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PubMed2002

Prevalence of H. pylori-infection in family members of H. pylori positive and its influence on the reinfection rate after successful eradication therapy: a two-year follow-up.

INTRODUCTION: Living conditions (e. g. domestic crowding) may influence the infection rate. Some studies suggested that the reappearance of H. pylori in H. pylori positive patients after successful eradication therapy might be a result of transmission by H. pylori positive spouses. Therefore this study has been performed to evaluate the effect of the H. pylori status of family members on the reinfection rate of H. pylori positive patients after successful eradication therapy. METHODS: 108 H. pylori positive patients (64 male, 44 female, aged 48.7 years, range 18-76 years) who presented with dyspeptic symptoms for upper GI-endoscopy have been included into this study. H. pylori status has been defined by culture and/or histology, rapid urease test and serology. For eradication therapy patients received omeprazole 20 mg bd, clarithromycine 250 mg bd and metronidazole 400 mg bd. H. pylori status was controlled by (13)C-urea breath test 28 days (n = 96), 6 (n = 35), 12 (n = 28) and 24 months (n = 25) after eradication therapy. Additionally H. pylori status of 170 family members (82 spouses, 68 children, 20 siblings/parents, aged 3-83 years) was defined by (13)C-urea breath test (n = 167), upper GI-endoscopy (n = 2) or serology (n = 1). RESULTS: The eradication rate was 98 % (94/96). H. pylori prevalence in all family members was 40 % (56 % in spouses, 20 % in children). No reinfection has been found in successful eradicated patients within the two-years follow-up. DISCUSSION: These results suggest that reinfection is not dependent on the H. pylori prevalence in family members and that H. pylori reinfection after successful eradication therapy is an unlikely event.

Adolescent↗
PubMed2000

Eradication of Helicobacter pylori compared with long-term acid suppression in duodenal ulcer disease. A randomized trial with 2-year follow-up. The Danish Ulcer Study Group.

BACKGROUND: Trials evaluating long-term management of duodenal ulcer disease have mainly been focused on recurrence of ulcers, disregarding effects on dyspeptic and reflux symptoms. Profound acid inhibition with a proton pump inhibitor is the gold standard therapy in acid-related diseases. We aimed to compare the symptomatic effects of eradication therapy with those of long-term omeprazole treatment in a design with periods both with and without acid inhibition. METHODS: Patients with active duodenal ulcer were randomized either to omeprazole, 20 mg twice daily until healing, followed by omeprazole, 20 mg/ day for 1 year, or to eradication therapy (metronidazole, amoxicillin, and omeprazole for 2 weeks) followed by placebo for 1 year. All patients were followed up passively for an additional year. Clinical controls were performed every 2 months the 1st year (maintenance phase) and every 6 months during the passive follow-up phase. The study was multicentric and double-blind. The primary end-point was discontinuation of treatment, irrespective of reason. RESULTS: Two hundred and seventy-six patients were randomized (139 in the eradication treatment group). In the maintenance phase there were no differences in the reporting of dyspeptic symptoms or in premature withdrawal. In the passive follow-up phase only five patients in the eradication therapy group discontinued owing to relapse of dyspeptic symptoms or ulcer, compared with 51 patients initially randomized to long-term omeprazole. There were no differences in reflux symptoms or in the development of reflux oesophagitis. CONCLUSIONS: Eradication therapy and long-term omeprazole are equally effective in controlling dyspeptic symptoms and reflux in duodenal ulcer patients with healed ulcers. One-quarter of the duodenal ulcer patients who start eradication therapy continue to be symptomatic or fail therapy for other reasons over a 2-year period. Eradication therapy does not increase the risk of reflux in ulcer patients.

Amoxicillin↗
PubMed2006

Helicobacter pylori eradication in the healing of atrophic gastritis: a one-year prospective study.

OBJECTIVE: Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. MATERIAL AND METHODS: Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58+/-12.6 years (mean+/-SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. RESULTS: Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication. The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). CONCLUSIONS: Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.

Aged↗
PubMed1999

Prevalence of resistance to clarithromycin and its clinical impact on the efficacy of Helicobacter pylori eradication.

