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PubMed1995

Adjuvant therapy for Helicobacter pylori eradication: role of lansoprazole in clinical studies.

Helicobacter pylori (Hp) eradication can lead to cure of duodenal ulcer. Eradication of Hp was first attempted with bismuth salts alone or in combination with one or two antibiotics. In 1990, triple therapy with bismuth, tetracycline or amoxicillin, and metronidazole or tinidazole was standard. Proton pump inhibitors are active in vitro against Hp and have therefore been tested in monotherapy, dual therapy, and triple therapy. When lansoprazole was used as monotherapy, the mean Hp eradication was 6% in four studies. When lansoprazole was used in dual therapy with amoxicillin, pooled data from four trials employing various dosage schedules showed Hp eradication in 38.9% of patients. When lansoprazole was used in dual therapy with clarithromycin, the eradication rate was about 47.7% with lansoprazole 30 mg daily and 69.1% with lansoprazole 30 mg twice daily. When lansoprazole was used in triple therapy, Hp eradication rates ranged from 80% to 96%, with the best results obtained with a combination of lansoprazole, amoxicillin, and clarithromycin. Lansoprazole together with one or preferably two antibiotics is effective in Hp eradication. With the new macrolides, which have a lower rate of Hp resistance than metronidazole or tinidazole, we can expect to achieve eradication of Hp in all patients who are compliant with antibiotic therapy and infected with sensitive strains.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Lansoprazole versus lansoprazole plus amoxicillin treatment for eradication of Helicobacter pylori in patients with gastric ulcer.

Helicobacter pylori is a major cause of gastritis and an important factor in duodenal ulcer relapse. Eradication of H. pylori has usually been achieved by triple therapy, a combination of bismuth salts and two antibiotics. The disadvantage of these regimens is the large number of tablets and the high incidence of side effects. A new H+,K(+)-ATPase inhibitor, lansoprazole (LPZ), has a strong acid inhibitory effect and an anti-H. pylori effect in vitro. These dual effects have an advantage for the eradication of H. pylori by LPZ alone or by a combination of LPZ and antibiotics. In this study, we investigated an anti-H. pylori effect of LPZ alone and LPZ plus low-dose amoxicillin and the relation between the status of H. pylori colonization and the endoscopic healing stage. LPZ monotherapy suppressed H. pylori but did not eradicate it. LPZ plus low-dose amoxicillin dual therapy eradicated H. pylori in 45.5% of patients with gastric ulcer disease. However, this rate is not satisfactory for eradication therapy. The optimal dosage and duration of treatment need to be specified. A high rate of healing to the endoscopic S2 stage was achieved by eradication of H. pylori and the recurrence of gastric ulcer was suppressed in patients in whom H. pylori was eradicated. The eradication of H. pylori may change the natural course of gastric ulcer disease as it does in duodenal ulcer disease.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Eradication of Helicobacter pylori with lansoprazole and clarithromycin in gastric ulcer patients.

This study attempted to determine the efficacy of lansoprazole plus clarithromycin therapy in the eradication of Helicobacter pylori in gastric ulcer patients. The influence of H. pylori eradication on healing and relapse of ulcers was also studied. Thirty-nine patients received either lansoprazole 30 mg daily for 8 weeks (group 1) or clarithromycin 200 mg twice daily for 2 weeks and lansoprazole 30 mg daily for 8 weeks (group 2). Before treatment, H. pylori status was evaluated by a rapid urease test and histologic examination. H. pylori clearance and eradication were evaluated by a rapid urease test, polymerase chain reaction, and a [13C]urea breath test. Clearance of H. pylori was 0% in group 1 and was 33% in group 2. Eradication of H. pylori was 0% in group 1 and 21% in group 2. Although all five ulcers were healed in patients with H. pylori eradication, ulcers were not healed in the five patients without eradication. Relapse of ulcer was observed in three patients in whom eradication had failed. In this study, for H. pylori-positive gastric ulcer patients, better results were obtained when lansoprazole plus clarithromycin therapy was used, and H. pylori eradication was achieved.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1998

Helicobacter pylori reinfection rates in children after eradication therapy.

