Active Duodenal Ulcer Research Articles

Prevalence of active duodenal ulcer in H. pylori-positive patients with past history of duodenal ulcer and relationship to symptoms

Prevalence of active duodenal ulcer in H. pylori-positive patients with past history of duodenal ulcer and relationship to symptoms

Omeprazole (OME), clarithromycin (CLA) and tinidazole (TIN) for 7 days vs ome, CLA and tin for 7 days plus ome for 21 days in the treatment and recurrence of active duodenal ulcer with H.pylori infection: a double blind placebo controlled trial Leonardo^Marzio

Omeprazole (OME), clarithromycin (CLA) and tinidazole (TIN) for 7 days vs ome, CLA and tin for 7 days plus ome for 21 days in the treatment and recurrence of active duodenal ulcer with H.pylori infection: a double blind placebo controlled trial Leonardo^Marzio

Rabeprazole is superior to ranitidine in the management of active duodenal ulcer disease: results of a double-blind, randomized North American study

OBJECTIVE: The primary purpose of this study was to compare the efficacy and tolerability of rabeprazole versus ranitidine in the treatment of patients with active duodenal ulcer disease. METHODS: This multicenter, double-blind, randomized, parallel-group study enrolled 376 patients. Patients were randomly assigned to receive rabeprazole 20 mg administered once daily in the morning ( q.a.m.) with matching ranitidine placebo twice daily ( b.i.d.) (n = 188), or ranitidine 150 mg b.i.d. with matching rabeprazole placebo q.a.m. (n = 188). Three visits were scheduled: wk 0 (baseline; days −3 to −1), wk 2 (day 15 ± 3 days), and wk 4 (day 29 ± 3 days). The primary efficacy response variable was defined as complete regeneration of the mucosa at the site of all ulcers identified during the study. Secondary efficacy variables included patients’ ratings of frequency and severity of ulcer pain, frequency of antacid use, and improvement of overall physical well-being. Tolerability was evaluated with analyses of adverse events, laboratory evaluations, fasting serum gastrin levels, vital signs, body weight, and electrocardiograms. RESULTS: Up to 4 wk of treatment with rabeprazole 20 mg q.a.m. produced significantly greater healing rates, compared to treatment with ranitidine150 mg b.i.d. (83% vs 73%; p = 0.017). Significant differences between treatment groups were also observed for secondary efficacy indices. At wk 2, rabeprazole was more likely than ranitidine to produce complete resolution of duodenal ulcer pain (39% vs 25%; p = 0.006), improvement in duodenal ulcer nighttime pain severity (76% vs 65%; p = 0.044), and improvement in overall well-being (55% vs 41%; p = 0.009). At wk 4, the proportion of patients with normalization of overall well-being was significantly higher in the rabeprazole group than in the ranitidine group (45% vs 29%; p = 0.003). Rabeprazole was safe and well tolerated in this study. CONCLUSIONS: In patients with active duodenal ulcer disease, rabeprazole 20 mg q.a.m. is superior to ranitidine 150 mg b.i.d. in healing, resolving ulcer pain frequency, improving nighttime pain severity, and improving overall well-being. Rabeprazole is an effective and well-tolerated alternative treatment for patients with active duodenal ulcer disease.

Cure of Helicobacter pylori-positive active duodenal ulcer patients: double-blind, multicentre, 12-month study comparing a two-week dual vs a one-week triple therapy

