Pylori Eradication In Patients Research Articles

Anti-Helicobacter pylori therapy followed by celecoxib on progression of gastric precancerous lesions

To evaluate whether celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, could reduce the severity of gastric precancerous lesions following Helicobacter pylori (H pylori) eradication. H pylori-eradicated patients with gastric precancerous lesions randomly received either celecoxib (n = 30) or placebo (n = 30) for up to 3 mo. COX-2 expression and activity was determined by immunostaining and prostaglandin E(2) (PGE(2)) assay, cell proliferation by Ki-67 immunostaining, apoptosis by TUNEL staining and angiogenesis by microvascular density (MVD) assay using CD31 staining. COX-2 protein expression was significantly increased in gastric precancerous lesions (atrophy, intestinal metaplasia and dysplasia, respectively) compared with chronic gastritis, and was concomitant with an increase in cell proliferation and angiogenesis. A significant improvement in precancerous lesions was observed in patients who received celecoxib compared with those who received placebo (P < 0.001). Of these three changes, 84.6% of sites with dysplasia regressed in patients treated with celecoxib (P = 0.002) compared with 60% in the placebo group, suggesting that celecoxib was effective on the regression of dysplasia. COX-2 protein expression (P < 0.001) and COX-2 activity (P < 0.001) in the gastric tissues were consistently lower in celecoxib-treated patients compared with the placebo-treated subjects. Moreover, it was also shown that celecoxib suppressed cell proliferation (P < 0.01), induced cell apoptosis (P < 0.01) and inhibited angiogenesis with decreased MVD (P < 0.001). However, all of these effects were not seen in placebo-treated subjects. Furthermore, COX-2 inhibition resulted in the up-regulation of PPARgamma expression, a protective molecule with anti-neoplastic effects. H pylori eradication therapy followed by celecoxib treatment improves gastric precancerous lesions by inhibiting COX-2 activity, inducing apoptosis, and suppressing cell proliferation and angiogenesis.

The effect of Helicobacter pylori eradication on dyspeptic symptoms, acid reflux and quality of life in patients with functional dyspepsia

Background The aims of this study were to investigate the effect of Helicobacter pylori eradication on gastroesophageal reflux, gastrointestinal symptoms and quality of life in patients with functional dyspepsia. Methods 20 H. pylori positive patients diagnosed as having functional dyspepsia according to Roma-II criteria completed the study period. Esophageal motility testing and pH recordings were obtained from each patient before and at the end of the study period. Each patient's gastrointestinal symptoms were evaluated according to Glasgow dyspepsia score. 36-Item short-form health survey (SF-36) and EDQ5 health survey were obtained form each patient. Results H. pylori eradication was accomplished in 13 patients (65%). Glasgow dyspepsia symptom score improved in H. pylori eradicated patients (10.3 vs 7.5, p < 0.05) compared to baseline. Fasting lower esophageal sphincter pressures increased (21.6 vs 25.4 mmHg, p < 0.05) after H. pylori eradication Neither the amplitude of peristaltic contractions in the esophageal body (59.4 vs 57.7 mmHg, p = ns) nor the velocity of peristaltic contractions changed before and after eradication. The percent time of esophageal pH < 4 (0.7 vs 2.6, p < 0.001), reflux events longer than 5 min (0 vs 0.7, p < 0.005) and total reflux number (10.3 vs 19.3, p < 0.005) significantly increased after eradication therapy. In the SF-36 health-related quality of life survey, general health score was 3.5 vs. 3.4, physical activity 25.2 vs. 26.4, physical role 5.9 vs. 6.3, emotional pain 4.6 vs. 4.5, social activity 2.0 vs. 1.9, physical pain 3.4 vs. 3.0, vitality 32.3 vs. 34.6, and mental health 11.9 vs. 11.5, before and at the end of treatment ( p = ns), respectively. Conclusions H. pylori eradication did not influence quality of life in patients with functional dyspepsia. Majority of the patients experienced a significant change in esophageal acid exposure after H. pylori eradication. H. pylori eradication significantly decreases gastrointestinal symptoms, however has no effect on quality of life in patients with functional dyspepsia.