BACKGROUND: There are few studies of Helicobacter pylori reinfection in childhood. In the current study the reinfection rate of H. pylori and ulcer recurrence were investigated during a follow-up period of 12 months or more in children who had undergone eradication therapy. METHODS: Twenty-seven patients aged 5 to 16 years (6 with gastric ulcer, 13 with duodenal ulcer, and 8 with nodular gastritis) were studied. Biopsy-based H. pylori tests performed 1 to 2 months after eradication therapy demonstrated that eradication was successful in 23 patients (5 with gastric ulcer, 11 with duodenal ulcer, and 7 with nodular gastritis) and unsuccessful in 4 (1 with gastric ulcer, 2 with duodenal ulcer, and 1 with nodular gastritis). Twenty-three successfully treated patients were observed for a mean of 22 months (a total of 42.2 patient years of follow-up). To assess H. pylori status, all 23 patients underwent a 13C-urea breath test 1 year after eradication therapy. If the test result was negative, the patients underwent the follow-up test once every year thereafter. In successfully and unsuccessfully treated patients, endoscopy was performed if a patient reported symptoms suggesting ulcer recurrence. RESULTS: The initial follow-up 13C-urea breath tests showed that all 23 patients remained free of infection at 12 to 19 months. Among 17 patients, the second test confirmed reinfection in 1 at 28 months. In two patients studied, the third test showed a negative result. The reinfection rate was 2.4% per patient year. Over the follow-up period, ulcer recurrence was found in 2 of 3 ulcer patients with eradication failure but in none of the 16 ulcer patients with successful eradication. The recurrence rate was significantly lower in successfully treated patients than in unsuccessfully treated patients (p < 0.05). CONCLUSIONS: Reinfection with H. pylori is rare in children aged more than 5 years, and successful eradication significantly reduces ulcer recurrence. This study supports the benefit of eradication therapy in older children.

Adolescent↗
PubMed2001

Helicobacter pylori eradication therapy is more effective in peptic ulcer than in non-ulcer dyspepsia.

AIM: To evaluate whether eradication therapy is more effective in peptic ulcer disease (PUD) than in non-ulcer dyspepsia (NUD). METHODS: We retrospectively studied 481 patients with NUD (183 patients) or PUD (298 patients) infected with Helicobacter pylori included in several prospective clinical trials. Three eradication regimens were given: (1) proton pump inhibitor (PPI) plus clarithromycin, plus either amoxycillin or metronidazole for 7 days (297 patients); (2) ranitidine bismuth citrate (RBC) plus clarithromycin plus amoxycillin for 7 days (79 patients); and (3) RBC plus clarithromycin plus amoxycillin plus metronidazole for 5 days (105 patients). H. pylori eradication was defined as a negative 13C-urea breath test 4 weeks after completing treatment. RESULTS: H. pylori eradication rates were 82% (95% CI 78-87%) with PPI plus two antibiotics for 7 days, 85% (95% CI 75-91%) with RBC plus two antibiotics for 7 days, and 91% (95% CI 86-97%) with RBC plus three antibiotics for 5 days (P < 0.05 compared with the first regimen). Overall, the H. pylori eradication rate in patients with NUD was 78% (95% CI 71-84%), while in patients with PUD it was 89% (95% CI 86-93%) (P < 0.001). Both the combination of PPI plus two antibiotics for 7 days and the combination of RBC plus three antibiotics for 5 days were more effective in PUD than in NUD patients. However, RBC plus clarithromycin plus amoxycillin for 7 days was equally effective in both diseases. RBC plus two antibiotics for 7 days achieved better results than the same therapy with PPI only in NUD patients (84% v. 59%, P < 0.01), but both regimens were similar when prescribed in PUD patients (86% v. 88%). In the multivariate analysis, the type of therapy, the diagnosis (NUD v. PUD), and the product variable of therapy (with RBC plus 2 antibiotics for 7 days) and diagnosis (interaction variable) were the only variables that influenced H. pylori eradication. The odds ratio (OR) for the effect of RBC versus PPI plus two antibiotics for 7 days in patients with NUD was 4 (95% CI 1.7-9.7; P < 0.01), whereas in patients with PUD no statistical significance was achieved (OR 0.79; 95% CI 0.2-3.9). CONCLUSION: Overall, H. pylori eradication therapy is more effective in PUD than in NUD patients. This advantage of eradication therapies in PUD patients seems to be observed with 7-day PPI-based triple regimens, and with 5-day RBC-based quadruple therapy, while the 7-day RBC-based triple regimen seems to be equally effective in both diseases.