Aims. To compare a two-week dual therapy to a one-week triple therapy for the healing of duodenal ulcer and the eradication of the Helicobacter pylori infection. Patients and Methods. A total of 165 patients with active duodenal ulcer were enrolled in the study. At entry, endoscopy, clinical examination and laboratory tests were performed. Histology and the rapid urease test were used to diagnose Helicobacter pylori infection. Patients received either lansoprazole 30 mg plus amoxycillin 1 g bid for two weeks (two-week, dual therapy) or lansoprazole 30 mg plus amoxycillin 1 g plus tinidazole 500 mg bid for one week plus lansoprazole qd for an additional week (one-week, triple therapy). Two and twelve months after cessation of therapy, endoscopy and clinical assessments were repeated. Results. Duodenal ulcer healing and Helicobacter pylori eradication were both significantly greater (p<0. 0001) in the triple therapy group (healing: 98.6%; Helicobacter pylori cure rate: 72.6%) than in the dual therapy group (healing: 77.3%; Helicobacter pylori cure rate: 33.3%). Ulcers healed more frequently in Helicobacter pylori-cured than in Helicobacter pylori-not cured patients (94.9% vs. 77.2%; p<0.0022). After one year, Helicobacter pylori eradication was re-confirmed in 46 58 patients previously treated with the triple therapy and in 10 40 patients treated with the dual therapy (p<0.0001). Only three duodenal ulcer relapses were observed throughout follow-up: all were in Helicobacter pylori-not cured patients. Conclusions. Triple therapy was more effective than dual both in curing Helicobacter pylori infection and healing active duodenal ulcers. The speed of ulcer healing obtained after only 7 days of antibiotics and 14 days of proton pump inhibitors confirmed that longer periods of anti ulcer therapy were not necessary. Helicobacter pylori -not cured patients had more slowly healing ulcers which were more apt to relapse when left untreated.

Pantoprazole versus ranitidine in the treatment of duodenal ulcer: a multicenter study in Brazil

OBJECTIVE: The aim of this study was to compare the effectiveness and tolerance of pantoprazole versus ranitidine in the treatment of duodenal ulcers in the Brazilian population. METHODS: A total of 222 patients with active duodenal ulcers (DU) were randomly allocated to a double dummy blind treatment, either with ranitidine (RAN) 300 mg (111, aged from 20–68 yr old, 56 female) or with pantoprazole (PANT) 40 mg (111 patients, 18–70 yr old, 45 female). After a 2-wk course of treatment, each patient was clinically and endoscopically assessed for ulcer healing. Failure to heal required a further 2-wk course of treatment and a new evaluation thereafter. RESULTS: In all, 77 of the 103 patients in the PANT group (74.8%) and 42 of the 94 patients in the RAN group (44.7%) who completed the study had ulcer healing after one 2-wk treatment course, and an additional 23 in the PANT group (22.3%) and 28 in the RAN group (29.8%) after the second 2-wk treatment course, totaling 100 (97.1%) and 70 (74.5%), respectively. Therapeutic gain in favor of pantoprazole was significant both at the end of the first and the second 2-wk treatment course ( p < 0.001). At 2 wk, symptoms remission was significantly higher in the PANT group (97.6%) than with the RAN group (77.5%) ( p < 0.001). The Intention-to-treat analysis showed results statistically similar to those observed in the per-protocol analysis. Minor adverse events were reported by four patients in the PANT group and three in the RAN group. No relevant laboratory abnormalities were seen. No patient withdrew from the study due to adverse events. CONCLUSIONS: Our results show that pantoprazole is more effective than ranitidine in the treatment of duodenal ulcer providing faster ulcer healing in most patients (97.1%), in 4 wk. Adverse events were rare and were similar in both groups, and had no influence on the therapeutic outcome.

Eradication of Helicobacter pylori Compared with Long-Term Acid Suppression in Duodenal Ulcer Disease: A Randomized Trial with 2-Year Follow-up

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.

