Changes in the first line Helicobacter pylori eradication rates using the triple therapy-a multicenter study in the Tokyo metropolitan area (Tokyo Helicobacter pylori study group).

BACKGROUND AND AIM: Helicobacter pylori (H. pylori) infection is a strong risk factor for the development of gastric cancer. In 2013, the Japanese government approved H. pylori eradication therapy in patients with chronic gastritis as well as peptic ulcer. However, the continuing decline in eradication rates for first-line H. pylori eradication therapies is an urgent problem. In this study, we investigated changes in the first-line eradication rate from 2001 to 2010. METHODS: Eradication rates for 7-day triple therapy [proton pump inhibitor (rabeprazole 20 mg, lansoprazole 60 mg, or omeprazole 40 mg)+amoxicillin 1500 mg + clarithromycin (CAM) 400 or 800 mg, daily] were collated from 14 hospitals in the Tokyo metropolitan area. The urea breath test was used for the evaluation of eradication. The cut-off value was less than 2.5%. RESULTS: The yearly eradication rates (intention to treat/per protocol) were 78.5/79.5% (2001, n=242), 71.2%/72.9% (2002, n=208), 67.8%/70.5% (2003, n=183), 75.6%/84.6% (2004, n=131), 56.4%/70.5% (2005, n=114), 70.5%/75.8% (2006, n=271), 67.4%/82.0% (2007, n=135), 64.0%/76.3% (2008, n=261), 60.5%/74.3% (2009, n=329), and 66.5%/78.8% (2010, n=370), respectively. Examination of eradication rates according to CAM dosage revealed an eradication rate of 65.6% (383/584) for CAM 400 mg daily, and 68.5% (1124/1642) for CAM 800 mg daily, with no significant difference seen between dosages. CONCLUSION: In recent years, eradication rates for first-line triple therapy have obviously decreased, but no noticeable decrease has occurred after 2001.

Trends of second-line eradication therapy for Helicobacter pylori in Japan: a multicenter study in the Tokyo metropolitan area.

BACKGROUND: In Japan, the eradication rate of first-line therapy for Helicobacter pylori (H. pylori) with a proton pump inhibitor (PPI), amoxicillin (AMPC) and clarithromycin (CAM) has been decreasing because of a high prevalence of CAM resistance. A possible decrease of the eradication rate for second-line therapy with a PPI, AMPC and metronidazole (MNZ) is of concern. The aim of this study is to assess the trends in second-line eradication therapy for H. pylori in Japan. MATERIALS AND METHODS: We accumulated data retrospectively on patients administered second-line eradication therapy for Helicobacter pylori with a PPI, AMPC, and MNZ for 1 week after failure of first-line eradication therapy with a PPI, AMPC and CAM at 15 facilities in the Tokyo metropolitan area in Japan from 2007 to 2011. Trends for second-line eradication rates in modified intention-to-treat (ITT) analyses were investigated. Second-line eradication rates were categorized by three PPIs (rabeprazole (RPZ), lansoprazole (LPZ) or omeprazole (OMZ)) and evaluated. RESULTS: We accumulated data on 1373 patients. The overall second-line eradication rate was 92.4%. Second-line eradication rates in 2007, 2008, 2009, 2010 and 2011 were 97.7, 90.6, 94.5, 91.8 and 91.8%, respectively, with no significant trends revealed. Second-line eradication rates categorized by three PPIs for the entire 5-year period were 91.6, 93.4 and 92.4% (RPZ, LPZ and OPZ, respectively) with no significant differences among the three PPIs. CONCLUSIONS: From 2007 to 2011, there were no significant trends in the second-line eradication rates and the rates remained consistently high. From the viewpoint of high prevalence of CAM resistance in Japan, triple therapy with PPI, AMPC and MNZ may be a better strategy for first-line therapy compared to triple therapy with PPI, AMPC and CAM.

Helicobacter pylori upregulates peripheral platelet counts mainly in female patients.