Amoxicillin↗
PubMed2004

A 1 year follow-up study of the consequences of Helicobacter pylori eradication in duodenal ulcer patients: unchanged frequency of erosive oesophagitis and decreased prevalence of non-erosive gastro-oesophageal reflux disease.

BACKGROUND AND AIM: Discussions concerning the increased incidence of gastro-oesophageal reflux disease (GORD) after Helicobacter pylori eradication continue. In this study we aimed to evaluate the presence of co-existing GORD in (1) duodenal ulcer patients after successful H. pylori eradication, (2) patients with persistent H. pylori infection after attempts at eradication, and (3) controls in whom H. pylori eradication had not been attempted. METHODS: A prospective study of 255 patients with duodenal ulcer who were assigned to H. pylori eradication or to control treatment (omeprazole for 4 weeks) and followed up for 1 year or until peptic ulcer relapse. GORD was determined in the patients who had reflux oesophagitis on endoscopy at the beginning of the study and/or in patients without reflux oesophagitis if they experienced heartburn and/or regurgitation at least twice a week associated with impairment of daily activities. RESULTS: The study revealed a significant decrease (from 44.6% to 21.7%; P < 0.001) of patients with GORD at the end of the follow-up among those in whom H. pylori eradication had been successful. There was no significant difference in the frequency of reflux oesophagitis before and after the follow-up regardless of H. pylori status. CONCLUSIONS: H. pylori eradication did not significantly influence the prevalence and incidence of reflux oesophagitis in patients with duodenal ulcer during a 1 year follow-up period, but there was a significantly lower prevalence of GORD after successful H. pylori eradication, as patients with non-erosive GORD had been cured.

Adult↗
PubMed2006

Helicobacter pylori isolated from patients who later failed H. pylori eradication triple therapy readily develop resistance to clarithromycin.

In this study, the ease of selection of clarithromycin resistance was investigated in clarithromycin-susceptible Helicobacter pylori strains isolated from patients with H. pylori infection prior to the administration of triple-combination eradication therapy (clarithromycin plus amoxicillin plus a proton pump inhibitor). Clarithromycin-susceptible strains isolated from ten patients in whom the eradication therapy was successful and from six patients in whom the eradication therapy was unsuccessful were exposed serially to subinhibitory concentrations of clarithromycin. The number of transfers required for the MICs of the strains to increase by 8- and 32-fold were 6.6 and 7.2, respectively, in the successful eradication group, and as few as 2.4 and 1.5, respectively, in the unsuccessful eradication group. The number of transfers required for the A2142G or A2143G point mutation of the 23S rRNA gene to be detected in the strains were 5 and 8, respectively, for the strains in the successful eradication group, and 1 and 2, respectively, for the strains in the unsuccessful eradication group. These results suggest that patients in the unsuccessful eradication group were infected with strains of H. pylori that readily became resistant to clarithromycin on exposure to the drug.

Amoxicillin↗
PubMed2004

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.

Adult↗
PubMed2004

Eradication of Helicobacter pylori induces apoptosis and inhibits proliferation of heterotopic proliferative glands in infected Mongolian gerbils.