Long-term efficacy of Helicobacter pylori eradication in patients with idiopathic thrombocytopenic purpura: 7-year follow-up prospective study

Helicobacter pylori eradication is useful for improvement of a half of patients with idiopathic thrombocytopenic purpura (ITP), but its long-term therapeutic efficacy has not been elucidated. We investigated the long-term efficacy of H. pylori eradication in 30 cases with ITP that were included in our previous study regarding the association between H. pylori infection and ITP. Twenty-one cases were positive and nine cases were negative for H. pylori infection. H. pylori eradication therapy including secondary regimen was successful in 20 cases, half (responder) of whom showed ITP remission 1 month later. Nine responders could be followed up for a long time and did not show re-infection of H. pylori. Eight of nine needed no medication except for eradication therapy. Another case remained in remission for 1 year but thereafter needed a steroid therapy due to the recurrence. Eight nonresponders could be followed up for a long time. All these cases showed a bad clinical course even though they received the other post-treatments including steroid therapy. Three of nine H. pylori-negative cases underwent eradication therapy after obtaining the written informed consent, but none of them showed improvement. Of these three cases, two cases could be followed up. Only one case remained a remission although receiving corticosteroid as a post-treatment. Conditions of H. pylori-negative ITP cases were usually unstable for a long time. H. pylori eradication has a short-term efficacy for about half of H. pylori-positive ITP patients, and the responders to the eradication therapy may receive a long-term clinical benefit without other therapies.

Endoscopic diagnosis and staging of mucosa-associated lymphoid tissue lymphoma

The role of endoscopy, including endoscopic ultrasound, in the diagnosis and management of mucosa-associated lymphoid tissue lymphomas of the stomach has evolved steadily in the last two decades. The present review summarizes recent findings and puts them in context with studies on the diagnosis and management of mucosa-associated lymphoid tissue lymphoma published earlier. Several recent studies have emphasized the crucial role of endoscopic ultrasound in treatment planning in patients with gastric mucosa-associated lymphoid tissue lymphoma. This is important as early-stage gastric mucosa-associated lymphoid tissue lymphomas can be managed just by the eradication of Helicobacter pylori by appropriate antibiotic regimens. However, the more advanced lesions are treated with much more invasive treatment regimens involving radical gastrectomy, chemotherapy or radiation, or all. Endoscopic ultrasound staging is highly accurate in predicting response to Helicobacter pylori eradication in patients with gastric mucosa-associated lymphoid tissue lymphoma. Normalization of gastric wall thickness and architecture can be used to monitor tumor regression following treatment. Endoscopic ultrasound findings can also be used to identify treatment failures and relapses and can help identify patients who need more aggressive therapy.

M1077 The Efficacy of Adding Sofalcone to One-Week, Low-Dose Triple Therapy for Helicobacter pylori Eradication in Patients with Chronic Gastritis

M1077 The Efficacy of Adding Sofalcone to One-Week, Low-Dose Triple Therapy for Helicobacter pylori Eradication in Patients with Chronic Gastritis

Helicobacter pylori eradication in patients with immune thrombocytopenic purpura. A novel therapy

Helicobacter pylori eradication in patients with immune thrombocytopenic purpura. A novel therapy

The long‐term efficacy of Helicobacter pylori eradication therapy in patients with idiopathic thrombocytopenic purpura