BACKGROUND: Triple therapy with a proton-pump inhibitor (PPI) in combination with metronidazole and clarithromycin is the method of choice for eradication of Helicobacter pylori. Failures have been primarily blamed on the development of resistance to clarithromycin. The present study investigated the prevalence and clinical significance of resistance to clarithromycin and metronidazole in determining therapeutic success of both triple therapy as a primary eradication method and high-dose dual therapy in non-responders. METHODS: On the basis of prior therapy, H. pylori-positive patients were assigned to one of two groups in the present prospective study. Group A (n = 93) included patients who had not undergone any prior eradication treatment, whereas group B (n = 15) consisted of patients who had received clarithromycin but in whom eradication had been unsuccessful. All patients underwent endoscopy with biopsy for bacterial culture and resistance studies. Patients in group A were treated with a 7-day regimen of pantoprazole (40 mg twice daily), metronidazole (500 mg twice daily), and clarithromycin (250 mg twice daily), whereas those in group B received omeprazole (40 mg three times a day) and amoxycillin (1000 mg three times a day ) for 14 days. Success of the eradication treatment was ascertained by means of the 13C urea breath test. RESULTS: In group A resistance to clarithromycin and metronidazole was identified in 3 patients (4.9%) and in 14 patients (22.9%), respectively. Eradication proved successful in 78 of 84 patients (92.6%) followed up. Two of the 3 patients with primary clarithromycin resistance and 1 of the 14 patients with metronidazole resistance did not respond to treatment. In group B isolated or combined resistance to clarithromycin was found in seven patients, whereas another four showed isolated resistance to metronidazole. Eradication proved successful in 10 of 13 controlled patients (76.9%) followed up, and only 2 patients reported severe side effects. CONCLUSION: Determination of antibiotic resistance before initiating therapy is not necessary, since primary resistance to clarithromycin is rare. The Italian triple therapy remains a highly effective primary therapeutic method. Further, routine determination of resistance in non-responders also seems to be superfluous because high-dose dual therapy is an effective and well-tolerated second-line therapy regardless of the patients' resistance status.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2004

Gastric MALT lymphomas are divided into three groups based on responsiveness to Helicobacter Pylori eradication and detection of API2-MALT1 fusion.

Gastric MALT lymphoma shows unique features including regression by Helicobacter pylori eradication and API2-MALT1 fusion. We performed a molecular and clinicopathologic study for 115 cases. All eradication-responsive cases were devoid of API2-MALT1 fusion. All tumors positive for the fusion and all negative for H. pylori infection were nonresponsive to the eradication. Consequently, gastric MALT lymphomas were divided into three groups: Eradication-responsive and fusion-negative (group A, n = 72), eradication-nonresponsive and fusion-negative (group B, n = 22), and eradication-nonresponsive and fusion-positive (group C, n = 21). Group A tumors were characterized by low clinical stage and superficial gastric wall involvement, and group C tumors by low H. pylori infection rate, advanced clinical stage, and nuclear BCL10 expression. All group C tumors showed exclusively low-grade histology. Group B tumors, which have not been well recognized, frequently showed nodal involvement, deep gastric wall involvement, and advanced clinical stage, and sometimes an increased large cell component. A multivariate discriminant analysis revealed that responsiveness to the eradication could be predicted accurately by negative API2-MALT1 fusion, positive H. pylori infection, low clinical stage, and superficial gastric wall invasion, the former being the most important factor for the prediction. This 3-group categorization may be helpful for a comprehensive understanding of gastric MALT lymphoma.

Adaptor Proteins, Signal Transducing↗
PubMed1995

Triple therapy eradicated H. pylori equally in patients pretreated with omeprazole or ranitidine. A 12-month follow-up.

