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Background: Although white light (WL) colonoscopy is a gold standard to detect colorectal polyps, substantial polyps are missed. Narrow band imaging (NBI) is a new technology that enables a more detailed visualization of the mucosal surface. The aim of the present study was to determine whether NBI can improve the detection of colorectal polyps. Methods: We prospectively enrolled 188 (M : F = 99:89, 21–80 years) subjects undergoing colonoscopy as a screening procedure in nine referral centers. After a careful WL examination of the whole colorectum, rectosigmoid colon (0–30 cm from the anal verge) was reobserved by NBI. Size, macroscopic morphology, and the histology of all the polyps detected during WL and NBI examination were analyzed. Results: WL examination detected 162 polyps in 188 subjects, of which 106 lesions were neoplastic, while NBI of rectosigmoid colon detected an additional 61 polyps of which eight lesions were neoplastic. Only 10 (6.2%) of 162 polyps discovered during WL examination were flat polyps compared to 10 (16.4%) of 61 newly detected polyps during NBI being flat type ( P = 0.002). The mean polyp size detected by NBI was smaller than that found by WL colonoscopy (2.8 ± 1.0 mm vs 6.5 ± 4.5 mm, P < 0.001). Conclusion: Many additional colorectal polyps, especially flat type, could be detected by NBI examination for normal-looking rectosigmoid mucosa. The role of NBI in colorectal neoplasm screening needs to be further investigated in future studies. [ABSTRACT FROM AUTHOR]

Background. Helicobacter pylori induces the expression of proinflammatory cytokines in vitro by activating nuclear factor-κB, a transcriptional regulator. However, it has not been clarified whether H. pylori-induced proinflammatory cytokines are also mediated through nuclear factor-κB in vivo. The aim of this study was to evaluate the role of nuclear factor-κB on the expressions of proinflammatory cytokines in H. pylori-infected mice. Materials and Methods. We evaluated nuclear factor-κB (p65) activation in the H. pylori-infected gastric mucosa of mice by immunofluorescent staining using antip65 polyclonal antibody, and the expressions of proinflammatory cytokines with inhibition of nuclear factor-κB pathway by using phosphorothioate antisense and sense oligonucleotide against the nuclear factor-κB (p65). Results. In the H. pylori-infected gastric mucosa of mice, immunofluorescent staining using antip65 polyclonal antibody showed nuclear factor-κB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor-α and interleukin-1β concentrations in gastric mucosa by enzyme-linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with nuclear factor-κB (p65) antisense oligonucleotide inhibited the activation of nuclear factor-κB and the expressions of tumor necrosis factor-α and interleukin-1β in H. pylori-infected gastric mucosa. Sense oligonucleotide did not influence on the expression of proinflammatory cytokines. Conclusions. H. pylori infection was found to activate the expressions of proinflammatory cytokines via nuclear factor-κB in vivo, and this may play an important role in the initiation of H. pylori-induced gastric inflammation. [ABSTRACT FROM AUTHOR]

Helicobacter pylori stimulates nuclear factor-kappa B (NF-κB) activation and chemokine interleukin-8 (IL-8) expression in gastric epithelial cells. Ecabet sodium (ecabet), a locally acting antiulcer drug, is known to have anti- H. pylori activity. However, there is little understanding of how ecabet induces anti-inflammatory activity in gastric epithelial cells infected with H. pylori. The aim of this study was to investigate the effects of ecabet on IL-8 gene expression and NF-κB activation in human gastric epithelial cells infected with H. pylori. After Hs746T, MKN-45, or SNU-5 gastric epithelial cell lines had been infected with cagA+cytotoxin+ H. pylori in the presence of ecabet, IL-8 mRNA expression was assessed by quantitative reverse transcription–polymerase chain reaction, and IL-8 secretion was measured by enzyme-linked immunosorbent assay. NF-κB and inhibitory kappa B-alpha (IκBα) signals were assayed by electrophoretic mobility shift assay and Western blot, respectively. The activation of NF-κB and IL-8 reporter genes was determined by luciferase assay. Ecabet showed no antimicrobial activiy against Gram-positive or -negative bacteria. However, ecabet inhibited transcription of the IL-8 gene and secretion of IL-8 by gastric epithelial cells infected with H. pylori at a concentration of 5 µg/ml. Moreover, ecabet inhibited the activation of NF-κB and the degradation of IκBα in gastric epithelial cells in response to H. pylori infection. In addition, the NF-κB signal inhibited by ecabet was comprised predominantly of heterodimers of p65/p50. Ecabet inhibited H. pylori-induced IL-8 gene transcription and secretion by suppressing the NF-κB signal. This inhibition might be one pathway by which ecabet exerts its anti-inflammatory effect on H. pylori-induced gastric inflammation. [ABSTRACT FROM AUTHOR]