A beneficial effect of Helicobacter pylori (H. pylori) eradication in patients with H. pylori-positive idiopathic thrombocytopenic purpura (ITP) has been reported by several investigators; however, it was not clear whether the recovered platelet count after H. pylori eradication was maintained for a long period. Thirty-eight ITP patients who were examined for H. pylori infection were assessed. H. pylori-positive patients received a standard antibiotic therapy for H. pylori eradication. We investigated the long-term effect of H. pylori eradication on platelet recovery in patients with H. pylori-positive ITP. Of the 38 ITP patients, 26 (68.4%) were positive for H. pylori. The response rate of platelet recovery was 56.5% (13/23 patients). Twelve patients showed complete response (CR) and one showed partial response (PR). The mean platelet counts 6 months after eradication significantly increased from 31 x 10(9)/L to 129 x 10(9)/L in 23 H. pylori-eradicated patients (P < 0.001). The median platelet counts of responders 1, 2, 3, and 4 years after eradication were 168 x 10(9)/L (n = 10), 193 x 10(9)/L (n = 9), 168 x 10(9)/L (n = 7), and 243 x 10(9)/L (n = 4) after a mean follow-up of 25.8 months. Eradication therapy for H. pylori-positive patients with ITP was effective and a favorable effect was maintained for long periods.

Increased prevalence of Helicobacter pylori infection in gastric cardia of patients with reflux esophagitis: A study from Jordan

The role of H. pylori infection in GERD is highly controversial. Our aim was to investigate the relationship between reflux esophagitis and H. pylori infection in Jordanian subjects and to examine the gastric site for H. pylori that is most strongly associated with reflux esophagitis. During endoscopy two biopsies from the cardia and another two biopsies from the antrum were taken from 100 consecutive patients with reflux esophagitis (RE group) and from a sex- and age-matched group of 50 patients, who were referred to the endoscopy unit for evaluation of upper gastrointestinal symptoms and whose endoscopic findings were normal (control group). The biopsies were examined histologically for the presence of gastritis and H. pylori. Antral histological gastritis, Barrett's esophagus and hiatus hernia were significantly more common in the RE group than in the control group. Out of the 100 patients, 68 (68%) in the RE group and 26 of 50 (52%) in the control group were found to have H. pylori infection. The presence of H. pylori in both antral and cardiac biopsies was significantly more frequent in patients of the RE group. Forty-four patients in the RE group had positive H. pylori in both antral and cardiac biopsies (44%), while only 12 out of 50 patients of the control group (24%) had positive H. pylori in both biopsies. In the control group the prevalence of H. pylori in the antrum was similar to that of patients of the RE group (52% vs. 59%), but colonization of H. pylori in the cardia was significantly much lower than that of the RE group (24% vs. 53%; P = 0.0007). The increased prevalence of H. pylori colonization in the cardia is associated with reflux esophagitis and further controlled clinical study is required to show the impact of H. pylori eradication in patients with reflux esophagitis.

Eradication of Helicobacter pylori Does Not Reduce the Incidence of Gastroduodenal Ulcers in Patients on Long‐term NSAID Treatment: Double‐Blind, Randomized, Placebo‐Controlled Trial

Helicobacter pylori and nonsteroidal antiinflammatory drugs (NSAIDs) are the major causes of gastroduodenal ulcers. Studies on the benefit of eradication of H. pylori in NSAID users yielded conflicting results. To investigate whether H. pylori eradication in patients on long-term NSAIDs reduces the incidence of gastroduodenal ulcers. Patients on long-term NSAID treatment and who are H. pylori positive on serologic testing, were randomly assigned to either H. pylori eradication (omeprazole, amoxicillin, and clarithromycin) or placebo. Primary endpoint was the presence of endoscopic gastric or duodenal ulcers 3 months after randomization. One hundred sixty-five (48%) of a total of 347 patients were on gastroprotective medication. At endoscopy, gastroduodenal ulcers were diagnosed in 6 (4%) and 8 (5%) patients in the eradication and placebo group, respectively (p = .65). During follow-up of 12 months, no symptomatic ulcers or ulcer complications developed. No significant differences were found in the development of gastroduodenal erosions, dyspepsia, or in quality of life. H. pylori eradication therapy in patients on long-term NSAID treatment had no beneficial effect on the occurrence of ulcers, erosions, or dyspepsia. Ulcer rates in both study arms are remarkably low, in both patients with and without gastroprotective therapy.