The aim of this study was twofold: first, to investigate the effectiveness of a standard triple therapy (tripotassium dicitrato bismuthate, 125 mg q.i.d., tetracycline hydrochloride 500 mg q.i.d., and metronidazole 500 mg t.i.d.) in eradicating Helicobacter pylori in patients with duodenal ulcer successfully healed with omeprazole or ranitidine; second, to examine the influence of the eradication on duodenal ulcer recurrence rate after 12 months. Two hundred forty-five consecutive H. pylori-positive patients with healed duodenal ulcer either with omeprazole (20 mg/day, 126 patients) or with ranitidine (150 mg b.i.d., 119 patients) given at random, began triple therapy for 15 days. H. pylori eradication was looked for 4-5 weeks later by culture of biopsy material, hematoxylin-eosin stain, and rapid urease test. H. pylori-eradicated patients were followed up for 12 months. Endoscopy was carried out at the end of the follow-up or whenever symptoms appeared. Five patients (2.0%) withdrew because of triple-therapy-related side effects. The eradication rate was 92% (220 of 240 patients); no difference was found between those healed with omeprazole (93%, 114 of 123 patients) or ranitidine (91%, 106 of 117 patients). Of 220 successfully treated patients, 132 completed the 12-month follow-up. The duodenal ulcer recurrence rate was 4% (5 of 132 patients); 3% (2 of 70) in the omeprazole group and 5% (3 of 62) in the ranitidine group healed. All the recurrences were asymptomatic. H. pylori recurrence rate was 11% (14 of 132 patients); no difference was found between patients healed with omeprazole (10%, 7 of 70 patients) or with ranitidine (11%, 7 of 62 patients). All the recurrent duodenal ulcers occurred in H. pylori-positive patients (36%, 5 of 14 patients). Standard triple therapy after duodenal ulcer healing with omeprazole or ranitidine eradicates H. pylori in comparable high rates. Side effects were mild and dropouts were only 2%. Ulcer recurrence rate 12 months after eradication was low and comparable between those healed with omeprazole or ranitidine.

Adolescent↗
PubMed1995

Efficacy of lansoprazole and amoxicillin in eradicating Helicobacter pylori: evaluation using 13C-UBT and Monoclonal H. pylori antibody testing.

Combination therapy with lansoprazole (LPZ) and amoxicillin (AMPC) was administered to eradicate Helicobacter pylori. Changes in eradication rates were monitored and serum antibody titers, levels of pepsinogens I and II (PI and PII), and gastrin were measured. The 40 subjects were divided into two groups: one group received LPZ 30 mg alone, and the other received LPZ 30 mg and AMPC 1,500 mg concomitantly. AMPC was administered for 2 weeks before completion of LPZ treatment. Maintenance therapy was cimetidine 400 mg. The presence of H. pylori was evaluated using the urea breath test (UBT). The clearance rate was 12.5% and the eradication rate was 0% in the LPZ group, and the corresponding rates in the LPZ with AMPC group were 41.6 and 25.0%, respectively. Serum monoclonal H. pylori antibody titers decreased in patients in whom bacterial eradication had been achieved. Serum PI was significantly reduced in those patients in whom eradication had been achieved. Serum PII and gastrin levels also tended to decrease in patients in whom eradication had been achieved, but no such changes were observed in the other patients. Further research into drug treatment and evaluation methods for bacterial eradication is required.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Enhancement of neutrophil infiltration in the corpus after failure of Helicobacter pylori eradication.