The author discusses the effectiveness of germinated barley foodstuff (GBF) in colitis-associated colon cancer prevention and treatment. The author denotes how the inflammatory bowel disease (IBD) can aggravate the risk of acquiring such cancer. The author notes the fermentation of the GBF through gut microbiota and it provokes the growth of prebiotics such as Bifidobacterium, Eubacterium, and Lactobacillus species which can prevent colitis as well as colon cancer.

Background and Aim: The number of patients with ulcerative colitis (UC) in Korea has increased. In addition, the number of patients with colorectal cancer (CRC) associated with UC has also increased. Therefore, this population-based nationwide study was conducted to investigate the incidence of CRC in patients with UC in Korea and compare these results to those of studies conducted in other countries. Methods: The Korean Association for the Study of Intestinal Diseases (KASID) reviewed 7061 cases of UC that occurred between 1970 and 2005 and found a total of 26 cases of CRC. Results: The overall prevalence of CRC in patients with UC was 0.37%. In addition, the estimated cumulative risk of UC-associated CRCs was 0.7% for patients that had UC for 10 years, 7.9% for patients that had UC for 20 years, and 33.2% for patients that had UC for 30 years. The mean age at the time of diagnosis with CRC was 49.6 years, and the mean duration of UC prior to the development of CRC was 11.5 years. Most UC-associated CRCs were diagnosed after they were already in advanced stages; however, the stage at diagnosis was lower in patients that had good compliance with medical treatment. Conclusion: The cumulative incidence of UC-associated CRCs in Korea was found to be comparable to that of western countries. The overall occurrence of UC-associated CRC in Korea may be growing, therefore, intensive surveillance colonoscopy and constructive chemoprevention should be encouraged to enable early detection and treatment of UC-associated CRCs in Korea. [ABSTRACT FROM AUTHOR]

A 59-year-old man underwent endoscopic mucosal resection (EMR) for gastric adenoma. He had suffered from end-stage renal disease for several years and had received renal transplantation some 5 months before EMR. Subsequently, he took immunosuppressive agents. Follow-up gastrofiberscopy 6 months after EMR showed a sessile polyp at the resection site twice as large as the original adenoma; biopsy specimens revealed a hyperplastic nature. At the time of writing, this hyperplastic polyp has neither increased in size nor developed adenomatous or carcinomatous changes by histological examinations over the past 5 years. Therefore, this is a case of hyperplastic polyp occurring at the gastric adenoma resection site, and suggests the possible effect of immunosuppressive therapy on the post-EMR healing process and hyperplastic polyp development. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the efficacy of a new polyclonal enzyme immunoassay for the detection of Helicobacter pylori ( H. pylori) antigen in stool by determination of the optimal cut-off value in the screening population. A consecutive 515 patients undergoing a routine health check-up were prospectively enrolled. H. pylori infection was defined if at least two of four tests (histology, rapid urease test, C-urea breath test, and serology) were positive. A stool antigen test (EZ-STEP H. pylori) was performed for the detection of H. pylori. The optimal cut-off value was determined by the receiver-operator characteristic curve. The diagnostic performance of each test was evaluated with regard to the histological diagnosis of atrophic gastritis (AG)/intestinal metaplasia (IM), degree of AG/IM, and old age. Sensitivity, specificity, positive and negative predictive values, and accuracy of the stool antigen test were 93.1%, 94.6%, 95.1%, 92.3%, and 93.8%, respectively. The sensitivity of histology, rapid urease test, and theC-urea breath test ranged from 89.1% to 97.6%, and their specificity was > 98%, while serology had high sensitivity, but low specificity. The accuracy of the stool antigen test was comparable to that of other methods (93.6-95.9%), whereas it was higher than that of serology. The stool antigen test still showed good diagnostic performance in the setting of progression of AG/IM and in patients over 40 years. The performance of a new stool antigen test was comparable to that of other methods in the diagnosis of H. pylori infection for the screening population, even with the presence of AG/IM. [ABSTRACT FROM AUTHOR]