Mongolian gerbils infected with Helicobacter pylori (H. pylori ) develop heterotopic proliferative glands (HPGs) in the glandular stomach submucosa. To investigate the effects of H. pylori eradication on cell turnover in HPGs, three antibiotics, lansoprazole, amoxicillin and clarithromycin, were administered at 50 or 75 weeks after inoculation of H. pylori, and the stomachs were excised for histological examination at 1, 2, 4, 8 or 25 weeks thereafter. The HPGs were classified into gastric type (G-type) and others (GI + I-type), which included both pure intestinal (I-type) and gastric-and-intestinal mixed type (GI-type). Apoptosis and cell proliferation were evaluated by means of TUNEL assay and BrdU labeling, respectively. At 8 weeks post-eradication, apoptotic indices were significantly increased in the eradication group (G-type: 2.5%; GI + I-type: 7.2%) compared to the non-eradication group (G-type: 0.6%; GI + I-type: 2.1%: P < 0.01), while BrdU labeling indices were significantly decreased (G-type: 1.9%; GI + I-type: 6.8% as compared with 4.3% and 13.2%, respectively, P < 0.01 for both). At 25 weeks, the apoptotic indices were similarly higher [G-type: 0.4 (eradication group) vs. 0.2% (non-eradication group); GI + I-type: 5.8 vs. 1.1%, both P < 0.01], and the BrdU labeling indices (G-type: 0.8 vs. 2.2%, P < 0.01; GI + I-type: 5.1 vs. 11%, P < 0.05) continued to be lower in HPGs. Furthermore, there were highly significant reductions in the areas of HPGs at 8 and 25 weeks post-eradication. These findings demonstrated that eradication results in apoptosis and reduction of proliferation of HPGs in H. pylori-infected gerbils, these lesions thus being apparently reversible through regulation of cell kinetics.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2005

Morphological changes in human gastric tumours after eradication therapy of Helicobacter pylori in a short-term follow-up.

BACKGROUND: It is controversial as to whether the development of gastric cancer is influenced by Helicobacter pylori eradication. If eradication itself influences the tumour morphology, this may affect the tumour discovery rate. AIM: To investigate the morphological changes in the gastric neoplasm after H. pylori eradication. METHODS: We studied 37 patients with eradication therapy. After a 1-month follow-up, endoscopic re-evaluation was performed and the appearance was compared with first image. All lesions were resected endoscopically, and were subjected to histological assessment and to immunohistochemistry. Serum gastrin levels were determined before and after eradication. RESULTS: Twenty-nine of 37 patients underwent successful eradication. The appearance of 11 lesions (33% of 33 lesions) became indistinct after successful eradication. All lesions were of the superficial-elevated type and the height of the lesions decreased. We detected normal columnar epithelium over the neoplasm in eight of the lesions. Higher expression of single-stranded deoxyribonucleic acid in the deep area was characteristic in tumours with an indistinct appearance. These changes did not correlate with the serum gastrin levels. CONCLUSIONS: The morphology of the gastric neoplasm change after eradication in the short-term. This may contribute to the decreased tumour discovery rate.

Adenocarcinoma↗
PubMed2005

Helicobacter pylori-associated ulcer bleeding: should we test for eradication after treatment?

BACKGROUND: Eradication of Helicobacter pylori after peptic ulcer haemorrhage reduces the risk of recurrence. Because H. pylori treatment is very effective, it is unclear whether testing to confirm eradication is worthwhile. AIMS: To examine whether patients with H. pylori-associated peptic ulcer haemorrhage should be tested for successful eradication after completion of antibiotic therapy. METHODS: A Markov cost-effectiveness model was developed to compare testing vs. non-testing of H. pylori eradication in peptic ulcer haemorrhage. Probability estimates and average costs were derived from published information. RESULTS: Testing for H. pylori eradication resulted in a benefit of 0.07 quality-adjusted life-years and cost 836 US dollars less than the strategy of not confirming eradication. Testing remained the superior strategy when varying the model regarding age, the initial success of eradication, various test and retreatment strategies, and the rate and costs of recurrent bleeding. Assuming a high eradication rate (95%), the test strategy becomes more expensive only if the cost of H. pylori testing reaches 265 US dollars; however, even under these conditions it remains cost-effective. CONCLUSIONS: Patients with H. pylori-associated peptic ulcer bleeding should be tested to confirm eradiation of H. pylori after completion of antibiotic treatment.