Symptomatic benefit 1–3 years after H. pylori eradication in ulcer patients: impact of gastroesophageal reflux disease

OBJECTIVES: Eradication of Helicobacter pylori ( H. pylori) infection markedly reduces the recurrence of duodenal and gastric ulcers. However, there is little information regarding its efficacy in resolving dyspeptic symptoms in ulcer patients. The primary aim of this study was to assess the effect of eradicating H. pylori infection on dyspeptic symptoms in ulcer patients. The secondary aim was to identify predictors of symptomatic response to H. pylori eradication. METHODS: A total of 97 dyspeptic patients with active duodenal and/or gastric ulceration associated with H. pylori infection and unrelated to NSAID use had the severity and character of their dyspeptic symptoms measured before and again 1–3 yr after H. pylori eradication therapy. RESULTS: Pretreatment, the median dyspepsia score was 12 (4–16). Posttreatment, 55% of those eradicated of H. pylori had resolution of dyspepsia (score <2) compared with 18% of those not eradicated of the infection (95% CI for difference, 11–62%). Of the ulcer patients 31% had symptoms and/or endoscopic evidence of coexisting gastroesophageal reflux disease (GERD) at initial presentation and this influenced the symptomatic response to eradication of H. pylori. Of the 22 patients with heartburn or acid reflux as the predominant presenting symptom, but no endoscopic esophagitis, only 27% experienced resolution of dyspepsia after H. pylori eradication, compared with 68% of the 59 without those as predominant symptoms (95% CI for difference, 18–63%). Only one of the five patients with coexisting endoscopic esophagitis at initial presentation experienced resolution of dyspepsia after H. pylori eradication. Symptomatic benefit was unrelated to time lapsed since the infection was eradicated. Only three of 50 subjects developed de novo GERD symptoms after eradication of H. pylori, whereas 21 of 36 subjects experienced resolution of GERD symptoms after eradication of the infection. CONCLUSIONS: A substantial proportion of ulcer patients have symptoms and/or signs of coexisting GERD at initial presentation and this reduces the symptomatic benefit from H. pylori eradication. However, we have found no evidence that eradicating H. pylori induces de novo GERD symptoms in ulcer patients.

Symptomatic benefit 1-3 years after H. pylori eradication in ulcer patients: impact of gastroesophageal reflux disease.

Eradication of Helicobacter pylori (H. pylori) infection markedly reduces the recurrence of duodenal and gastric ulcers. However, there is little information regarding its efficacy in resolving dyspeptic symptoms in ulcer patients. The primary aim of this study was to assess the effect of eradicating H. pylori infection on dyspeptic symptoms in ulcer patients. The secondary aim was to identify predictors of symptomatic response to H. pylori eradication. A total of 97 dyspeptic patients with active duodenal and/or gastric ulceration associated with H. pylori infection and unrelated to NSAID use had the severity and character of their dyspeptic symptoms measured before and again 1-3 yr after H. pylori eradication therapy. Pretreatment, the median dyspepsia score was 12 (4-16). Posttreatment, 55% of those eradicated of H. pylori had resolution of dyspepsia (score <2) compared with 18% of those not eradicated of the infection (95% CI for difference, 11-62%). Of the ulcer patients 31% had symptoms and/or endoscopic evidence of coexisting gastroesophageal reflux disease (GERD) at initial presentation and this influenced the symptomatic response to eradication of H. pylori. Of the 22 patients with heartburn or acid reflux as the predominant presenting symptom, but no endoscopic esophagitis, only 27% experienced resolution of dyspepsia after H. pylori eradication, compared with 68% of the 59 without those as predominant symptoms (95% CI for difference, 18-63%). Only one of the five patients with coexisting endoscopic esophagitis at initial presentation experienced resolution of dyspepsia after H. pylori eradication. Symptomatic benefit was unrelated to time lapsed since the infection was eradicated. Only three of 50 subjects developed de novo GERD symptoms after eradication of H. pylori, whereas 21 of 36 subjects experienced resolution of GERD symptoms after eradication of the infection. A substantial proportion of ulcer patients have symptoms and/or signs of coexisting GERD at initial presentation and this reduces the symptomatic benefit from H. pylori eradication. However, we have found no evidence that eradicating H. pylori induces de novo GERD symptoms in ulcer patients.