To determine genome-wide DNA methylation profiles induced by Helicobacter pylori ( H. pylori) infection and to identify methylation markers in H. pylori-induced gastric carcinogenesis. Gastric mucosae obtained from controls (n = 20) and patients with gastric cancer (n = 28) were included. A wide panel of CpG sites in cancer-related genes (1505 CpG sites in 807 genes) was analyzed using Illumina bead array technology. Validation of the results of Illumina bead array technique was performed using methylation-specific PCR method for four genes ( MOS, DCC, CRK, and PTPN6). The Illumina bead array showed that a total of 359 CpG sites (269 genes) were identified as differentially methylated by H. pylori infection ( p < .0001). The correlation between methylation-specific PCR and bead array analysis was significant ( p < .0001, Spearman coefficient = 0.5054). Methylation profiles in noncancerous gastric mucosae of the patients with gastric cancer showed quite distinct patterns according to the presence or absence of the current H. pylori infection; however, 10 CpG sites were identified to be hypermethylated and three hypomethylated in association with the presence of gastric cancer regardless of H. pylori infection ( p < .01). Genome-wide methylation profiles showed a number of genes differentially methylated by H. pylori infection. Methylation profiles in noncancerous gastric mucosae from the patients with gastric cancer can be affected by H. pylori-induced gastritis. Differentially methylated CpG sites in this study needs to be validated in a larger population using quantitative methylation-specific PCR method. [ABSTRACT FROM AUTHOR]

Background and Aim: Colorectal cancer screening is recommended for average-risk persons beginning at age 50. However, information about the incidence and risk factors of precursor adenoma in preceding decades is limited. The aim of this study was to determine the prevalence and risk factors of colorectal adenoma in persons aged 40–49 years and to compare the data with those aged 30–39 years and 50–59 years. Methods: A cross-sectional study of 5254 asymptomatic subjects who underwent screening colonoscopy was conducted. Data were stratified by age into three groups: 608 aged 30–39 years, 1930 aged 40–49 years, and 2716 aged 50–59 years. Results: Prevalence of overall adenomas was 10.4% in the 30–39 years age group, 22.2% in the 40–49 years age group, and 32.8% in the 50–59 years age group. Advanced adenoma was found in 0.7% of the 30–39 years age group, 2.7% of the 40–49 years age group, and 4.1% of the 50–59 years age group. In the 40–49 years age group, male sex and current smoking habits showed associations with low-risk adenoma after multiple adjustments. Moreover, male sex (odds ratio [OR] = 1.55, 95% confidence interval [CI]: 1.02–3.23), current smoking (OR = 1.58, 95%CI: 1.06–3.50), and family history of colorectal cancer (OR = 2.54, 95%CI: 1.16–5.56) were independent predictors of advanced adenoma in this age group. Conclusions: Prevalence of adenoma in subjects aged 40–49 years was higher than in previous studies. Male sex and current smoking habits along with a family history of colorectal cancer were associated with advanced adenoma in this age group. [ABSTRACT FROM AUTHOR]