Cost-Benefit Analysis↗
PubMed2006

Systematic review and meta-analysis: importance of CagA status for successful eradication of Helicobacter pylori infection.

BACKGROUND: Some, but not all studies have provided evidence that the CagA status of Helicobacter pylori strains is a predictive factor for the outcome of eradication therapy. AIM: To clarify the association between CagA status and eradication outcome. METHODS: We included studies reporting the numbers of successful and failed cases in H. pylori-eradication therapy according to the CagA status. Fourteen studies (1529 patients) were included of 325 articles identified in the search. The pooled risk ratio for H. pylori-eradication failure in CagA-negative relative to CagA-positive strains and the pooled risk difference in eradication success between the two groups were used as summary statistics. Meta-regression was used for examining the source of heterogeneity. RESULTS: The summary risk ratio for eradication failure in CagA-negative relative to CagA-positive was 2.0 (95% CI: 1.6-2.4, P < 0.001), corresponding with the summary risk difference for eradication success between the groups of 11% (95% CI: 3-19%, P = 0.011). Meta-regression analysis demonstrated that usage of polymerase chain reaction examination for CagA status and a high proportion of non-ulcer dyspepsia patients were factors for heterogeneity among studies. CONCLUSIONS: Our meta-analysis confirmed the importance of the presence of CagA as a predictor for successful eradication of H. pylori.

Antigens, Bacterial↗
PubMed2004

Effect of Helicobacter pylori eradication on gastroesophageal function.

BACKGROUND: To elucidate the cause of possible occurrence of reflux esophagitis after Helicobacter pylori eradication, gastric and esophageal function among H. pylori infected Japanese patients were evaluated both before and after eradication therapy. METHODS: Nine H. pylori-positive patients were studied before and 6 months after successful H. pylori eradication. Studies included gastric emptying, esophageal manometry, gastric and esophageal pH monitoring as well as measuring serum levels of gastrin, pepsinogen I and pepsinogen II. RESULTS: Helicobacter pylori eradication was associated with a significant change in serum gastrin and pepsinogen levels, consistent with the improvement in mucosal inflammation. There was no significant change in gastric emptying, fasting or postprandial lower esophageal sphincter (LES) pressure, esophageal primary peristaltic contractions, frequency of transient LES relaxation, or gastroesophageal reflux, as assessed by 24 h pH monitoring. The percent time of the gastric pH>4 at night decreased significantly. A 41-year-old male developed erosive gastroesophageal reflux disease (GERD) (Los Angeles Classification Grade A) after eradication. Physiological studies showed he had abnormal esophageal motility prior to H. pylori eradication. CONCLUSIONS: With the exception of gastric pH at night, most patients did not experience a significant change in gastric or esophageal function after H. pylori eradication. Development of GERD post H. pylori eradication likely reflects an increase in the acidity of the refluxate superimposed on pre-existing abnormalities in gastroesophageal motility.

Adult↗
PubMed2005

Impact of Helicobacter pylori eradication on the anti-secretory efficacy of lansoprazole in gastroesophageal reflux disease patients.

