Decreased Prevalence of Helicobacter pylori Infection in Gastroesophageal Reflux Disease

Background.   An increased incidence of reflux esophagitis has been reported after eradication of H. pylori in patients with duodenal ulcer. To determine if H. pylori is associated with lower rates of esophagitis, we studied the prevalence of H. pylori infection in patients with and without reflux esophagitis and a subgroup of patients with concomitant peptic ulcer disease.
Methods.   Patients who underwent esophagogastroduodenoscopy and had diagnostic testing for H. pylori over a 30-month period were studied. H. pylori infection was determined by rapid urease testing, gastric histopathology, or serology. Reflux esophagitis was determined by endoscopic and/or histologic criteria.
Results.   Of 514 patients, 39.5% had H. pylori infection and 22.2% had reflux esophagitis. The prevalence of H. pylori infection in patients with reflux esophagitis was 30.7%, compared with 42.0% in patients without esophagitis ( p = 0.039). The odds ratio for esophagitis risk with H. pylori infection was 0.61 (95% CI, 0.39–0.95). Neither patient age nor gender affected H. pylori prevalence. In patients with duodenal ulcer, H. pylori was present in 36.4% of patients with esophagitis and in 69.2% of patients without esophagitis ( p = 0.018). The odds ratio for esophagitis with H. pylori infection in these patients was 0.25 (95% CI, 0.09–0.73).
Conclusions.   Our study demonstrates that H. pylori infection is significantly less prevalent in patients with reflux esophagitis and may protect against its development. In duodenal ulcer patients, this effect was more dramatic. Further study is required to confirm these findings and elucidate mechanisms underlying possible beneficial effects of H. pylori.     

Long-term follow-up after eradication of Helicobacter pylori with omeprazole, clarithromycin, and tinidazole (OCT regimen) in a Japanese population

BACKGROUND: The long-term benefit of Helicobacter pylori eradication treatment that includes metronidazole on peptic ulcer disease in Japan is unclear. We investigated the rate of H. pylori re-infection and ulcer relapse after H. pylori eradication. MATERIALS AND METHODS: A total of 266 patients with endoscopically confirmed peptic ulcer disease and H. pylori infection were treated with triple therapy of omeprazole 40 mg (20 mg b.i.d.), clarithromycin 800 mg (400 mg b.i.d.), and tinidazole 1000 mg (500 mg b.i.d.) for 7 days. Endoscopy with gastric biopsy was performed before and 1 month, 6 months, 1.5 years, and 3.5 years after therapy. H. pylori status was determined by H. pylori culture, rapid urease test, and histopathology. 13C-urea breath test was done at 6 months after eradication therapy. Treatment was deemed successful when all tests were negative at 6 months after therapy by endoscopic biopsy. RESULTS: Successful H. pylori eradication was achieved in 262/266 (98.5%) patients with peptic ulcer. Total relapse of peptic ulcer occurred in 8/262 (3%) patients after eradication, with 3/262 (1.1%) occurring within 1.5 years after treatment and 5/262 (1.9%) within 3.5 years. All relapsed patients were found to be H. pylori-positive at the time of relapse. Of the 262 patients who experienced eradication, 20 (7.6%) were subsequently re-infected, six (2.3%) within 1.5 years and 14 (5.3%) within 3.5 years. CONCLUSION: Triple therapy with omeprazole, clarithromycin, and tinidazole (OCT) is useful for H. pylori eradication in Japan, but there is an appreciable re-infection rate in this population.     