To evaluate the influence of Helicobacter pylori and sex difference on peripheral platelet counts, dyspeptic patients without immunohaematologic disorders were evaluated. H. pylori infection was verified with the rapid urease test and serum anti-H. pylori IgG antibody. Platelet counts were analysed with a reference to H. pylori infection and sex difference. Among H. pylori-eradicated patients, changes in platelet counts were separately evaluated. Totally, 655 patients were enrolled: 340 patients were infected with H. pylori and 178 patients received eradication therapy, with a success rate of 88.2% (157/178). Females with H. pylori infection definitely manifested elevated platelet counts (infected vs. uninfected 244 ± 57 vs. 219 ± 54 × 10(9)/l; p < 0.0001). H. pylori eradication reduced peripheral platelets by 8 weeks, 5-6 months, 1, 2 and ≥3 years after eradication in females from 248 ± 54 to 237 ± 49, 237 ± 54, 229 ± 48, 238 ± 61 and 232 ± 50 × 10(9)/l (p = 0.0003, 0.0182, 0.0041, 0.0398 and 0.0289), respectively. In males, the reduction was verified by 8 weeks, 1 year and ≥3 years from 226 ± 52 to 217 ± 47, 214 ± 44 and 200 ± 49 × 10(9)/l (p = 0.0464, 0.0164 and 0.0016), respectively. In conclusion, H. pylori infection upregulates platelet counts mainly in females, and eradication reduced peripheral platelets in both sexes. Females appeared more susceptible to H. pylori infection than males with regard to upregulation of platelet counts.

Long term changes in platelet counts after H. pylori eradication in non-ITP patients.

Helicobacter pylori eradication is becoming a first-line therapy against idiopathic thrombocytopenic purpura (ITP) and its long term efficacy has already been reported. In contrast, eradication therapy reduced peripheral platelets in non-ITP patients 8 weeks later. To confirm the long term efficacy of Helicobacter eradication on platelet counts in non-ITP patients, we evaluated changes in peripheral platelet counts in endoscopically diagnosed patients with Helicobacter infection. Endoscopically diagnosed patients with Helicobacter infection received eradication therapy using amoxicillin (1500 mg/day), clarithromycin (400 mg/day) and lansoprazole (60 mg/day). The changes in platelet counts after Helicobacter eradication were serially evaluated for as long as 3 years or more. In total, 294 patients were enrolled: 243 patients successfully received eradication therapy and 51 were unsuccessfully treated. As a whole, peripheral platelet counts significantly decreased after Helicobacter eradication, being reduced by more than 1.0 × 109/l by 5-6 months, 1 year, 2 years and 3 years or more (from 24.2+/-5.6 to 23.1+/-5.0, 23.0+/-5.0, 22.1+/-4.5, 22.4+/-5.6, and 21.6+/-5.3 × 109/l: p = <0.0001, <0.0001, 0.0001, 0.0052, and <0.0001, respectively). Helicobacter pylori eradication finally reduced peripheral platelet counts around 2.0 × 109/l in non-ITP patients. There was a definite difference in platelet regulation by Helicobacter pylori between ITP and non-ITP patients. These bivalent effects, upregulation and downregulation, on the peripheral platelet induced by Helicibacter pylori infection appeared to originate from quite different mechanisms.

Current status of first- and second-line Helicobacter pylori eradication therapy in the metropolitan area: a multicenter study with a large number of patients.