Neutrophil accumulation plays an important role in Helicobacter pylori-associated gastric mucosal injury. In this study, the mucosal content of myeloperoxidase (MPO), which is a measure of neutrophil accumulation and interleukin-8 (IL-8) was assayed and changes in MPO and IL-8 content were determined before and after H. pylori eradication therapy. Thirty-seven H. pylori-positive patients (11DU/26GU) underwent H. pylori eradication therapy with lansoprazole (30 mg/day, 6 weeks) and amoxicillin (2 g/day, 2 weeks), followed by famotidine (20 mg/day, 8 weeks). H. pylori-infection status was evaluated by routine endoscopic examinations (culture, CLO, histology). Immediately and 8 weeks after cessation of the anti-H. pylori therapy, these tests were repeated. Intragastric urease activity was estimated by delta 13CO2, which was obtained by the [13C]urea breath test (UBT). Mucosal samples were taken and tissue MPO and IL-8 contents were assayed by EIA and ELISA, respectively. Histologic examination was also performed. Among the 37 patients, 21 cases of H. pylori infection were eradicated (56.8%). Intragastric urease activity was dramatically reduced immediately after the anti-H. pylori therapy, whereas, it was re-elevated 8 weeks later in the relapsed cases. Antral MPO content was decreased in the eradicated and relapsed cases. MPO in the corpus was also decreased in the eradicated cases. Nevertheless, it was enhanced (3.5-fold) in the relapsed cases at 8 weeks after therapy. Changes in mucosal IL-8 content were similar to those of MPO. In eradicated cases, neutrophil infiltration is improved in both the antrum and corpus. However failure of eradication therapy results in the enhancement of neutrophil accumulation in the corpus. Further study is necessary to clarify the mechanism of neutrophil accumulation after therapy for H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Preliminary clinical study on gastric ulcer scars and ulcer relapses after Helicobacter pylori eradication therapy.

To determine the effect of Helicobacter pylori eradication on the healing of gastric ulcers, endoscopic examinations of gastric ulcer scars and ulcer relapse after eradication therapies or antisecretory therapy were carried out in 24 H. pylori-positive patients with recurrent gastric ulcers located in the gastric angle. Sixteen patients were initially treated with 2-week triple eradication therapy. Subsequently, seven of eight noneradicated cases were retreated with triple therapy, which included metronidazole. Eight patients received antisecretory monotherapy. Endoscopic examinations were performed at 4 weeks and 6 months after the treatments. Gastric ulcer scars were classified endoscopically into three types: Sa, a central depression surrounded by a coarse pattern: Sb, a coarse regenerated pattern; and Sc, a fine pattern indicating matured scar of high quality. Transformations of the scar patterns and ulcer relapse were assessed in 19 patients who showed an ulcer scar at 4 weeks after initial therapy. Thirteen cases in which H. pylori was successfully eradicated, either after initial or re-eradication therapies, mainly showed Sc scars and had no ulcer relapse. Sa scar was mainly observed during H. pylori-positive conditions. Transformation from the Sa to the Sc was observed after successful re-eradication. Ulcer relapses occurred in three patients who showed Sa scar after antisecretory therapy. Although a random study would be needed to obtain a definite conclusion, we suspect that the H. pylori-negative condition after eradication therapies may result in good ulcer healing and may subsequently reduce ulcer relapse.

Anti-Bacterial Agents↗
PubMed1998

Relationship between the eradication of Helicobacter pylori and the healing pattern of peptic ulcer.

We investigated the relationship between the eradication of Helicobacter pylori and the stage after the eradication of this bacterium. Eighty-six patients with H. pylori who had gastric ulcer (n=45) or duodenal ulcer (n=41) were enrolled in the study. As eradication therapy, patients received 1,500 mg amoxicillin, 400 mg clarithromycin, and 30 mg lansoprazole for 2 weeks, followed by 30 mg lansoprazole for 6 weeks in patients with gastric ulcer or for 4 weeks in those with duodenal ulcer. The ulcer stages were evaluated using the indigocarmine method at the third and sixth month after entry. The overall eradication rate of H. pylori was 85% in this study. In the gastric ulcer group, 62% of H. pylori-eradicated patients and 37.5% of H. pylori-uneradicated patients showed the S2 stage (white scar) at the sixth month. In the duodenal ulcer group, 61% of H. pylori-eradicated patients showed the S2 stage and none of the H. pylori-uneradicated patients showed the S2 stage (p < 0.05). We concluded that H. pylori eradication might promote not ulcer healing but maturity of the ulcer scar, especially in duodenal ulcer patients, and that this might also be related to the reduction of ulcer relapse.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1998

Long-term effect of Helicobacter pylori eradication on gastric metaplasia in patients with duodenal ulcer.