Eradication of Helicobacter pylori for the prevention of peptic ulcer rebleeding

AIM: To evaluate the effect of Helicobacter pylori eradication on ulcer bleeding recurrence in a prospective, long-term study including more than 400 patients. METHODS: Patients with peptic ulcer bleeding were prospectively included. H. pylori infection was confirmed by rapid urease test, histology or (13)C-urea breath test. Several eradication regimens were used. Ranitidine 150 mg was administered daily until eradication was confirmed by breath test 8 weeks after completing eradication therapy. Patients with therapy failure received a second or third course of therapy. Patients with eradication success did not receive maintenance anti-ulcer therapy, and were controlled yearly with a repeated breath test. RESULTS: Four hundred and twenty-two patients were followed up for at least 12 months, with a total of 906 patient-years of follow up. Mean age was 59 years, and 35% were previous nonsteroidal anti-inflammatory drug (NSAID) users. Sixty-nine percent had duodenal, 24% gastric, and 7% pyloric ulcer. Recurrence of bleeding was demonstrated in two patients at 1 year (incidence: 0.22% per patient-year of follow up), which occurred after NSAID use in both cases. CONCLUSION: Peptic ulcer rebleeding does not occur in patients with complicated ulcers after H. pylori eradication. Maintenance anti-ulcer (antisecretory) therapy is not necessary if eradication is achieved.     

Influence of oral Helicobacter pylori on the success of eradication therapy against gastric Helicobacter pylori

Background. The goal of this study was to see whether Helicobacter pylori ( H. pylori ) in the oral cavity might adversely affect the outcome of eradication therapy for gastric H. pylori.
Materials and Methods. Forty-seven patients (36 males, 11 females) with gastric H. pylori infection were enrolled in this study. Gastric H. pylori infection was confirmed by both immunohistological staining with anti- H. pylori antibody and bacterial culture of biopsy specimens. The therapeutic regimen consisted of 30 mg/day lansoprazole, 750 mg/day metronidazole, and 400 mg/day clarithromycin administered for 2 weeks. A fragment of the H. pylori urease gene was amplified by nested PCR for DNA extracted from saliva and dental plaque from the same patients. We examined the correlation between the gastric eradication success rate and the prevalence of H. pylori in the oral cavity as determined by PCR before and after the eradication therapy.
Results. The eradication success rate was significantly lower in the oral H. pylori -positive cases (12/23, 52.1%) than in the negative cases (22/24, 91.6%) at 4 weeks after the therapy (p = .0028). Two years later, only 16 of the 23 (69.5%) oral H. pylori -positive cases were disease-free, as compared to 23 of the 24 (95.8%) oral H. pylori -negative cases (p = .018).
Conclusions. H. pylori in the oral cavity affected the outcome of eradication therapy and was associated with a recurrence of gastric infection. We recommend that oral H. pylori should be examined by nested PCR and, if positive, should be considered a causal factor in refractory or recurrent cases.     

Helicobacter pylori–Positive Duodenal Ulcer: A Long-Term Double-Blind Randomized Study in Patients Healed with H2-Receptor Antagonists

Background. The NIH Consensus Conference in 1994 (1) concluded that all patients with peptic ulcr disease should be tested and treated for Helicobacter pylori and that further evaluation was needed for patients in remission.
Materials and Methods. We evaluated in a double blind randomization 30 patients whose duodenal ulcers had been healed with H₂-receptor antagonists and who remained in remission on maintenance therapy. After ulcer healing and the presence of H. pylori had been confirmed, these patients were randomized to receive eradication therapy or placebo and were followed for a mean period of 23 months.
Results. Almost all patients receiving placebo had ulcer recurrence, whereas the patients treated with antibiotics demonstrate a low recurrence rate.
Conclusion. These data suggest, for the first time to our knowledge, the importance of treating with antibiotics duodenal ulcer patients whose disease is in remission.     