BACKGROUND: The environment surrounding Helicobacter pylori eradication treatment is dramatically changing. Recently, vonoprazan, a first-in-class potassium-competitive acid blocker (P-CAB), was introduced onto the market in 2015. The aging of Japan's demographic structure is becoming pronounced. In this study, we examined the trend of the eradication rate of H. pylori in the metropolitan area and examined factors concerning successful eradication. METHODS: We collected data from 20 hospitals in the Tokyo metropolitan area on patients who received first-line eradication therapy with a proton-pump inhibitor (PPI)/P-CAB, amoxicillin, and clarithromycin for 1 week and second-line eradication therapy with a PPI/P-CAB, amoxicillin, and metronidazole for 1 week from 2013 to 2018. The annual eradication rate and associated factors for successful eradication were analyzed. RESULTS: We collected data of 4097 and 3572 patients in the first- and second-line eradication therapies, respectively. The eradication rate decreased from 2013 to 2014 and increased again from 2015 to 2018 with the first-line therapy [the eradication rates in 2013, 2014, 2015, 2016, 2017 and 2018 were 71.8%, 63.7%, 78.5%, 84.6%, 89.7 and 90.1%, respectively, in the per protocol (PP)]. The second-line eradication rates were 90.0%, 82.6%, 88.8%, 87.5%, 91.8% and 90.1% in 2013, 2014, 2015, 2016, 2017 and 2018, respectively, in PP. Vonoprazan was an independent factor for successful eradication in not only first-line, but also second-line eradication. Age over 75 years was an independent factor for eradication failure in both first- and second-line eradication therapies. CONCLUSION: The eradication rate improved from 2015 to 2018 with the first-line therapy because of the introduction of vonoprazan in the market. The eradication rates with first- and second-line regimens in elderly patients were lower than those in younger patients.

Endoscope images of Schönlein-Henoch purpura.

BACKGROUND/AIMS: Schönlein-Henoch purpura (SHP) is a systemic condition characterized by purpura associated with leukocytoclastic vasculitis. SHP diagnosis is more difficult in infrequent cases where gastrointestinal (GI) symptoms precede purpura. This report examines 11 cases of SHP at our hospital with specific regard to the incidences and details of GI symptoms. METHODS: The clinical manifestations and endoscopic findings were investigated for their utility in SHP diagnosis. RESULTS: Among the 11 cases, 3 showed GI symptoms prior to other manifestations. In terms of GI symptoms, abdominal pain was reported in all 11 cases, diarrhea in 4 cases, and bloody stools in 3 cases. Endoscopic findings were seen in the stomach in 7/10 cases, in the small intestine including the duodenum in 10/11 cases, and in the large intestine in 6/10 cases. The frequency of ulcer formation was significantly higher in the small intestine (including the duodenum) than in the stomach. Multiple specific erythematosus lesions were observed in the stomach and large intestine. CONCLUSION: Familiarity with characteristic endoscopic findings and careful observation of all GI findings are essential for diagnosing SHP in cases in which GI tract symptoms precede cutaneous findings.

Prophylactic impact of endoscopic treatment for esophageal varices in liver resection: a prospective study.

BACKGROUND: Prophylactic treatment for esophageal varices has been performed without adequate supporting evidence. We assessed the feasibility of prophylactic and follow-up treatment for high-risk esophageal varices in patients with hepatocellular carcinoma (HCC). METHODS: Patients with HCC were screened prospectively and followed up for esophageal varices and gastroduodenal ulceration. High-risk esophageal varices (huge F3 varices or intermediate F2 varices positive for red color signs) were treated prophylactically. Follow-up endoscopy was performed to assess the impact of prophylaxis and changes in varices at 1 week, 1 month, and 6 months after operation. If high-risk varices were found during follow-up, secondary prophylaxis was performed according to the same criteria. RESULTS: Among 251 patients with HCC, 81 (32.3 %) had esophageal varices on screening endoscopy. Prophylactic endoscopic treatment was required by 13 patients (1 with F3 varices and 12 with F2 varices positive for red color signs). Ten varices worsened, and 4 varices progressed to high-risk varices requiring endoscopic treatment. No F0 or F1 varices at screening endoscopy progressed to high-risk varices, and no bleeding event occurred during 6 months of preplanned follow-up. A preoperative platelet count of less than 10 × 10(4)/µL (odds ratio: 4.21, 95 % confidence interval 3.11-10.6; p < 0.001), the presence of splenomegaly (2.87, 2.16-21.8; p = 0.011), and an indocyanine green retention rate at 15 min of greater than 30 % (2.31, 1.88-24.6; p = 0.026) were independent predictors of worsening varices. CONCLUSIONS: Our protocol for prophylactic and follow-up treatment of high-risk esophageal varices was feasible in patients with HCC.