Background and Aim: Proton pump inhibitors (PPI) are mainly metabolized by cytochrome P450 2C19 (CYP2C19) in the liver. We investigated whether the CYP2C19 genotype plays a role in the eradication rate of Helicobacter pylori ( H. pylori) infection in patients receiving pantoprazole- or esomeprazole-based triple therapy. Methods: A total of 327 patients infected with H. pylori were treated with either pantoprazole or esomeprazole, plus amoxicillin and clarithromycin for 7 days. The presence of the CYP2C19 genotype was determined by pyrosequencing. Results: The overall H. pylori eradication rate was 85%; 82.6% for the PAC regimen, and 88.3% for the EAC regimen; the differences were not statistically significant. The overall eradication rate in the poor metabolizer groups (PM) was significantly higher than in the extensive metabolizer groups (EM) (97.4% vs 83.3%; P = 0.016). The eradication rates in the EM and PM groups were 80.8% and 95.7% for the PAC regimen and 86.8% and 100% for the EAC regimen, respectively. Conclusion: The results of this study suggest that the CYP2C19 genotype status may play a role in the H. pylori eradication rate in patients receiving pantoprazole or esomeprazole-based triple therapy. [ABSTRACT FROM AUTHOR]

Background: This study was performed to evaluate whether the addition of probiotics to proton pump inhibitor (PPI)-based triple therapy increases the likelihood of successful Helicobacter pylori eradication. Materials and Methods: Three hundred and forty-seven H. pylori-infected patients were randomized into a triple-plus-yogurt group (yogurt group, n = 168) or a triple-only group (control group, n = 179). Triple therapy consisted of PPI b.i.d., clarithromycin 500 mg b.i.d., and amoxicillin 1 g b.i.d. for 7 days. Yogurt group received triple therapy for 1 week and one bottle of Will yogurt per day for at 3 weeks, starting on the first day of triple therapy. Will yogurt (a Korean brand) contains Lactobacillus acidophilus HY2177, Lactobacillus casei HY2743, Bifidobacterium longum HY8001, and Streptococcus thermophilus B-1. 13C-urea breath test was performed at least 4 weeks after completion of triple therapy. Eradication rates, compliances, and adverse events were compared. Results: By intention-to treat analysis the H. pylori eradication rates in the yogurt group 79.2% (133 of 168) was similar to that in the control group 72.1% (129 of 179) ( p = .124). However, by per-protocol (PP) analysis, the eradication rate in the yogurt group, 87.5% (133 of 152) was higher than that in the control group, 78.7% (129 of 164) ( p = .037). Common adverse events were metallic taste (11.8%) and diarrhea (8.6%). The frequency of adverse effects in the yogurt group 41.1% (69/168) were higher than in the control group, 26.3% (47 of 179) ( p = .003). However, most adverse events were mild to moderate in intensity, and the severities of adverse effects were similar in both groups ( p = .401). Conclusions: The addition of Will yogurt to triple therapy did not reduce the side-effects of triple therapy. But it increased the H. pylori eradication rate by PP analysis, encouraging more research in this field. [ABSTRACT FROM AUTHOR]