Helicobacter pylori and the Surface Mucous Gel Layer of the Human Stomach

Background The colonization of Helicobacter pylori in the surface mucous gel layer (SMGL) was investigated.
Materials and Methods. Surgically removed stomachs were obtained from patients and included gastric ulcer (4 cases), duodenal ulcer (2), and gastric cancer (24). Five of these cases were examined at 8, 19, 28, 143, and 171 days after the end of eradication therapy. For the preservation of the SMGL, these specimens were fixed in cold Carnoy's solution, cleared in xylene, and embedded in paraffin. Serial sections were obtained and were stained by dual staining with the galactose oxidasecold thionin Schiff reaction followed by paradoxical Concanavalin A staining and immunostaining for H. pylori.
Results. H. pylori characterstically attached to surface mucous cells and colonized in the SMGL. H. pylori in the SMGL was more abundant than that attached to the surface mucous cells. The degree of H. pylori infection both on the surface of surface mucous cells and in the SMGL correlated well with the severity of gastritis. In the SMGL, this organism obviously preferred to colonize in the layer of surface mucous cell-type mucins, and the multilaminated structure of the SMGL deteriorated markedly. Eradication of H. pylori restored the structure of the SMGL, and the inflammatory reaction decreased gradually.
Conclusion. The SMGL is an indispensable site of H. pylori colonization, and this organism damaged the gastric mucosa partially by causing deterioration of the SMGL. Removal of the organism from the SMGL should be considered for eradication of this organism.     

Effect of Omeprazole Therapy on the Survival of Helicobacter pylori, Urease Activity, and Antral Gastric Histology in Patients with Duodenal Ulcer

Background. Helicobacter pylori is associated with chronic active gastritis and peptic ulceration (PU). Omeprazole is a proton pump inhibitor that is effective in healing PU and reducing gastritis. Previously it has been found that omeprazole has some bacteriostatic activity against H. pylori both in vitro and in vivo and in inhibiting urease activity in vitro. Our aim was to evaluate the effect of omeprazole on H. pylori colonization of the gastric mucosa, urease activity in vivo, and the presence of associated gastritis in patients with duodenal ulcer (DU).
Materials and Methods. We studied 12 patients (7 men and 5 women, ages 22–68 yr) with Du larger than 5 mm in diameter with a positive CLOtest (Delta West Ltd., Australia). Omeprazole, 20 mg bid, was given for 8 weeks to each patient, patients were endoscoped at the end of this period to check for healing of DU, and repeat biopsies were obtained from the gastric antrum for histologyical analysis, CLOtest, and culture.
Results. DU healed completely in all patients. Likewise in all patients there was significant reduction in the urease activity, from 22.1=4.17 to 1.58 ± 0.92 units/ml ( p <.001; 95% confidence interval of the difference between means, 32.7–14.1), and reduced H. pylori density, from 1,403.46 ± 128.23 to 422.5 ± 172.39 colony-forming units (CFU) per milligram of tissue biopsy ( p < .001; 95% confidence interval of the difference between means, 1,486.1–590.5). The numbers of H. pylori were reduced on the gastric mucosa after omeprazole therapy and disappeared in six patients, a result that correlated with a negative CLOtest reading after 24 hours.
Conclusion. Omeprazole, 20 mg bid, is capable of reducing H. pylori numbers and urease activity in vivo. There was no significant reduction in the severity of antral gastritis in DU patients studied.     

Pathophysiology and clinical relevance of Helicobacter pylori.