Spontaneous Regression of Polyposis following Abdominal Colectomy and Helicobacter pylori Eradication for Cronkhite-Canada Syndrome.

The etiology of Cronkhite-Canada syndrome (CCS) remains unknown and many cases are refractory to treatment. Therefore, new therapies are urgently needed. Furthermore, a number of CCS cases with gastrointestinal carcinoma have been reported. Our patient had rapid onset of CCS and early development of colon carcinoma associated with adenomas. High anterior resection of the sigmoid colon and ileostomy were performed, and her symptoms and endoscopic and histological findings improved. Helicobacter pylori eradication was carried out 2 years later, surgical closure of an ileal fistula the following year. After 4 months, upper gastrointestinal endoscopy and colonoscopy showed that the CCS lesions had completely disappeared, and biopsies confirmed a normal stomach, duodenum, ileum and colon histologically. The patient has maintained remission for 2 years. The clinical course of this case, showing complete regression of CCS lesions following abdominal colectomy and H. pylori eradication, suggests the significance of H. pylori infection in the treatment of CCS.

Multi-center randomized controlled study to establish the standard third-line regimen for Helicobacter pylori eradication in Japan.

BACKGROUNDS: The present study sought to establish a standard third-line eradication regimen for Helicobacter pylori in Japan. METHODS: Subjects were 204 patients with H. pylori infection in whom the standard Japanese first- and second-line eradication therapies had proven unsuccessful. Patients were randomly assigned to one of the following third-line eradication therapy groups: (1) LA group: lansoprazole (LPZ) 30 mg 4 times a day (qid) + amoxicillin (AMPC) 500 mg qid for two weeks; (2) LAL group: LPZ 30 mg twice a day (bid) + AMPC 750 mg bid + levofloxacin (LVFX) 300 mg bid for one week; (3) LAS group: LPZ 30 mg bid + AMPC 750 mg bid + sitafloxacin (STFX) 100 mg bid for one week. Patients for whom these therapies failed underwent a crossover fourth-line eradication regimen. Drug sensitivity was also tested for AMPC, clarithromycin (CAM), MNZ, LVFX, and STFX. RESULTS: Drug resistance rates prior to third-line eradication therapy were 86.4 % for CAM, 71.3 % for MNZ, 57.0 % for LVFX, 8.2 % for AMPC, and 7.7 % for STFX. Intention-to-treat analysis of third-line eradication therapy eradication rates showed a significantly higher rate in the LAS group (70.0 %) compared with the LA group (54.3 %; p < 0.05) and the LAL group (43.1 %; p < 0.001). The significantly lower rate in the LAL group than the LAS group was caused by bacterial resistance to LVFX. CONCLUSIONS: The findings suggest that triple therapy with PPI, AMPC, and STFX for one week would be an effective standard third-line eradication regimen for H. pylori in Japan.

Anti-inflammatory activity of probiotic Bifidobacterium: enhancement of IL-10 production in peripheral blood mononuclear cells from ulcerative colitis patients and inhibition of IL-8 secretion in HT-29 cells.