Long-Term Re-Infection Rate after Helicobacter pylori Eradication in Bangladeshi Adults

Background and Aim: Bangladesh is a developing country with a very high prevalence of Helicobacter pylori infection, which has been ascribed to overcrowding and poor sanitary conditions. It has generally been accepted that the re-infection rate is higher in countries with a high prevalence of H. pylori infection. Short-term follow-up studies support this assumption but no long-term studies are available to confirm or refute this assertion. The present study was aimed to define the long-term H. pylori re-infection rate (6 years after successful eradication) in duodenal ulcer patients. Methods: In a previous study, 90 patients were successfully eradicated for H. pylori and followed-up for 24 months. 17/90 were found to be re-infected (18% re-infection rate per year in the first 12 months) [Gastroenterology 2001;792–798]. The remaining 73 patients were targeted for long-term follow-up. 26/73 were lost to follow-up; 6 symptomatic patients were tested H. pylori positive in the period between 24 and 60 months post-eradication. The remaining 41 patients were evaluated 72 months after successful eradication. The evaluation included clinical history taking, a ¹³C-urea breath test (UBT), and endoscopy. Results: Of the 41 H. pylori-eradicated patients analyzed after 72 months, 16 were H. pylori-positive. If the 6 patients, who were tested positive between 24 and 60 months, are added, the total re-infection cases amount to 22 subjects in the period between 24 and 72 months. Therefore, an overall annual re-infection rate 6 years after eradication of 5.02% can be calculated. Six of the 23 symptomatic patients had duodenal ulcer relapse, 5/6 were H. pylori re-infected and one was H. pylori-negative at 72 months post-treatment. Conclusion: The long-term annual H. pylori re-infection rate in Bangladeshi adults is markedly higher than in Western countries but lower than anticipated. In this study, duodenal ulcer relapse is clearly related to H. pylori re-infection.

Nonsteroidal anti-inflammatory drug use does not affect short-term endoscopic and histologic outcomes after Helicobacter pylori eradication in patients with rheumatoid arthritis

We evaluated the effects of the use of nonsteroidal anti-inflammatory drugs (NSAIDs) on endoscopic and histological findings in patients with rheumatoid arthritis (RA) before and after the eradication of Helicobacter pylori infection. Helicobacter pylori (H. pylori) eradication using lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week was conducted in 44 patients (mean age: 56.5 years) with RA. Using the updated Sydney system, endoscopic and histological findings of the greater curvature of the antrum, the greater curvature of the upper corpus, and the lesser curvature of the lower corpus were compared before and after eradication, for a mean follow-up period of 3.5 months. Overall, H. pylori eradication was successful in 32 patients (72.7%). Of these 32 patients, 23 were NSAID users. In the successful eradication group, (1) there was no significant change on endoscopic findings, including gastric erythema and erosion in all three regions irrespective of NSAIDs use; (2) of 17 active ulcers before eradication in NSAIDs users, all healed except for one duodenal ulcer that persisted, where one patient newly developed a gastric ulcer, one developed erosive duodenitis, and two developed reflux esophagitis, all in NSAID users; (3) neutrophil infiltration and chronic inflammation were significantly improved in all three regions after H. pylori eradication irrespective of use of NSAIDs, while atrophic change and intestinal metaplasia did not change. In the eradication failure group; (1) there was no significant change on endoscopic and histological findings in the three regions; (2) two of three ulcers present before eradication on NSAID users persisted even after eradication, and no new cases of gastric ulcer or erosive duodenitis occurred. In conclusion, over a mean follow-up period of 3.5 months, use of NSAIDs in Japanese patients with RA did not impair the healing process of gastric and duodenal ulcers nor did it affect the endoscopic and histological improvements associated with H. pylori eradication.