Alto índice de erradicación de Helicobacter pylori en pacientes con úlcera duodenal tras fracaso de un tratamiento previo

To analyze the effectiveness of a second-line treatment of Helicobacter pylori infection in patients with duodenal ulcer based on previous antibiotic regimen. Open, prospective, uncontrolled study, but guided by protocol including 30 consecutive patients with endoscopic diagnosis of active duodenal ulcer and failure of a first-line H. pylori eradication treatment diagnosed by urea breath test or a new endoscopy with histology and positive urease test. Treatment consisted in 10 days with omeprazole (20 mg/12 h), bismuth subcitrate (120 mg/6 h), tetracycline (500 mg/6 h) and metronidazole (500 mg/8 h) (OBTM) if previous regimen was with clarithromycin; or 10 days with omeprazole (20 mg/12 h), clarithromycin (500 mg/12 h) and amoxycillin (1g/12 h) (OCA) if previous regimen did not include clarithromycin; using metronidazole (500 mg/8 h) instead of amoxycillin (OCM) in case of allergy. Eradication was defined as a negative 13C-urea breath test 2 months after the end of therapy. One patient had to stop treatment due to the side effects and in 2 patients urea breath test was not performed (3 patients due to the OBTM group). Per protocol eradication was achieved in 25 out of 27 patients (92.6%) and by intention-to-treat eradication was attained in 25 out of 30 cases (83.3%). When both groups analyzed separately, the OCA combination was successful in 5 from 6 patients (83.3%; 95% CI 35.9-99.6); while the OBTM combination was successful in 20 from 21 valuable patients (95. 2%; 95% CI 76.2-99.9). In this second case we make an intention to treat analysis and eradication was achieved in 20 from 24 (83.3%; 95% CI 62.6-95.3). The eradicative treatment for H. pylori based in different antibiotics used in subsequent attempts get high eradication rates in patients with duodenal ulcer.

The role of the host versus the environment in duodenal ulcer disease

Gastric functions can be understood only in the context of a network including the brain gut axis, neuro-endocrine and paracrine mechanisms and growth factors. These host factors including parietal cell sensitivity (PCS) may well interact with an important environmental factor, Helicobacter pylori (Hp), and help to explain its actions. The aim of this study was to investigate PCS related to Hp status and duodenal ulcer (DU). PCS was assessed by constructing dose-response curves after pentagastrin and calculating the D 50. Five groups of patients were studied: I) active DU, Hp pos. (8); II) history of DU, Hp pos. (8); III) asymptomatic Hp pos. (8); IV) asymptomatic Hp neg. (10); V) DU on maintenance H 2 blocker therapy, Hp pos. (20). PCS was repeated after Hp eradication. PCS was lowest in group IV, and in Hp pos. groups, was significantly higher, with insignificant differences among them, irrespective of DU. PCS declined significantly after Hp eradication. Group V showed an insignificant decline in PCS during treatment, not preventing recurrence. A higher PCS in Hp infection irrespective of DU, declining after eradication, suggests that this may be a reversible epiphenomena related to Hp infection. This may offer an explanation as to why DU develops only in some subjects with Hp, suggesting the importance of the host in the pathogenesis of DU.

DOES THE ERADICATION OF HELICOBACTER PYLORI CURE DUODENAL ULCER DISEASE IN COMMUNITIES WITH A HIGH PREVALENCE RATE? COMPARISON WITH LONG‐TERM ACID SUPPRESSION