Considerable knowledge has recently accumulated on the mechanism by which Helicobacter pylori (H. pylori) induces chronic gastritis. Although H. pylori is not an invasive bacterium, soluble surface constituents can provoke pepsinogen release from gastric chief cells or trigger local inflammation in the underlying tissue. Urease appears to be one of the prime chemoattractants for recruitment and activation of inflammatory cells. Release of cytokines, such as tumor necrosis factor alpha, interleukin 1 and 6, and oxygen radicals, leads to a further tissue inflammation accompanied by a potent systemic IgA and IgG type of immune response. Chronic inflammation and antigens on glandular epithelial cells lead to a progressive destruction with loss of the epithelial barrier function. Within the gastric mucosa, patches of intestinal metaplasia develop, which may be a risk factor for subsequent development of gastric carcinoma. Hyperacidity in duodenal ulcer patients induces gastric metaplasia in the duodenal bulb, which represents a target for H. pylori colonization and ulcer formation. H. pylori can be detected in the majority of patients with peptic ulcers and, compared to age-matched healthy people, it is also found more often in patients with dyspepsia and gastric carcinoma. Although H. pylori can be detected in healthy people, the marked reduction of the ulcer recurrence rate by eradication of H. pylori (80 percent versus 20 percent relapse within one year) suggests that H. pylori is a major risk factor for duodenal ulcer formation. The potential role of H. pylori in non-ulcer dyspepsia and carcinogenesis is under investigation. Current regimens aimed at eradicating H. pylori use a combination of several drugs that are potentially toxic. Since the risk of complications may exceed the potential benefit in most patients, eradication treatment should be limited to clinical trials and to patients with aggressive ulcer disease. New drug regimens, e.g., the combination of proton pump inhibitors with one antibiotic, may provide less toxic alternatives. Beyond ulcer treatment, effective and well-tolerated eradication regimens may have a place in prophylaxis of gastric carcinoma.     

Normalization of phospholipids concentration of the gastric mucosa was observed in patients with peptic ulcer after eradication of Helicobacter pylori

Background. Phospholipids concentration in the gastric mucosa decreased in patients with Helicobacter pylori infection. The aim of this study is to examine the effects of eradication of H. pylori on decreasing the phospholipids concentration in the gastric mucosa in patients with gastric or duodenal ulcer. Materials and Methods. Phospholipids (phosphatidylcholine, phosphatidylethanolamine, and sphingonomyeline) were measured in biopsy specimens from the antrum and corpus using thin‐layer chromatography. In H. pylori positive patients with gastric ulcer (n = 26) and duodenal ulcer (n = 13), and H. pylori negative controls (n = 20), the biopsy specimens were obtained before and 3 months after eradication. Eradication was performed using lansoprazole, amoxycillin, and clarithromycin. Results. Compared with the H. pylori negative control group, the concentrations of phosphatidylcholine and phosphatidylethanolamine decreased significantly in the gastric ulcer group in both antrum and corpus mucosa, and in the duodenal ulcer group in antrum mucosa. This decrease returned to the control level after eradication. Conclusions. This study demonstrates that the eradication of H. pylori in patients with peptic ulcer normalized the decrease of phosphatidylcholine and phosphatidylethanolamine in the gastric mucosa.     

Four-day, twice daily, quadruple therapy with amoxicillin, clarithromycin, tinidazole and omeprazole to cure Helicobacter pylori infection: a pilot study

Background. The best regimen for the treatment of Helicobacter pylori infection has yet to be defined. Four-day quadruple therapy with tetracycline, metronidazole, bismuth, and a proton pump inhibitor has been shown to obtain a very high cure rate. However, the fact that it must be taken four times daily may interfere with compliance. The objective of the study was to test the efficacy and tolerability of a new 4-day therapy with 4 drugs taken every 12 hours to cure H. pylori infection.
Patients and Methods. Fifty-six consecutive patients with peptic ulcer disease and H. pylori infection were treated with an oral 4-day course with omeprazole (20 mg/12 hours), clarithromycin (500 mg/12 hours), amoxicillin (1 g/12 hours) and tinidazole (500 mg/12 hours). Efficacy of the treatment was determined at least 2 months after therapy either by biopsy (in the case of gastric ulcer) or by ¹³C-urea breath test. A second breath test was performed at least 6 months after therapy.
Results. Two patients were lost to follow-up. Forty-nine of the remaining 54 patients were cured at the first control [intention-to-treat cure rate: 87.5% (CI 95% 75–94%); per protocol cure rate: 90.7% (CI 95% 81–98%)]. Forty-three of these 49 cured patients returned for a second ¹³C urea breath-test at 6–12 months. Two of them were not cured, giving a long-term cure rate of 85.5% per protocol and 73.2% by intention-to-treat. Compliance was good, although 25 patients had mild side effects.
Conclusion. This particular four-day therapy is well tolerated, easy to follow, and achieves an acceptably high cure rate.     