AIM: To determine the anti-inflammatory activity of probiotic Bifidobacteria in Bifidobacteria-fermented milk (BFM) which is effective against active ulcerative colitis (UC) and exacerbations of UC, and to explore the immunoregulatory mechanisms. METHODS: Peripheral blood mononuclear cells (PBMNC) from UC patients or HT-29 cells were co-cultured with heat-killed probiotic bacteria or culture supernatant of Bifidobacterium breve strain Yakult (BbrY) or Bifidobacterium bifidum strain Yakult (BbiY) to estimate the amount of IL-10 or IL-8 secreted. RESULTS: Both strains of probiotic Bifidobacteria contained in the BFM induced IL-10 production in PBMNC from UC patients, though BbrY was more effective than BbiY. Conditioned medium (CM) and DNA of both strains inhibited IL-8 secretion in HT-29 cells stimulated with TNF-alpha, whereas no such effect was observed with heat-killed bacteria. The inhibitory effect of CM derived from BbiY was greater than that of CM derived from BbrY. DNAs of the two strains had a comparable inhibitory activity against the secretion of IL-8. CM of BbiY induced a repression of IL-8 gene expression with a higher expression of IkappaB-zeta mRNA 4 h after culture of HT-29 cells compared to that in the absence of CM. CONCLUSION: Probiotic Bifidobacterium strains in BFM enhance IL-10 production in PBMNC and inhibit IL-8 secretion in intestinal epithelial cells, suggesting that BFM has anti-inflammatory effects against ulcerative colitis.

Serum p53 antibodies as a prognostic indicator in oral squamous cell carcinoma.

The purpose of the present study was to investigate the clinical usefulness of the detection of serum p53 antibodies (p53 Abs) in patients with oral squamous cell carcinoma (SCC). Preoperative values of p53 Abs were measured by enzyme-linked immunosorbent assay in 113 patients with primary oral SCC and seropositive patients were reevaluated postoperatively. The positivity rate of p53 Abs was 16%, and the 5-year survival rate of patients positive for p53 Abs was significantly lower than that of patients negative for p53 Abs (56.2% vs. 80.7%; P = 0.018). The preoperative presence of p53 Abs was found to be an independent prognostic factor in a multivariate analysis (P = 0.028, hazards ratio = 3.34), and its positivity was significantly related to secondary cervical lymph node metastases (P = 0.029). Six of nine patients who remained seropositive for p53 Abs through the disease course and the one with seropositive reversion from temporary negative status developed treatment failure. Therefore, the detection of p53 Abs in the serum of patients with SCC may be a useful prognostic marker.

Helicobacter pylori eradication reduces platelet count in patients without idiopathic thrombocytopenic purpura.

Discrepant outcomes of Helicobacter pylori eradication in patients with idiopathic thrombocytopenic purpura have been reported. Here patients with dyspepsia and no other complications underwent gastroendoscopic examination and evaluation for Helicobacter pylori infection. Helicobacter pylori-infected patients with gastritis and gastric ulcer received eradication therapy: lansoprazole (60 mg/day), clarithromycin (400 mg/day), and amoxicillin (1500 mg/day) for 1 week. Lansoprazole 30 mg/day was administrated additional 7 weeks. Peripheral platelets were counted before treatment, 8 weeks after initiation of therapy, and at follow-up periods. Platelet counts in patients with both gastritis and gastric ulcer were evaluated with reference to the presence of Helicobacter pylori infection. Eighty-seven patients with gastritis and 35 of those with gastric ulcer underwent successful eradication therapy. Peripheral platelet counts in patients with gastritis decreased from 235+/-55 to 228+/-58 (10(3)/microL) (p=0.0337), and those with gastric ulcer decreased from 248+/-60 to 232+/-48 (10(3)/microL) (p=0.020) 8 weeks after initiation of therapy. Non-eradicated patients did not show such a tendency. Helicobacter pylori eradication reduced peripheral platelet counts in patients with gastritis and gastric ulcer. Amelioration of thrombocytopenia by eradicating Helicobacter pylori appears to involve mechanisms specific to idiopathic thrombocytopenic purpura.

Usefulness of rectally administering [1-(13)C]-butyrate for breath test in patients with active and quiescent ulcerative colitis.

