is important for surveillance and prevention of gastric cancer. Having first-degree relatives diagnosed with gastric cancer is a strong and consistent risk factor for gastric cancer, but the pathogenic mechanisms behind this familial aggregation are unclear. Against this background, we reviewed the risk factors for gastric cancer in those with a first-degree relative with gastric cancer, and the possible causes for familial clustering of gastric cancer including bacterial factors, inherited genetic susceptibility, environmental factors or a combination thereof. Among individuals with a family history, current or past Helicobacter pylori infection, having two or more first-degree affected relatives or female gender was associated with an increased risk of developing gastric cancer. To date, no specific single nucleotide polymorphism has been shown to be associated with familial clustering of gastric cancer. H. pylori eradication is the most important strategy for preventing gastric cancer in first-degree relatives of gastric cancer patients, particularly those in their 20s and 30s. Early H. pylori eradication could prevent the progression to intestinal metaplasia and reduce the synergistic effect on gastric carcinogenesis in individuals with both H. pylori infection and a family history. Endoscopic surveillance is also expected to benefit individuals with a family history. Further large-scale, prospective studies are warranted to evaluate the cost-effectiveness and optimal time point for endoscopy in this population. Moreover, genome-wide association studies that incorporate environmental and dietary factors on a ‘big data’ basis will increase our understanding of the pathogenesis of gastric cancer.
Carcinogenesis ; Endoscopy ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Helicobacter pylori ; Humans ; Metaplasia ; Mortality ; Polymorphism, Single Nucleotide ; Prospective Studies ; Risk Factors ; Stomach Neoplasms*

No abstract available.
Esophagus*