Helicobacter pylori and Non-malignant Diseases

It is well known that Helicobacter pylori infection is associated with many nonmalignant disorders such as gastritis, peptic ulcer, gastroesophageal reflux disease (GERD), gastric polyp, nonsteroidal anti-inflammatory drug (NSAID)/aspirin-induced gastric injury, and functional dyspepsia. In 2008, interesting articles on the association of H. pylori infection with these disorders were presented, some of which intended to reveal the mechanisms of inter-individual differences in response to H. pylori infection, and have demonstrated that genetic differences in host and bacterial factors as well as environmental factors account for these differences. A decline in the occurrence of peptic ulcer related to H. pylori was confirmed. An inverse relationship between H. pylori infection and GERD was also confirmed but the impact of gastric atrophy on the prevention of GERD remained debatable. For NSAID-induced gastric injury, eradication of H. pylori infection has been recommended. During this year, eradication of H. pylori infection was recommended for patients treated with antiplatelet therapy as well as aspirin and NSAID. It was also reported that for patients with functional dyspepsia, eradication of H. pylori offers a modest but significant benefit.     

Gastric Ulcer Formation after the Hanshin-Awaji Earthquake: A Case Study of Helicobacter pylori Infection and Stress-Induced Gastric Ulcers

Background. Both Helicobacter pylori ( H. pylori ) infection and various stresses are known to induce peptic ulcer disease of the upper gastrointestinal tract. However, the pathogenetic relationship between the two factors has not yet been clarified. We conducted a case - control study to examine whether H. pylori infection played a role in the development of gastric ulcer (GU) induced by life-event stresses that were experienced after the Hanshin-Awaji earthquake.
Materials and Methods. Serum samples from patients in the devastated area who developed GUs during the 2 months following the Hanshin-Awaji earthquake and those from GU patients in the same area during the corresponding period of the previous year, and from gender-, age- and institute-matched ulcer-free controls were tested for the presence of the H. pylori IgG antibody.
Results. A significant association between H. pylori infection and the development of GU in uninjured patients was observed in all sets [matched odds ratio (OR) = 3.23, 95% confidence interval: 1.95–5.35]. Moreover, the prevalence of H. pylori infection in patients who developed GUs after the earthquake was not different from that for GU patients in the previous year. In contrast, there was no association between H. pylori infection and the development of GU in the physically injured patients after the earthquake.
Conclusions. H. pylori infection may play an important role in the development of GUs that are induced by emotional life-event stresses.     

胃癌与幽门螺杆菌cagA、hrgA基因相关性的研究

目的:探讨幽门螺杆菌(Hpylori)菌株中cagA和hrgA基因对胃癌的致病作用及其检测的意义。方法:胃癌及消化性溃疡术后切除标本,组织学检查,快速尿素酶法和PCR检测。结果:40例标本经组织学检查24例为胃腺癌,2例为胃黏膜相关淋巴样组织(MALT)瘤,14例为消化性溃疡。经快速尿素酶法检测,胃腺癌中,12例H pylori( ),消化性溃疡中,12例H pylori( )。经PCR检测,胃腺癌中,18例hrgA( ),6例hrgA(-),20例cagA( ),4例cagA(-);消化性溃疡中,6例hrgA( ),8例hrgA(-),12例cagA( ),2例cagA(-)。结论:H pylori感染与胃癌的发生有密切关系。PCR检测较快速尿素酶法准确。检测cagA和hrgA基因对了解Hpylori菌株的致病性、估计疾病程度、了解病变预后及临床治疗都具有重要意义。     