SUMMARYThe long‐term effect of Helicobacter pylori eradication on the natural history of duodenal ulcer has been investigated and compared with long‐term acid suppression treatment in an endemic community for infection. Seventy‐three patients with endoscopically verified H. pylori positive active duodenal ulcer disease were included in this prospective study. Patients were divided into two groups. Group A patients (n=39) were given an omeprazole‐based triple eradication regimen, while group B patients (n=34) were given omeprazole alone followed by long‐term famotidine 20 mg daily as maintenance treatment. A control endoscopy was performed at the third month of treatment. The bacterium was eradicated in 32 (82%) of group A patients. All patients were followed up for two years and an endoscopy performed at the end of each year. H. pylori recurred in 13 patients and the reinfection rate was 44.8% over two years. Duodenal ulcer recurred in seven of these patients at two years (24.1%). There was a close association between H. pylori reinfection and ulcer relapse. Group B patients remained H. pylori positive during the study and the ulcer recurred in five of these patients (16.6%) despite continuous famotidine treatment. There was no statistically significant difference in ulcer relapse rate between the groups. These results suggested that H. pylori eradication is not an absolute solution for duodenal ulcer disease in high endemic regions and continuous maintenance treatment with H2‐receptor antagonists is still an alternative approach in some chronic recurrent cases.

Impact of ELISA and immunoblot as diagnostic tools one year after eradication of Helicobacter pylori in a multicentre treatment study.

The performance of serological tests for Helicobacter pylori infections is hampered by the persistence of antibodies after eradication therapy or spontaneous healing. Detection of different antigens or immunoglobulin classes might have an impact on the validity of serodiagnosis. The aim of this study was to assess the decrease in IgA and IgG antibody levels after eradication of H. pylori. Serum samples of 242 patients with active duodenal ulcer were tested with the ELISA and the immunoblot (IB) techniques for H. pylori-specific IgA and IgG antibodies before therapy and 1 year after successful eradication. From a total of 81 patients paired sera were available. At the end of the follow-up period ELISA antibody titres from the IgA class had decreased from a mean value of 6.69 to 4.26 units (P = 0.0001), and IgG class antibody titres from a mean value of 21.9 to 12.1 units (P = 0.0001). Regarding seroreversion, from 34 initially IgA positive sera 16 (47%), and from 74 IgG positive sera 18 (24%), had definitively reverted to 'negative'. One year after eradication, when tested with the immunoblot, the antibody responses against specific antigens of 37% IgA-positive sera (23/62) and 8% IgG-positive sera (6/78) reverted to 'negative', compared to a seroreversion rate of 27% of the anti-CagA IgA-positive sera (18/67) and of 9% of the anti-CagA IgG-positive sera (7/79). In conclusion, despite an overall significant decrease of H. pylori antibodies, both tests cannot be recommended for monitoring treatment success.

Impact of ELISA and immunoblot as diagnostic tools one year after eradication of Helicobacter pylori in a multicentre treatment study

The performance of serological tests for Helicobacter pylori infections is hampered by the persistence of antibodies after eradication therapy or spontaneous healing. Detection of different antigens or immunoglobulin classes might have an impact on the validity of serodiagnosis. The aim of this study was to assess the decrease in IgA and IgG antibody levels after eradication of H. pylori. Serum samples of 242 patients with active duodenal ulcer were tested with the ELISA and the immunoblot (IB) techniques for H. pylori-specific IgA and IgG antibodies before therapy and 1 year after successful eradication. From a total of 81 patients paired sera were available. At the end of the follow-up period ELISA antibody titres from the IgA class had decreased from a mean value of 6.69 to 4.26 units ( P=0.0001), and IgG class antibody titres from a mean value of 21.9 to 12.1 units ( P=0.0001). Regarding seroreversion, from 34 initially IgA positive sera 16 (47%), and from 74 IgG positive sera 18 (24%), had definitively reverted to ‘negative’. One year after eradication, when tested with the immunoblot, the antibody responses against specific antigens of 37% IgA-positive sera (23/62) and 8% IgG-positive sera (6/78) reverted to ‘negative’, compared to a seroreversion rate of 27% of the anti-CagA IgA-positive sera (18/67) and of 9% of the anti-CagA IgG-positive sera (7/79). In conclusion, despite an overall significant decrease of H. pylori antibodies, both tests cannot be recommended for monitoring treatment success.