Nonsteroidal anti-inflammatory drug use does not affect short-term endoscopic and histologic outcomes after Helicobacter pylori eradication in patients with rheumatoid arthritis

We evaluated the effects of the use of nonsteroidal anti-inflammatory drugs (NSAIDs) on endoscopic and histological findings in patients with rheumatoid arthritis (RA) before and after the eradication of Helicobacter pylori infection. Helicobacter pylori (H. pylori) eradication using lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week was conducted in 44 patients (mean age: 56.5 years) with RA. Using the updated Sydney system, endoscopic and histological findings of the greater curvature of the antrum, the greater curvature of the upper corpus, and the lesser curvature of the lower corpus were compared before and after eradication, for a mean follow-up period of 3.5 months. Overall, H. pylori eradication was successful in 32 patients (72.7%). Of these 32 patients, 23 were NSAID users. In the successful eradication group, (1) there was no significant change on endoscopic findings, including gastric erythema and erosion in all three regions irrespective of NSAIDs use; (2) of 17 active ulcers before eradication in NSAIDs users, all healed except for one duodenal ulcer that persisted, where one patient newly developed a gastric ulcer, one developed erosive duodenitis, and two developed reflux esophagitis, all in NSAID users; (3) neutrophil infiltration and chronic inflammation were significantly improved in all three regions after H. pylori eradication irrespective of use of NSAIDs, while atrophic change and intestinal metaplasia did not change. In the eradication failure group; (1) there was no significant change on endoscopic and histological findings in the three regions; (2) two of three ulcers present before eradication on NSAID users persisted even after eradication, and no new cases of gastric ulcer or erosive duodenitis occurred. In conclusion, over a mean follow-up period of 3.5 months, use of NSAIDs in Japanese patients with RA did not impair the healing process of gastric and duodenal ulcers nor did it affect the endoscopic and histological improvements associated with H. pylori eradication.

Helicobacter pylori eradication reduced the incidence of gastric cancer, especially of the intestinal type

Although Helicobacter pylori infection is closely associated with gastric cancer development, follow-up studies after H. pylori eradication are still scarce. To clarify the cancer preventive effect of H. pylori eradication, with special attention to differences in effect according to histology. Patients who underwent H. pylori eradication therapy and were followed-up endoscopically for at least 1 year were analysed. The incidence of gastric cancer and factors associated with cancer development were investigated. A total of 1807 patients were enrolled. Six of 1519 H. pylori eradicated and five of 288 persistent subjects developed gastric cancer. Four of the eradicated subjects developed the intestinal type and two the diffuse type, while four of the persistent subjects developed the intestinal type and one the diffuse type. Kaplan-Meier analysis indicated a significantly lower incidence in eradicated patients than in persistent patients. The incidence of intestinal type was significantly lower than in eradicated patients, while the diffuse type could not be evaluated because of the low incidence. Helicobacter pylori-eradicated patients had a reduced incidence of gastric cancer compared with H. pylori-persistent patients, particularly the intestinal type, suggesting that H. pylori is strongly associated with intestinal-type gastric cancer.

Eradication of Helicobacter pylori for primary gastric cancer and secondary gastric cancer after endoscopic mucosal resection

Because most gastric cancers develop from a background of Helicobacter pylori-infected gastric mucosa, H. pylori plays an important role in gastric carcinogenesis. Therefore, eradication of H. pylori may inhibit the incidence of gastric cancers. In experimental studies, H. pylori eradication has proved to act as a prophylaxis against gastric cancer. However, the results of recent randomized controlled studies are absolutely contradictory. In Japan, mucosal gastric cancer is usually resected by endoscopic treatment. As only a small part of the gastric mucosa is resected, secondary gastric cancer after endoscopic resection of the primary gastric cancer often develops at another site in the stomach. A nonrandomized Japanese study involving 132 early gastric cancer patients reported that eradication of H. pylori after endoscopic resection tended to reduce the development of secondary gastric cancer. Also, a retrospective multicenter survey indicated that the incidence rate of secondary gastric cancer in H. pylori-eradicated patients was about one-third that among patients in the non eradication group. We conducted a large-scale multicenter randomized trial to confirm the effect of H. pylori eradication on secondary and residual gastric cancer after endoscopic resection. This study was begun in 2003 and is ongoing at present. Diagnosis of a new carcinoma at another site of the stomach is defined as the primary end point, and recurrence of tumors at the resection site as a secondary end point. A total of 542 subjects have been enrolled in the study. This study will have the statistical power to demonstrate whether H. pylori eradication decreases the incidence and recurrence of gastric cancer.