OBJECTIVE: Impaired butyrate metabolism plays a part in ulcerative colitis (UC). To assess the usefulness of measuring butyrate metabolism as an indication of inflammatory activity, we investigated the rate of butyrate metabolism by breath test after administering [1-(13)C]-butyrate rectally to patients with UC. MATERIAL AND METHODS: Thirty-eight UC patients (22 active, 16 quiescent) and 15 healthy controls were given [1-(13)C]-butyrate enemas. The (13)CO2 production rate was measured by breath test using an infrared spectrometric analyzer. RESULTS: The quantity of expired (13)CO2 was significantly lower in the active than in the quiescent UC and control groups. Cumulative (13)CO2 production at 240 min showed significant negative correlations with the clinical activity index (r=-0.65, p<0.0001), endoscopic activity index (r=-0.63, p=0.0001) and histology (r=-0.71, p<0.0001) in the active UC group. The (13)CO2 production rate was significantly increased in the quiescent stage as compared with the active stage in six UC patients, in whom clinical remission was achieved, in accordance with improvements in the clinical activity index, the endoscopic activity index, histology and fecal butyrate concentrations. Significant inverse correlations between the cumulative (13)CO2 production rate and these three parameters were seen in these six UC patients assessed in both the active and quiescent stages. CONCLUSIONS: Measurement of expired (13)CO2 after rectally administering [1-(13)C]-butyrate in active and quiescent UC appears to be a promising and reliable method for evaluating disease activity and metabolic changes associated with amelioration of inflammation.

Expression of cyclo-oxygenase-2 in gastrointestinal carcinoid tumors.

BACKGROUND: Cyclo-oxygenase (COX)-2 overexpression is observed in various neoplasms and COX-2 inhibition has been attempted as prevention and/or therapy in these neoplasms. Carcinoid tumors are thought to arise from neuroendocrine cells and originate mainly in the gastrointestinal tract. Cyclo-oxygenase-2 is reportedly expressed in neuroendocrine cells of normal colorectal mucosa. The role of COX in carcinoids has not previously been investigated. The aim of the present paper was to clarify the expression of COX-1 and -2, and their role in human gastrointestinal carcinoids. METHODS: Expression of COX-1 and -2 was studied immunohistochemically in 38 gastrointestinal carcinoids. Five bronchopulmonary and seven metastatic carcinoids were also examined, for comparison with gastrointestinal carcinoids. The immunohistochemical score (IHS) was calculated from staining intensity and immunoreactive cell population, and ranked according to four grades (negative to strong). RESULTS: Cyclo-oxygenase-2 was expressed in all gastrointestinal carcinoids (weak, 1; moderate, 13; strong, 24) and bronchopulmonary carcinoids (weak, 1; moderate, 4), as well as their metastases (moderate, 3; strong, 4). The IHS of COX-2 in larger tumors was significantly lower than that in smaller tumors. However, the IHS of COX-2 at the advancing tumor edge was significantly higher than that at the centers of tumors >or=10 mm in size. Faint COX-1 expression was detected in only one duodenal, one rectal and four bronchopulmonary carcinoids. CONCLUSIONS: Enhanced COX-2 expression was observed in gastrointestinal as well as bronchopulmonary carcinoids and their metastases, especially at the advancing edges of the tumors. Cyclo-oxygenase-2 may play a role in carcinoid progression.

Oral peppermint oil is a useful antispasmodic for double-contrast barium meal examination.

BACKGROUND AND AIM: Intraluminally administered peppermint oil (PO) is reportedly a safe and useful antispasmodic for gastroscopy, colonoscopy and double-contrast barium enema. The aim of this study was to examine the efficacy of oral PO for double-contrast barium meal examination (DCBM) without other antispasmodics. METHODS: Two hundred and five randomly chosen subjects (PO group) and 215 sex- and age-matched controls were enrolled. All participants underwent DCBM. The PO group was orally administered PO and a barium suspension mixture at the start of DCBM. Radiographs were blindly evaluated for spasm and overlapping with barium-filled duodenal loops (scored 0-3, indicating none to severe). The quality of barium coating of the mucosa and overall diagnostic quality (scored 0-3, indicating not acceptable to excellent) were also evaluated. RESULTS: There was no significant difference in subject acceptance between PO group and controls, and no adverse effects in either group. Scores for spasm at the esophagus, lower stomach and duodenal bulb were significantly lower in the PO than in the control group (P < 0.001). Scores for overlapping at the lower stomach and duodenal bulb were significantly lower in the PO than in the control group (P < 0.05, P < 0.01, respectively). Scores for overall diagnostic quality at the esophagus, lower stomach and duodenal bulb were significantly higher in the PO than in the control group (P < 0.001). Oral PO reduces spasm of the esophagus, lower stomach and duodenal bulb, inhibits barium flow to the distal duodenum, and improves diagnostic quality without other antispasmodics. CONCLUSIONS: Oral PO is a safe, easy to use and effective antispasmodic for DCBM.