Dyspepsia on withdrawal of ranitidine in previously asymptomatic volunteers

OBJECTIVE: H 2 receptor antagonist therapy has been shown to produce rebound acid hypersecretion. The clinical significance of this phenomenon is not known. We performed this study to determine whether withdrawal of H 2 receptor antagonist therapy results in dyspepsia in previously asymptomatic volunteers. METHODS: Thirty-five Helicobacter pylori-positive asymptomatic volunteers were randomized in double-blind fashion to receive 2 months’ treatment with either ranitidine 300 mg nocte or placebo. Dyspeptic symptoms were measured before starting treatment and over the course of 10 days after stopping treatment by means of a validated questionnaire. RESULTS: Thirty-one subjects completed the study; 17 were randomized to ranitidine. The pretreatment median aggregate dyspepsia score of the placebo group was 0 (0–4), as was that of the ranitidine group (0–8) (N.S.). During the 10 days after completion of ranitidine, the median aggregate dyspepsia score was 1.4 (0–30), compared with 0 (0–6.3) after placebo ( p < 0.01). Of those given ranitidine, 59% experienced dyspepsia after treatment, compared with only 14% who took placebo. In the subgroup that developed dyspepsia after active therapy, the median duration of symptoms was 2 days, symptom severity being maximal on the second day after completion of the tablets. On the days when dyspepsia was experienced, the median daily dyspepsia score was 5 (range, 2–10), which was similar to that of a control group with active duodenal ulcer disease (5; range, 0–11). CONCLUSIONS: Withdrawal of a 2-month course of ranitidine 300 mg nocte results in the development of dyspeptic symptoms in a proportion of previously asymptomatic subjects. Patients receiving ranitidine should be warned about this rebound dyspepsia and advised not to immediately resume treatment, as rebound symptoms are likely to improve within a few days.

Prevalence of Helicobacter pylori Infection in Peptic Ulcer Patients of Highly Endemic Kashmir Valley

Objective This study aimed to find out prevalence of Helicobacter pylori (H. pylori) in peptic ulcer disease (PUD) which is highly endemic disease in Kashmir. Method This study consisted of 50 PUD patients and 30 asymptomatic volunteers. Peptic ulcer was diagnosed by endoscopic examination and H. pylori was detected by histology (using Giemsa stain), one minute endoscopy room test (OMERT) and modified Gram's staining. Positive results from OMERT plus histology were considered as the “gold standard” for the presence of H. pylori. Results Out of 50 patients, 46 had duodenal ulcer (DU), 2 had benign gastric ulcer (GU) and 2 had both DU and GU. The sensitivity and specificity of OMERT were 94% and 96.70%, histology 97.90% and 96.90% and Gram's staining 91.30% and 85.30%, respectively, as compared to our gold standards. H. pylori was present in 76.09% of DU, 50% of GU, whereas patients with duodenitis, channel ulcers, chronic active DU and those with multiple ulcers were 100% H. pylori positive. H. pylori was present in 10 (33.33%) of healthy volunteers. Conclusion A significant association between H. pylori infection and PUD was found in this study. However, there seem to be other causative factors as well which contribute for this highly endemic disease.

Oxidant stress, anti-oxidants, nitric oxide and essential fatty acids in peptic ulcer disease

In patients with duodenal ulcer (DU), the plasma levels of nitrite and lipid peroxides, the anti-oxidant content of red cells and plasma phospholipid fatty acid analysis were performed both before and after healing of the ulcer following treatment with lansoprazole, a proton pump inhibitor. These results showed that during the phase of active DU, the concentrations of antioxidants (superoxide dismutase, SOD, catalase and glutathione peroxidase) in red cells were low where as those of lipid peroxides and nitric oxide were high. Of the fatty acids measured, the concentration of palmitic acid (16:0) was increased during the active ulcer phase whereas those of arachidonic acid, alpha-linolenic acid and docosahexaenoic acid were low. These biochemical abnormalities reverted to normal following healing of the ulcer with lansoprazole. These results coupled with the observation that polyunsaturated fatty acids (PUFAs) can inhibit the growth of Helicobacter pylori and heal the ulcer suggest that free radicals, anti-oxidants, nitric oxide and PUFAs may play a significant role in the pathogenesis of DU. If this is true, it suggests that PUFAs can be exploited as potential anti-peptic ulcer drugs.