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 (103/µL) (p = 0.0337), and those with gastric ulcer decreased from 248+/−60 to 232+/−48 (103/µL) (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.

Helicobacter pylori-associated immune thrombocytopenia

Idiopatic thrombocytopenic purpura (ITP), a disorder characterized by autoantibody-mediated platelet destruction, may be primary or secondary to various illnesses including lymphoproliferative, autoimmune, or infectious diseases. There are increasing data on the association between Helicobacter pylori infection and idiopathic thrombocytopenic purpura and the significant increase in platelet count after bacterial eradication. The aim of this review is to consider the studies so far published on Helicobacter pylori infection and idiopathic thrombocytopenic purpura in order to evaluate a possible pathogenic correlation between these two conditions. A review of the literature data show that Helicobacter pylori eradication in patients with idiopathic thrombocytopenic purpura is effective in increasing platelet count in approximately half of the cases. However, since the studies so far published are few, sometimes controversial and involve small series of patients, further controlled studies on larger numbers of patients with longer follow-up are needed to confirm these preliminary findings.

Importance of Helicobacter pylori eradcation for maintenance of remission of drug associated peptic ulcer disease

The role of Helicobacter pylori (H. pylori) eradication in non-steroidal anti inflammatory drug (NSAID) users with peptic ulcer disease is controversial especially in countries with a high prevalence of the infection. Furthermore the value of low dose omeprazole for maintenance of remission is not yet known. 138 symptomatic out-patients receiving continuous COX 1 NSAID therapy, were treated with omeprazole 40 mg/day upon endoscopic confirmation of gastro-duodenal ulceration or erosions while those infected with H. pylori received in addition clarithromycin 500 mg and amoxycillin 1000 mg twice daily during the first week of treatment. After endoscopic confirmation of healing at the end of week 5, the patients were randomized to receive omeprazole 10 mg (n=50) or 20 mg once daily (n=66) and endoscopy repeated after 20 weeks. The overall healing rate (per protocol) at five weeks (116/128) was 90.6% while in 85.5% (65/76) eradication was successful. The healing rate for the H. pylori eradicated patients (58/65) was 89.2%. For those who failed eradication (8/11) it was 72.7% (NS), while for patients not infected with H. pylori at entry to the study (50/52) it was 96.2% (NS). An intention to treat analysis showed that after 20 weeks of omeprazole prophylaxis with the 10mg dose 86% (43/50) had maintained healing while for the 20mg dose a similar figure was observed (87.9; 58/66). Only three patients in the two groups (pp) had persistent H. pylori infection, all of whom relapsed. No patients discontinued treatment because of adverse effects of the drugs. H. pylori eradication was not associated with impaired ulcer healing in a Middle Eastern population with symptomatic NSAID induced gastro/duodenal lesions, when a high healing dose of omeprazole (40 mg) was used. After eradication, omeprazole 10 or 20 mg per day were highly and equally effective for maintenance of gastroduodenal mucosal integrity during continued NSAID use. H. pylori should be eradicated from symptomatic Middle Eastern NSAID users with peptic ulcer disease.

Long‐term follow‐up of 13C‐urea breath test results after Helicobacter pylori eradication: frequency and significance of borderline δ13CO2 values

The precise choice of cut-off point for the 13C-urea breath test to define whether it is positive or negative represents a controversial issue. To quantify the 13C-urea breath test result for several years following Helicobacter pylori eradication, and to evaluate the frequency and the significance of borderline delta13CO2 values. Two-hundred H. pylori eradicated patients confirmed by 13C-urea breath test (100 mg of urea, citric acid), and having had repeated this test yearly up to 5 years, were studied. Delta13CO2 values between 2 and 5/1000 were considered as borderline results. Eight H. pylori recurrences were observed during 406 patient-years of follow-up (1.97% yearly). In two of eight reinfected patients, the reinfection was preceded by a negative delta13CO2 value >2/1000. Borderline delta13CO2 values were detected in 4% of the 606 urea breath tests performed, and in 25% when only patients in whom H. pylori recurrence was detected in subsequent urea breath tests were included (P < 0.05). The negative-predictive value of a post-treatment delta13CO2 >2/1000 for the diagnosis of H. pylori recurrence was 99%. Positive and negative urea breath test results tend to cluster outside the range between 2/1000 and 5/1000. Nevertheless, a borderline urea breath test delta value (e.g. very close to the selected cut-off point) should be interpreted cautiously, and the result should probably be confirmed either by repeating the urea breath test or by other diagnostic methods. On the contrary, a delta13CO2 value <2/1000 very confidently confirms H. pylori eradication.