BACKGROUND: Helicobacter pylori eradication was recommended for the prevention of atrophic gastritis in gastroesophageal reflux disease (GERD) patients on long-term omeprazole treatment. It has been also shown that the treatment with proton pump inhibitors produces lower intragastric pH after H. pylori eradication in subjects with peptic ulcer and healthy individuals. The aim of the present study was to test the hypothesis of whether the efficacy of lansoprazole is reduced after the eradication of H. pylori in GERD patients with peptic esophagitis. METHODS: Eight-hour intragastric pH recordings were performed before and after an 8-day course of lansoprazole (30 mg once daily) in 10 H. pylori-positive male patients with reflux esophagitis and were repeated after the H. pylori eradication. Intragastric acidity was measured by using an antimony electrode placed 10 cm below the cardia. RESULTS: Baseline median preprandial, post-prandial, total intragastric pH and the percentage of time with pH < 3 were not different before and after H. pylori eradication without lansoprazole treatment. During lansoprazole treatment, median post-prandial intragastric pH was lower (4 vs 2.7; P < 0.05) and the percentage of time with pH < 3 was longer (3.4%vs 41.8%; P < 0.05) after H. pylori eradication. Median total intragastric pH tended to be lower after eradication but no difference was found in preprandial median pH. CONCLUSIONS: In patients with reflux esophagitis treated with lansoprazole, intragastric pH increased significantly when H. pylori was present, especially in the post-prandial period, whereas baseline pH remained unchanged after H. pylori eradication.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2006

Effects of Helicobacter pylori eradication therapy on gastric emptying measured using the 13C-octanoic acid breath test and the acetaminophen method.

BACKGROUND: The relationship between Helicobacter pylori eradication and gastric emptying has been reported; however, the effect of eradication therapy on gastric emptying is still unclear. This study evaluated the relationship between three gastric emptying techniques, the scintigraphic technique, the 13C-octanoic acid breath test, and the acetaminophen method, measured simultaneously, and the effect of H. pylori eradication therapy on gastric emptying and abdominal symptoms in patients with functional dyspepsia who were H. pylori positive. METHODS: Fifty-three consecutive patients with positive H. pylori infection were enrolled in this study. In the first 14 patients, gastric emptying was measured using the three gastric emptying techniques. In 42 patients cured of H. pylori infection, the 13C-octanoic acid breath test and the acetaminophen method were performed before and 3 months after eradication. RESULTS: Significant correlations were found between the scintigraphic technique, the 13C-octanoic acid breath test, and the acetaminophen method. Gastric emptying determined by the 13C-octanoic acid breath test and the acetaminophen method was not changed after eradication, on average. In 14 (33.3%) patients a decrease in symptom score after eradication was observed. In four (9.5%) patients, accelerated gastric emptying after eradication may have led to a reduction in the abdominal symptoms. CONCLUSIONS: The 13C-octanoic acid breath test and the acetaminophen method are appropriate for investigating gastric emptying. A causal relationship between improvement of symptoms and accelerated gastric emptying was not found, and the efficacy of H. pylori eradication therapy in patients with functional dyspepsia was minimally exhibited.

Acetaminophen↗
PubMed1997

Time of Helicobacter pylori eradication assessment following treatment.

BACKGROUND: The most appropriate time to assess accurately Helicobacter pylori eradication following treatment has been debated, with recommendations ranging from 1 to 3 months. The purpose of this study was to validate the assessment of H. pylori eradication 1 month following treatment. MATERIALS AND METHODS: Three randomized, double-blind, active-controlled clinical trials were conducted in patients with endoscopically verified, active duodenal ulcers and H. pylori infection. Patients were treated with various treatment regimens of omeprazole plus amoxicillin. Ulcer healing, H. pylori eradication, and ulcer relapse were examined. Patients underwent repeat endoscopy and biopsy at 1 and 6 months following treatment (or sooner if symptoms returned) to determine the recurrence of ulcers and H. pylori status. To determine the accuracy of measuring H. pylori eradication at 1 month posttreatment, we compared the H. pylori status at 1 month and 6 months following treatment. RESULTS: In a combination of treatment groups and studies, a total of 384 evaluable patients represented data at both time points and were included in the analysis. Of those eradicated at 1 month posttreatment, 94% (141 of 150) remained eradicated at 6 months posttreatment. The proportion of patients with H. pylori eradicated at 1 month posttreatment did not differ significantly from that at 6 months posttreatment for each study. The overall efficiency of the two tests (agreement between tests) was 93% (359 of 384). Agreement between the 1-month and 6-month posttreatment H. pylori assessment was apparent, regardless of the treatment used. CONCLUSION: H. pylori eradication measured 1 month following cessation of treatment accurately reflects successful treatment of the infection.