Seasonal changes in symptomatic duodenal ulcer activity in Taiwan: a comparison between subjects with and without haemorrhage.

To examine if climatic changes may influence the presentation of pain and haemorrhage in patients with duodenal ulcers. Cross-sectional study. Tertiary referral centre. A total of 10,331 symptomatic duodenal ulcer diseases were diagnosed from 1989 to 1996. The patients who had any extrinsic factors that might influence the exacerbation of duodenal ulcer were not included. Patients were divided into those whose ulcer bled once or repeatedly as distinct from those whose ulcers caused pain without haemorrhagic complications. Patients with acute cholangitis diagnosed in the same period were studied as controls. During the 7-year period, 10,331 symptomatic duodenal ulcer diseases were diagnosed. Amongst these, 5328 showed active duodenal ulcer without haemorrhage, 2088 showed acute duodenal ulcer with stigmata of recent haemorrhage, and 2915 showed a deformed bulb. The incidence of total duodenal ulcers showed significant monthly variation and was found to be more common from November to March (P < 0.001). The monthly incidence of total episodes of upper gastrointestinal tract bleeding peaked from November to March (P < 0.001) with significant variation. The monthly incidence of bleeding episodes from duodenal ulcer only was the same (P < 0.001). In patients whose duodenal ulcers repeatedly caused pain without haemorrhage, there were significant monthly fluctuations, with peak months from December to March (P < 0.001). In the control diagnosis, there were no significant calendar variations (P = 0.85). Our study has shown that both groups of patients demonstrated similar monthly fluctuations. The incidence is significantly higher during the cold seasons. These data suggest that climatic changes may influence the presentation of pain and haemorrhage in duodenal ulcer patients.

Biopsy forceps disinfection technique does not influence Helicobacter pylori culture

Objectives: Culturing Helicobacter pylori ( Hp) has a low sensitivity rate, and is affected by factors such as the number of biopsies, transport, and culture conditions. Hp detection is also influenced by omeprazole, antibiotics, bismuth salts, or benzocaine use. Disinfection procedures based on glutaraldehyde are highly effective in eliminating any Hp contamination of endoscopic equipment. However, the possibility that some residual glutaraldehyde present in biopsy forceps after decontamination could affect Hp viability has not yet been investigated. Methods: Antral specimens from 25 patients with active gastric or duodenal ulcer obtained with three forceps (sterilized with ethylene oxide, glutaraldehyde, or glutaraldehyde-phenolate) were streaked on appropriate media, and results of culture evaluated. Results: Helicobacter pylori was isolated in 17 patients. Positivity of culture was independent of the way the forceps were sterilized, and the number of colonies (mean ± SD) was similar for the three types of forceps (475 ± 312, 533 ± 242, and 550 ± 225 colony-forming units [CFUs] for ethylene oxide, glutaraldehyde, and glutaraldehyde-phenolate, respectively). Moreover, the incubation time since isolation was also similar (6.0 ± 1.3, 5.8 ± 1.2, and 5.7 ± 1.2 days for ethylene oxide, glutaraldehyde, and glutaraldehyde-phenolate disinfected forceps, respectively). Conclusion: The use of glutaraldehyde to sterilize biopsy forceps is not responsible for the false-negative results of Hp culture.