The Clinical Efficacy of Helicobacter pylori Eradication in Patients with Helicobacter pylori-Positive Chronic Thrombocytopenic Purpura.

Background: Helicobacter pylori (H pylori) has been implicated in the pathogenesis of some autoimmune diseases including idiopathic thrombocytopenic purpura (ITP). Several studies recently showed a high prevalence of H pylori infection in patients with ITP and reported a platelet recovery after bacterial eradication therapy. The prevalence of H pylori infection and effect of its eradication in Korea patients with chronic ITP were investigated.Methods: The study included among 35 patients with chronic ITP from eight hospitals. H pylori infection was assessed by urea breath test, rapid urease test or microbial culture. H pylori eradication was performed with amoxicillin, clarithromycin and omeprazol regimen for 7 days or bismuth, metronidazol and tetracycline regimen for 10 days. Eradication was assessed by urea breath test 4 weeks after treatment. Platelet counts were monitored serially after the end of treatment.Results: Thirty five patients with chronic ITP were evaluated, including 12 males and 23 females. Median age was 57 years (range 30–79). The median platelet count before eradication was 23,000/uL (range 4,000–66,000/uL). Sixteen patients were performed the splenectomy previously. H pylori infection was found in 23 (65%) of 35 patients. In 21 patients performed the eradication, 6 patients (28.5%) had a significant increase in platelet count after 2 weeks and 2 months. The response duration was 1–27 (median 7.6) months.Conclusions: This study confirmed the efficacy of H pylori eradication in increasing platelet in adult chronic ITP patients. We must consider the investigation and eradication of H pylori infection in ITP patients as a simple, inexpensive tool in management of the chronic disease.

Prognostic Value of Translocation t(11;18) in Tumoral Response of Low-Grade Gastric Lymphoma of Mucosa-Associated Lymphoid Tissue Type to Oral Chemotherapy

To determine the impact of translocation t(11;18) on response to oral alkylating agents in gastric mucosa-associated lymphoid tissue lymphoma (GML). Fifty-three patients with a GML were studied. Helicobacter pylori-positive patients (n = 34) received anti-H pylori treatment and H pylori-negative patients (n = 19) or patients who failed to respond to anti-H pylori treatment received oral alkylating agents. t(11;18) was detected by reverse transcription polymerase chain reaction from frozen gastric biopsies. t(11;18) was detected in 32% of patients. It was more prevalent in H pylori-negative as compared with H pylori-positive patients (12 of 19 v five of 34 patients; P = .0005). Among 31 H pylori-eradicated patients, t(11;18) was detected in three patients, all of whom experienced treatment failure, and it was absent in 28 patients: 21 patients (75%) were in remission and seven patients (25%) experienced treatment failure (P = .03). Among 21 patients who received an alkylating agent, t(11;18) was detected in 12 patients: five patients (42%) were in remission and seven patients (58%) experienced treatment failure. t(11;18) was absent in nine patients: eight patients (89%) were in remission and one patient (11%) experienced treatment failure by the end of treatment. Four patients in remission relapsed during follow-up (median, 7 years): they all had t(11;18). Durable remission was obtained in eight (89%) of the nine patients without t(11;18) versus one of the 12 patients (8%) with t(11;18) (P = .0003). Presence of t(11;18) in GML is predictive of resistance to oral alkylating agents, with less than 10% of durable remission at long-term follow-up.