There have been conflicting reports on the effect of Helicobacter pylori eradication on gastric metaplasia in the duodenal bulb (DGM). In the present study, we have investigated the relationships between DGM and H. pylori by examining whether or not H. pylori-positive patients had more DGM than H. pylori-negative patients with nonulcer dyspepsia (NUD) or duodenal ulcer (DU), and by examining the effect of eradication of H. pylori on the prevalence and the extent of DGM during the long-term up to 4 years. Fifty H. pylori-positive and seven H. pylori-negative patients with DU and 23 H. pylori-positive and 23 H. pylori-negative NUD subjects were studied. Two duodenal bulb biopsy specimens were taken for histologic evaluation and the presence and the extent of DGM were evaluated. The extent of DGM was classified as none (grade 0), focal (grade 1), multifocal (grade 2), and diffuse type (grade 4). In H. pylori-positive patients with DU, follow-up gastroscopy was conducted 4 weeks, 1 year, and 4 years after H. pylori eradication. DGM was significantly (p < 0.001) more common (DU: 93%, NUD: 22%) and significantly (p < 0.001) greater in extent for patients with DU than for NUD subjects (DU: 1.89, NUD: 0.28). Neither the prevalence nor the extent of DGM was affected by H. pylori status in patients with DU or NUD; the prevalence (extent) of DGM of H. pylori-positive and -negative patients with DU were 96% (1.94) and 71% (1.57), respectively. In the 43 "H. pylori-eradicated" group, initial prevalence of DGM was 95% and those of 4 weeks, 1 year, and 4 years after eradication were 91%, 96%, and 79%, respectively. The initial extent of DGM was 1.93, and those of 4 weeks, 1 year, and 4 years after eradication were 1.90, 1.88, and 1.57, respectively. In conclusion, the prevalence and the extent of DGM were not related to H. pylori in patients with DU or NUD. In addition, the prevalence and the extent of DGM did not change until 1 year after H. pylori eradication in patients with DU, and decreased to the initial level of the H. pylori-negative DU group but without statistical significance after 4-year follow-up.

Adolescent↗
PubMed1999

After the eradication of Helicobacter pylori infection, relapse is a serious problem in Turkey.

Eradication of Helicobacter pylori (Hp) infection is strongly recommended in duodenal and gastric ulcer. In developed countries the recurrence rate is low; however, in Turkey, the Hp recurrence rate is suspected to be high as the prevalence of Hp infection is--as high as 70-80% in the asymptomatic population. We planned this study to determine the relapse rate of Hp infection after successful eradication therapy in Turkey. Fifty-two cases including 24 patients with duodenal ulcer and 28 patients with nonulcer dyspepsia were examined in this study. The eradication regimen was omeprazole 20 mg twice daily, clarithromycin 500 mg twice daily, and metronidazole 500 mg three times a day for 1 week. All patients underwent upper gastrointestinal tract endoscopy. At least four samples from antrum and corpus were taken to enable histologic diagnosis of Hp infection. After the eradication therapy, endoscopy was repeated at 1, 3, 6, and 12 months, and Hp-positive patients were dropped from study. With the use of this regimen, the Hp eradication rate was 92.3% (48/52). After the eradication of Hp infection, relapse rates were 6.97%, 27.5%, and 11.11% at 3, 6, and 12 months, respectively. The cumulative relapse rate for 1 year was 41.46%. The results of this study revealed that after the eradication of Hp infection, recurrence is encountered very often as a problem in Turkey. We concluded that hygienic and environmental factors can affect these high relapse rates.

Adult↗
PubMed2004

Helicobacter pylori eradication rate and glycemic control in young patients with type 1 diabetes.