Amoxicillin↗
PubMed1998

Evaluation of the PyloriTek test for detection of Helicobacter pylori infection in cases with and without eradication therapy.

OBJECTIVE: The accuracy of the PyloriTek test (a 1-h rapid urease test) used after eradication therapy of Helicobacter pylori (H. pylori) has not been well clarified. This study was done to evaluate the accuracy of the PyloriTek test results for cases with and without eradication therapy, using culture and histology as gold standard methods, and to establish the suitable timing of the PyloriTek test after eradication treatment. METHODS: One hundred sixty-three patients undergoing upper endoscopy were randomly selected; 100 patients had not received eradication therapy and 63 had. Three biopsy specimens each were obtained from the gastric antrum and the body for examination by PyloriTek, culture, and histology. The absence of H. pylori was established with negative results from both culture and histology. RESULTS: In cases without eradication therapy, PyloriTek, correctly identified 66 of 67 H. pylori-positive cases and 30 of 33 H. pylori-negative cases, yielding 98.5% sensitivity and 90.9% specificity. In cases with eradication therapy, PyloriTek gave correct diagnoses in 10 of 17 H. pylori-positive cases and in 45 of 46 H. pylori-negative cases, for 58.8% sensitivity and 97.8% specificity. However, when PyloriTek was used more than 4 months after the end of eradication therapy, both the sensitivity and the specificity increased to 100%. CONCLUSION: Considering time and cost, the use of PyloriTek alone may be satisfactory for detecting H. pylori infection in cases without eradication therapy. When patients are examined more than 4 months after intervention, the use of PyloriTek alone may be sufficient for correctly diagnosing H. pylori infections.

Amoxicillin↗
PubMed1999

Increase in apoptosis and decrease in ornithine decarboxylase activity of the gastric mucosa in patients with atrophic gastritis and gastric ulcer after successful eradication of Helicobacter pylori.

OBJECTIVE: Recent reports have shown that patients infected with Helicobacter pylori (H. pylori) have a higher risk of gastric cancer. However, the mechanism of this increased risk is still unclear. In the gastric mucosa, the size of a continuously renewed population of cells is determined by the rates of cell production and of cell loss. Ornithine decarboxylase (ODC) activity is elevated in various gastrointestinal cancers and serves as a marker of mucosal proliferative activity. Apoptosis occurs throughout the gut and is associated with cell loss. Both cell proliferation and cell loss have important roles in H. pylori-associated gastric carcinogenesis. Therefore, we investigated the effect of H. pylori eradication on ODC activity and apoptosis in the gastric mucosa of patients with atrophic gastritis and gastric ulcers. METHODS: Biopsy specimens of the gastric antrum were obtained at endoscopy from 17 H. pylori-positive gastric ulcers patients and 15 H. pylori-positive gastritis patients before and 4 wk after eradication therapy with amoxicillin, omeprazole, and a new anti-ulcer agent, ecabet sodium, and from 10 gastric ulcer patients in whom ulcer healed but H. pylori was left untreated. ODC activity and induction of apoptosis were determined immunohistochemically. RESULTS: H. pylori was successfully eradicated with the triple therapy in 12 (80%) of 15 gastritis patients and 13 (76%) of 17 gastric ulcer patients. ODC activity was present in the gastric mucosa in 21 (84%) patients before eradication but in only four (16%) patients after successful eradication (p = 0.0005). The apoptotic index increased significantly (p = 0.0006) from 4.2% +/- 0.4% before treatment to 7.4% +/- 0.5% after successful eradication. CONCLUSIONS: Successful eradication of H. pylori decreases mucosal ODC activity and increases apoptosis in the gastric mucosa. These findings indicate that by decreasing mucosal cell proliferation and increasing epithelial cell loss, H. pylori eradication may help decrease the subsequent risk of gastric cancer.

Adult↗