Abnormal gastroesophageal flap valve is highly associated with endoscopic reflux esophagitis after Helicobacter pylori eradication.

BACKGROUND: Whether or not eradicating Helicobacter pylori worsens reflux esophagitis remains controversial. We investigated the relationship between gastroesophageal flap valve grading and endoscopic reflux esophagitis (in patients with peptic ulcer and gastritis) before and after H. pylori eradication in a case controlled study. Whether endoscopic assessment of the gastroesophageal flap valve allows prediction of endoscopic reflux esophagitis development or exacerbation was also assessed. MATERIALS AND METHODS: A total of 220 patients with peptic ulcer or chronic gastritis, who received H. pylori eradication therapy, were followed for at least 6 months (range, 6-34 months) for endoscopic changes. Another 88 age- and disease-matched H. pylori-positive controls, without eradication therapy, were also enrolled. Gastroesophageal flap valve grade (I-IV) was assessed using the Hill classification. RESULTS: Endoscopic reflux esophagitis incidence was significantly (p < .01) higher in abnormal gastroesophageal flap valve (grades III and IV) than in normal gastroesophageal flap valve (grades I and II) cases in both H. pylori eradication and control groups. The rate of new endoscopic reflux esophagitis after eradication was significantly (p < .01) higher in the abnormal than in the normal gastroesophageal flap valve group (54.5% vs. 9.1%). By contrast, the endoscopic reflux esophagitis exacerbation rate in patients with endoscopic reflux esophagitis before eradication was low (4.5%) and endoscopic reflux esophagitis improvement was observed in 40.9% of these patients. CONCLUSIONS: These results suggest gastroesophageal flap valve grading by endoscopy to be useful for predicting the risk of newly developing endoscopic reflux esophagitis after H. pylori eradication, in addition to predicting the presence of endoscopic reflux esophagitis.

Gene expression analysis in the stomachs of water immersion-restraint stress rats using high-density oligonucleotide array.

BACKGROUND AND AIM: Research on gastric lesions developing in response to stress is essential to elucidating the pathogenesis of these lesions as well as the interplay with other factors, including Helicobacter pylori infection and non-steroidal anti-inflammatory drug use. Genes expressed individually or in sets, such as heat shock proteins, growth factors, proto-oncogenes and cyclooxygenases, have been investigated in the stomach. However, gene expression in the stomach after stress exposure have not yet been comprehensively examined. We investigated the gastric gene expression profile in response to stress. METHODS: A high-density oligonucleotide array, representing approximately 850 genes, was used to determine gene expression changes in the stomachs of water immersion-restraint stress (WIRS) rats. RESULTS: Fifty-eight genes including expressed sequence tag (EST) genes were upregulated more than twofold in the 30 min-WIRS rat stomach as compared with the control. Concomitantly, five genes were downregulated. Numbers of up- or downregulated genes decreased rapidly at 1 and 2 h of WIRS. Altered gene expression of heat shock proteins, cell cycle regulators, proto-oncogenes and metabolic enzymes were recognized. Several of these genes, including p38 mitogen-activated protein kinase, did not reportedly show gastric expression changes in response to stress. CONCLUSION: These results suggest that, in addition to the previously identified stress-induced genes, expression of a number of other genes in the stomach is also involved in stress response.