OBJECTIVES: Eradication of Helicobacter pylori is more difficult in adult patients with diabetes than in patients with dyspepsia. It has also been suggested that eradication of H. pylori in children with type 1 diabetes mellitus improves their metabolic control. The aim of the current study was to assess the eradication rate of a standard triple therapy and its effects on glycemic control in young patients with type 1 diabetes. METHODS: The authors enrolled 29 type 1 diabetic patients with H. pylori, 29 type 1 diabetic patients without H. pylori, and 29 dyspeptic children with H. pylori. Groups were matched for gender and age and had similar geographical origin and socioeconomic status. H.pylori status was investigated before and 6 weeks after therapy by C-urea breath test. All enrolled patients with H. pylori were prescribed a standard triple therapy for eradicating H. pylori. Glycosylated hemoglobin A and daily insulin requirement were evaluated at enrollment and 6 months later in all patients with diabetes. The prevalence of the most common gastrointestinal symptoms also was investigated by means of a questionnaire in all subjects at enrollment and 6 months later. RESULTS: Eradication of H. pylori was similar in patients with diabetes (24/29) and those with dyspepsia (23/29) (83%v 79%; P = NS). No difference in metabolic control was observed before or after antibiotic treatment in the patients who experienced H. pylori eradication. No difference in glycemic control was observed after 6 months of follow-up. CONCLUSIONS: The eradication rate of H. pylori infection was similar for young patients with type 1 diabetes and those with dyspepsia and did not improve metabolic control in a short-term follow-up.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Eradication of Helicobacter pylori in peptic ulcer disease with amoxycillin, 2.0 g, and omeprazole, 80 or 120 mg: a prospective randomized trial.

BACKGROUND: The appropriate dose of proton pump inhibitors needed for eradicating Helicobacter pylori by dual therapy is still controversial. DESIGN: The study was conducted as a single-blind, single-centre trial. METHODS: Fifty-four patients with active duodenal ulcers were treated with amoxycillin tablets, 750 mg three times daily, and omeprazole, either 40 mg twice daily (group 1) or 40 mg three times daily (group 2), for 14 days in a prospective randomized trial. H. pylori eradication was assessed 10 weeks after starting treatment. Biopsies were taken for rapid urease tests and histological analysis and 13C-urea breath tests were ordered. RESULTS: In both groups ulcer healing was complete in 96.3% of patients after 10 weeks. Ten weeks after starting treatment, Helicobacter pylori was eradicated in 76.9% of the patients in group 1 and 74.1% of those in group 2, as shown by rapid urease tests and histological analysis. In the subgroup of fully compliant patients (n = 49) the eradication rates were 80% and 79.2%, respectively. Hyperacidity significantly reduced the eradication rates. Patients showing successful H. pylori eradication were significantly older (59 +/- 14.0 years vs. 49 +/- 15.6 years; P = 0.025). Eradication rates were lower in smokers than in non-smokers (36.4% vs. 83.9%; P = 0.006). CONCLUSION: It is concluded that higher omeprazole doses should be reserved for younger patients and smokers; in others they are not needed.

Adult↗
PubMed1997

Erosive duodenitis: prevalence of Helicobacter pylori infection and response to eradication therapy with omeprazole plus two antibiotics.

OBJECTIVES: To study the prevalence of Helicobacter pylori infection in patients with erosive duodenitis (ED), the associated gastric histological lesions and their response to eradication therapy with omeprazole plus two antibiotics. METHODS: A prospective study was made of 57 patients with ED (mean age 46 +/- 16 years, 72% males). At endoscopy, biopsies from gastric antrum and body were obtained for histological study (haematoxylin and eosin). A 13C-urea breath test was also performed. Omeprazole 20 mg twice daily plus two antibiotics (amoxycillin 1 g twice daily, clarithromycin 500 mg twice daily, metronidazole 500 mg twice daily) were administered for 1 week. Endoscopy and breath test were repeated 1 month after completing therapy, and the breath test was performed again at 6 months. RESULTS: All patients were H. pylori positive. Overall eradication was achieved in 86% (95% CI 75-93%). Duodenal erosion healing was obtained in 45 patients (79%). Healing was achieved in 86% (CI 73-93%) of cases with successful eradication therapy, but only in 3/8 (37%; CI 8.5-75%) patients with therapy failure (P < 0.01). In the multivariate analysis, H. pylori eradication was the only variable which correlated with erosion healing (odds ratio 10; CI 2-51; P < 0.01). Histological improvement, in both the gastric antrum and body, was demonstrated when eradication was achieved (P < 0.001). Six months after diagnosis H. pylori absence was confirmed in all patients with initial therapy success (all of them asymptomatic), and infection was confirmed in the eight patients who were H. pylori positive after therapy (six of them symptomatic). At 6-month follow-up, endoscopy was normal in 6/7 H. pylori-negative patients with previously persistent ED, while erosions were still present in 4/5 H. pylori-positive patients with previously persistent ED. CONCLUSION: A high prevalence (100%) of H. pylori infection in patients with ED was observed. A 1-week twice daily therapy with omeprazole plus two antibiotics (clarithromycin plus amoxycillin or metronidazole) was very effective in H. pylori eradication, duodenal erosion healing, symptomatic improvement, and in disappearance of associated histological gastritis. These observations suggest that ED should be considered a variant form of duodenal ulcer disease and treated accordingly; that is, with H. pylori eradication therapy.