Triple Therapy with Omeprazole, Amoxicillin and Clarithromycin Is Effective against Helicobacter Pylori Infection in Gastric Ulcer Patients as well as in Duodenal Ulcer Patients

Background/Aims: There have been few reliable published studies permitting assessment of therapeutic regimens for Helicobacter pylori infection in gastric ulcer (GU) patients. The aim of the present study was to evaluate the efficacy of omeprazole-based dual and triple therapy regimens, both including clarithromycin, for the cure of H. pylori infection in active GU and duodenal ulcer (DU) patients. The study was conducted in Japan, a country in which GU is more prevalent than DU. Methods: Two hundred and thirty-four consecutive peptic ulcer patients (GU: n = 124; DU: n = 103; GDU: n = 7) suffering from H. pylori infection were randomly treated with either omeprazole 20 mg b.i.d. + amoxicillin 500 mg q.i.d. + clarithromycin 400 mg b.i.d. (OAC) or with omeprazole 20 mg b.i.d. + clarithromycin 400 mg b.i.d. (OC) for 14 days. H. pylori infection was evaluated by histology and culture from antral and corpus biopsies 6 weeks after completing antimicrobial therapy. Results: Follow-up data were available in 202 patients. The cure rates of H. pylori infection in GU patients were 83.9% (47/56) with OAC and 59.2% (29/49) with OC. Corresponding rates in DU patients were 91.5% (43/47) and 70.5% (31/44), respectively. The cure rates with OAC were significantly higher than those with OC (p < 0.001, χ² test). The cure rates in GU patients were lower than those in DU patients for both regimens, but these differences were not statistically significant. Side effects were generally mild and did not interfere with compliance. One patient in the OAC group and 2 patients in the OC group complained of severe side effects that led to therapy discontinuation. Conclusions: Triple therapy with omeprazole, amoxicillin and clarithromycin is a safe and effective regimen for the cure of H. pylori infection in GU patients as well as in DU patients. We recommend this triple regimen as a first-line treatment in all patients with peptic ulcers associated with H. pylori infection in Japan.

Helicobacter pylori eradication as a surrogate marker for the reduction of duodenal ulcer recurrence.

An abundance of data exists documenting the association of H. pylori eradication with the reduction in duodenal ulcer recurrence. To evaluate the validity of using H. pylori eradication as a surrogate marker for the reduction in duodenal ulcer recurrence using rigorously controlled studies. Three controlled clinical trials were conducted in patients with uncomplicated, active duodenal ulcers. Patients were treated with various combinations of omeprazole and amoxycillin. Ulcer healing and H. pylori eradication were assessed. For patients whose duodenal ulcer healed, duodenal ulcer recurrence was determined over a 6-month period in patients with H. pylori eradication and those remaining positive for H. pylori at least 4 weeks after treatment. To support the data obtained from these clinical trials, a search of the medical literature was conducted to identify additional human clinical trials in which duodenal ulcer recurrence rates were measured and categorized by H. pylori status at least 1 month post-treatment. In 11 controlled trials, the overall 6-18-month duodenal ulcer recurrence rate was 54% among patients remaining positive for H. pylori at least 4 weeks after treatment compared to 6% among patients with H. pylori eradication following treatment. This finding was corroborated by the uncontrolled trials, in which the duodenal ulcer recurrence rate was 64% among patients found to be H. pylori-positive and 6% for patients found to be H. pylori-negative at least 4 weeks after treatment. A time course of duodenal ulcer recurrence rates using pooled data from both controlled and uncontrolled studies demonstrated that duodenal ulcer recurrence rates for H. pylori-negative patients persisted for up to 4 years following treatment. Duodenal ulcer recurrence rates for H. pylori-positive patients increased for the first year, then levelled off. A comparison of the duodenal ulcer recurrence rates for different treatment regimens revealed that eradication regimens based on omeprazole plus antibiotics and bismuth plus antibiotics exhibited similar duodenal ulcer recurrence rates for H. pylori-positive and -negative patients. Regardless of treatment regimens, H. pylori eradication produced a consistent and significant reduction in duodenal ulcer recurrence. Therefore H. pylori eradication, 4 weeks post-therapy, can be used as a surrogate marker for reduced duodenal ulcer recurrence in investigational clinical trials.