Background and Aim: Interactions between released proteins by Helicobacter pylori ( H. pylori) and the cells of gastric epithelium to which it adheres may contribute to gastric inflammation and epithelial damage. The present study was performed to evaluate the gene expression of AGS gastric cancer cells stimulated with released proteins by H. pylori. Methods: Gene expression of AGS cells to the stimulation by H. pylori-released proteins (G27 strain) were monitored using oligonucleotide microarrays. Results: Eighty-eight genes (0.88%) and eight genes (0.08%) were up- or downregulated, respectively, by treating AGS cells with H. pylori-released proteins but not by H. pylori adhesion after 12 h of coculture. Out of the selected 40 up- and five downregulated genes, 29 upregulated genes classified as general RNA polymerase II transcription factor activity ( GTF2B, PPARGC1A), SH3/ SH2 adaptor activity ( CRKL), transferase activity ( ACLY, CRKL, PIGC, PLK4), and oxidoreductase activity ( IDH1) were confirmed to be upregulated by released proteins and not by H. pylori adhesion by real-time reverse transcription–polymerase chain reaction. When the concentrated H. pylori-cultured supernatant prepared by our protocol was treated by boiling, the upregulations of 26 of these 29 genes (89.7%) except for CD160, ZNF268, and PSAT1 disappeared. This confirmed that most of these upregulations were caused by released proteins. Conclusion: Host genes involving transcription, signaling and stress are significantly modulated by the proteins released by H. pylori. This might strengthen the gastroduodenal pathogenesis induced by H. pylori. [ABSTRACT FROM AUTHOR]

Background and Aim: This study was performed to determine whether serum pepsinogen (PG) and gastrin testing can be used to detect gastric cancer in Korea. Methods: Serum levels of PG I (sPGI) and sPGII, PG I/II ratios, and gastrin levels were measured in 1006 patients with gastroduodenal diseases including cancer. Follow-up tests were performed 1 year after Helicobacter pylori eradication. Results: sPGI and sPGII levels increased and PG I/II ratios decreased in line with the severity of activity, chronic inflammation, and the presence of H. pylori ( p < .01). In contrast, sPGI levels and PG I/II ratios decreased in proportion with the severity of atrophic gastritis (AG)/intestinal metaplasia ( p < .01). Gastrin levels were found to be correlated with chronic inflammation negatively in the antrum but positively in the corpus. H. pylori eradication reduced sPGI, sPGII, and gastrin levels, and increased PG I/II ratios to the levels of H. pylori-negative patients, and was found to be correlated with reductions in activity and chronic inflammation of gastritis. The sensitivity and specificity of a PG I/II ratio of ≤ 3.0 for the detection of dysplasia or cancer were 55.8–62.3% and 61%, respectively. In addition, sPGI and sPGII levels of intestinal-type cancer were significantly lower than those of the diffuse type, respectively ( p = .008 and p = .05, respectively). Gastric cancer risk was highest in the H. pylori-positive, low PGI/II ratio (≤ 3.0) group with an odds ratio of 5.52 (confidence interval: 2.83–10.77). Conclusion: PG I/II ratio (≤ 3.0) was found to be a reliable marker for the detection of dysplasia or gastric cancer, especially of the intestinal type. This detection power of PG I/II ratio (≤ 3.0) significantly increased in the presence of H. pylori, and thus, provides a means of selecting those at high risk of developing gastric cancer in Korea. [ABSTRACT FROM AUTHOR]

Background and aim: The aim of this study was to test the efficacy of 10-day moxifloxacin-based triple therapy versus 2-week quadruple therapy for the second-line treatment of Helicobacter pylori infection. Methods: One hundred and ninety-two patients who had failed previous H. pylori eradication on standard triple therapy were randomized to one of two regimens: 1, moxifloxacin (400 mg q.d.), amoxicillin (1000 mg b.i.d.), and esomeprazole (20 mg b.i.d.) for 10 days (the 10MEA group), or 2, esomeprazole (20 mg b.i.d.), tripotassium dicitrate bismuthate (300 mg q.i.d.), metronidazole (500 mg t.i.d.), and tetracycline 500 mg (q.i.d.) for 14 days (the 14EBMT group). The eradication rates, drug compliances, and side-effect rates of these two regimens were compared. Results: Eradication rates by intention-to-treat and per-protocol analyses in the 10MEA and 14EMBT groups were 71.9% and 82.6%, and 71.7% and 90.5% ( p = .973 and .321), respectively. The 10MEA group was significantly superior to the 14EMBT group in terms of side-effect rates (12.2% vs. 39.6%, p = .001), and discontinuation rates due to side-effects were lower in the 10MEA group than in the 14EMBT group (0.7% vs. 13.2%, p < .001). Moreover, compliance was higher in the 10MEA group (94.2% (131/139)) than in the 14EBMT group (83.0% (44/53)) ( p = .014). Conclusion: The 10-day moxifloxacin-based triple therapy was found to have a high eradication rate with few side-effects and good drug compliance. These findings suggest that this regimen is a safe and effective second-line treatment option for H. pylori infection in Korea. [ABSTRACT FROM AUTHOR]