Adult↗
PubMed1998

Results of Helicobacter pylori screening and eradication in a multi-ethnic community in central England.

OBJECTIVES: To determine the prevalence of Helicobacter pylori and risks for infection in a multi-ethnic inner city population, and to assess the effectiveness with which the infection can be eradicated in a relatively asymptomatic population of this type. DESIGN: Analysis of results from a small research-based community programme of screening and eradication. Tests were offered to matched groups of Asians and non-Asians from the general population. METHODS: Those who attended for screening had a serological screening test for infection with H. pylori. Data concerning possible risk factors for infection were collected by means of questionnaires. Subjects testing positive were offered a prescription for eradication therapy (ranitidine bismuth citrate and clarithromycin) through their general practitioner, and success of eradication therapy was assessed by urea breath test. RESULTS: The overall prevalence of infection in 155 subjects was found to be 51%. The difference between positive test rates in Asians (53%) and non-Asians (47%) was not significant (P=0.611). In Asians, age and social class were risk factors for infection, but not gender or birth outside the UK. Results were similar in those born in India and East Africa. Of the 79 people who tested positive, 64 (81%) elected to take eradication therapy. Compliance with medication was estimated to be 95% and successful eradication was achieved in 92% of cases. CONCLUSION: Social class is more important than Asian ethnic origin as a predictor of H. pylori status. Good rates of H. pylori eradication can be achieved in subjects from the general population living in inner city communities.

Breath Tests↗
PubMed1999

Insulin-dependent diabetes mellitus affects eradication rate of Helicobacter pylori infection.

BACKGROUND: Patients with insulin-dependent diabetes mellitus (IDDM) are often affected by chronic infections; however, antibiotic absorption may be influenced by the disease. Helicobacter pylori, the most common gastric infection worldwide, is the main acquired factor in the pathogenesis of gastritis and peptic ulcer. The aim of the study was to compare the H. pylori eradication rate obtained with a standard 7-day antibiotic regimen in a group of IDDM H. pylori infected patients and in a control group of infected dyspeptic patients. METHODS: Thirty-one patients (18 male, 13 female, 39+/-12 years) affected by IDDM and H. pylori infection, and 50 dyspeptic infected patients (23 male, 17 female, 37+/-10 years) were evaluated. H. pylori infection was assessed through 13C-urea breath test. A triple therapy with amoxycillin (1 g b.i.d.), clarithromycin (250 mg t.i.d.) and pantoprazole (40 mg b.i.d.) was given to both groups at the time of diagnosis for 7 days. Cure was defined as the absence of H. pylori infection, assessed by 13C-urea breath test, 6 weeks after completing anti-microbial therapy. Effects of H. pylori eradication on gastrointestinal symptoms (pyrosis, epigastric pain, belching, bloating, halitosis and nausea) were also evaluated. RESULTS: All enrolled patients completed the study. When compared to dyspeptic patients, the eradication rate was significantly lower in IDDM patients: 92% (46/50) versus 65% (20/31), respectively (P < 0.002). IDDM patients infected by H. pylori showed a different prevalence of some of the gastrointestinal symptoms assessed when compared to the infected dyspeptic patients; in particular, pyrosis, epigastric pain and belching were significantly more prevalent in the infected dyspeptic group. After H. pylori eradication, both groups showed a significant reduction of the intensity of all the gastrointestinal symptoms evaluated, except for nausea. CONCLUSIONS: IDDM patients showed a significantly lower H. pylori eradication rate when compared to that observed in dyspeptic subjects. The dosage and/or the duration of a standard eradication regimen does not appear to be sufficient to eradicate the infection in IDDM patients. The impairment of the gastrointestinal mucosa microvasculature with a reduction of antibiotic absorption, or the frequent use of antibiotics for other infections with development of resistant strains, may be the mechanisms underlying the observation.

Adult↗
PubMed1999

The effect of eradicating Helicobacter pylori infection on the course of adenomatous and hyperplastic gastric polyps.

OBJECTIVE: Histopathological and clinical data strongly suggest that Helicobacter pylori is the cause of chronic gastritis and peptic ulceration. However, little has been written about the potential causal relation of H. pylori infection to hyperplastic and adenomatous gastric polyps. We therefore carried out a prospective study to determine the effect of eradicating H. pylori infection on the course of hyperplastic and adenomatous gastric polyps. METHODS: From November 1996 to December 1997, 6700 patients who had undergone upper gastrointestinal endoscopy at the two centres in Zagreb, Croatia, were candidates for participation in the study. Hyperplastic and adenomatous polyps were diagnosed on a basis of at least three histological samples taken from the polyp. In seven patients endoscopy had to be repeated because forceps biopsy sampling either provided inadequate tissue for correct histological diagnosis, or accurate characterization of gastric polyp histology was not possible. Upon completion of all endoscopic examinations before and after treatment, biopsy samples were taken from the antrum (two) and the body of the stomach (two) so that gastritis could be graded and classified, and the presence of H. pylori sought by histology. Two other samples were taken from the antrum for a rapid urease test. Follow-up examinations were performed by using endoscopy. Control endoscopy was performed at least 4 weeks after the treatment of H. pylori infection had been completed, and then every 3-4 months. The follow-up ranged from 4 to 17 months, with a median of 14 months. The treatment of H. pylori infection consisted of a 1-week course of either omeprazole (20 mg twice daily) or pantoprazole 40 mg twice daily), and a 1-week course of amoxicillin 2g twice daily) and metronidazole (400 mg three times daily), and clarithromycin (500 mg twice daily). Eradication of H. pylori infection was assessed by repeated histology and rapid urease test. RESULTS: Twenty-one patients (nine women, 12 men; median age 52 years) with histologically proven hyperplastic gastric polyps, and seven patients (two women, five men; median age, 67 years) with adenomatous gastric polyps were included in the study. Among 21 patients with hyperplastic gastric polyps, 16 patients (76%) were positive for H. pylori infection. Only two patients (29%) with adenomatous gastric polyps were positive for the infection. Complete eradication of H. pylori was initially achieved in all patients positive for H. pylori. Total regression of the gastric polyps was observed only among the patients with hyperplastic gastric polyps in whom H. pylori had been eradicated. Complete regression of the hyperplastic gastric polyps was observed in seven of the 16 evaluable patients (44%; 95% CI, 19-68%) after H. pylori eradication. The endoscopic snare polypectomy was carried out in nine patients with hyperplastic polyps and two patients with adenomatous gastric polyps in whom regression of the polyps was not observed after H. pylori eradication, as well as in five patients with hyperplastic and four with adenomatous gastric polyps who were negative for H. pylori. Exploratory laparotomy and gastrotomy with polyps excision were carried out in one patient with multiple adenomatous gastric polyps. In only one patient who was not positive for H. pylori recurrence of hyperplastic gastric polyp was recorded during follow-up, and no re-infection with H. pylori has been detected. CONCLUSIONS: Our results suggest that the development of hyperplastic gastric polyps may be directly related to chronic active gastritis and concomitant H. pylori infection. Cure of H. pylori infection associated with hyperplastic gastric polyps resulted in complete polyp regression in more than 40% of patients. Therefore, for patients with hyperplastic gastric polyps and concurrent H. pylori infection an antibiotic treatment designed to eradicate H. pylori appears to be recommended before further therapeutic options are consi

Adenomatous Polyps↗