Objective: To evaluate whether or not genetic polymorphism of IL-1B, IL-1RN, and TNF-Α is an important factor in the different expression of gastroduodenal diseases after Helicobacter pylori infection. Methods: This study consisted of 1360 subjects: control, gastric cancer (GC, intestinal type, and diffuse type), benign gastric ulcer (BGU), duodenal ulcer, and first-degree gastric cancer relative (GCR). IL-1Β-511 and TNF-A-308 biallelic polymorphism were genotyped by 5′ nuclease polymerase chain reaction (PCR) assays, and PCR-restriction fragment length polymorphism (PCR-RFLP). IL-1RN penta-allelic variable number of tandem repeats was genotyped by PCR. Results: There was no difference in the genetic polymorphism of IL-1Β-511, IL-1RN and TNF-A in the patients with gastric cancer regardless of H. pylori positivity compared with control. However, the frequencies of IL-1B-511 C/T (OR: 0.5, 95% CI: 0.3–0.7) and T carrier (OR: 0.6, 95% CI: 0.4–0.8) were lower in the H. pylori-positive BGU patients. The IL-1RN 2/2 was higher (OR: 5.5, 95% CI: 1.1–28.5) in the H. pylori-positive GCR. There was no significance in the polymorphism of TNF-Α-308 regardless of H. pylori-induced gastroduodenal diseases. Conclusions: The IL-1Β-511 T-carrier polymorphism has a negative effect on the development of H. pylori-positive BGU, and high frequency of IL-1RN 2/2 was found in the H. pylori-positive relatives of GC patients, which suggest that this genetic polymorphism could play some role in the H. pylori-induced gastroduodenal diseases in Korea. [ABSTRACT FROM AUTHOR]

Background and Aim: Metronidazole and tetracycline-based second-line quadruple therapy, widely used for Helicobacter pylori infection, often ends up in failure due to antibiotic resistance and poor compliance in Korea. Our aim is to evaluate the efficacy and tolerability of moxifloxacin-based triple therapy as an alternative second-line treatment for H. pylori infection. Methods: The subjects consisted of 85 patients infected with H. pylori, in whom initial proton pump inhibitor triple therapy had failed. They were randomized to receive the following 7-day therapy: 1, moxifloxacin 400 mg q.d., esomeprazole 20 mg b.i.d., and amoxicillin 1 g b.i.d.; and 2, esomeprazole 40 mg b.i.d., tripotassium dicitrate bismuthate 300 mg q.i.d., metronidazole 500 mg t.i.d., and tetracycline 500 mg q.i.d. Eradication rates, drug compliance, and side-effect rates of each group were evaluated. Results: The eradication rates were 75.6 and 83.8% with moxifloxacin triple therapy, and 54.5 and 72.7% with quadruple therapy by intention-to-treat ( p = .042) and per-protocol analyses ( p = .260), respectively. Moxifloxacin triple therapy was significantly superior to quadruple therapy in terms of side-effect rates ( p = .039). Compliance for therapy, i.e., the percentage of tablets taken (> 85%), was 90.2 and 75.0%, numerically higher in moxifloxacin triple therapy group than in quadruple therapy group, but without statistical difference ( p = .065). Conclusions: Moxifloxacin-based triple therapy showed high eradication rates with few side effects and good drug compliance, suggesting this regimen could be a safe and effective option as second-line therapy for H. pylori infection in Korea. [ABSTRACT FROM AUTHOR]