Helicobacter pylori and Nonmalignant Diseases

The incidence of peptic ulcer disease has declined over the last few decades, particularly in Western populations, most likely as a result of the decrease in Helicobacter pylori infection and the widespread use of proton-pump inhibitors (PPI) in patients with dyspepsia. The hospital admission rate for uncomplicated duodenal and gastric ulcers has significantly decreased worldwide. In contrast, admissions for complicated ulcer disease, such as bleeding peptic ulcers and perforation, remained relatively stable. Prophylactic H.?pylori eradication was found to be associated with a reduced risk of both gastric and duodenal ulcers and their complications, including bleeding in chronic users of nonsteroidal anti-inflammatory drugs. The recent Helicobacter Eradication Relief of Dyspeptic Symptoms trial presented important data relating to symptoms and quality of life of H.?pylori-positive patients with functional dyspepsia (FD) and also demonstrated significant benefits from eradication compared with the control group. The new Asian consensus report on FD recommended that dyspepsia accompanied by H.?pylori infection should be considered a separate disease entity from FD and that H.?pylori infection should be eradicated before diagnosing FD. The association of H.?pylori with gastroesophageal reflux disease (GERD) is still controversial. Treatment for H.?pylori does not seem to increase GERD symptoms or reflux esophagitis. However, documented eradication of H.?pylori appears to significantly improve GERD symptoms. Additional long-term intervention studies are needed to provide more information on which to base clinical decisions.     

Helicobacter pylori recurrence in patients with duodenal ulcer: Clinical, endoscopic, histologic, and genotypic aspects. A 10-year Brazilian series

BACKGROUND: Recurrence infection following successful eradication of Helicobacter pylori is usually low, except for countries with high prevalence of H. pylori. The aim of this study was to verify H. pylori recurrence rate in patients with duodenal ulcer after eradication and the possible relationship with environmental factors, histologic pattern of the mucosa and bacterial genotype. MATERIALS AND METHODS: One-hundred and ninety-four patients with an active duodenal ulcer and who were successfully treated for H. pylori infection from 1990 to 1999 were studied. A questionnaire was answered about their living conditions, and a 14C-urea breath test was performed. Patients with a positive breath test underwent an upper endoscopy to investigate for possible ulcer recurrence; gastric biopsy samples were than collected for rapid urease test and for histologic assessment. H. pylori vacA and cagA genotype was determined by polymerase chain reaction in those samples with positive urease test. RESULTS: H. pylori infection was detected in 11 patients (recurrence rate of 5.7%) that were not associated with the type of bacterial virulence. In 10 patients the ulcer was healed and all of them were clinically asymptomatic. In eight, histology showed an intensification of gastritis. All 11 patients had adequate housing and sanitary conditions and no other risk for H. pylori recurrence was identified. CONCLUSIONS: The recurrence rate of H. pylori in Brazil was higher than that reported in developed countries, but lower than usually reported in developing ones. Ulcer relapse rarely occurs even in long-term follow up.     

Helicobacter pylori Reinfection in Brazilian Patients with Peptic Ulcer Disease: A 5-Year Follow-Up

Background:  The Helicobacter pylori reinfection seems to be higher in developing countries, than in developed ones. The aim of the study was to determine the annual recurrence rate of H. pylori , in Brazilian patients with peptic ulcer disease, in a 5-year follow-up.
Methods:  Patients, with peptic ulcer disease diagnosed by upper digestive endoscopy (UDE) and H. pylori infection verified by histological analysis, rapid urease test, polymerase chain reaction, and urea breath test (UBT), were treated for bacterial eradication. The cure of the infection was verified using the same tests, 3 months after. Clinical evaluation and UBT were performed after sixth and ninth month. After 1 year of follow-up, UBT and UDE were repeated. Up to the fifth year, patients were assessed twice a year and an UBT was performed annually. The patients included and all the reinfected were tested for 15 different genes of the H. pylori .
Results:  One hundred and forty-seven patients were followed: 19 for 1 year, eight for 2 years, four for 3 years, five for 4 years, and 98 for 5 years, totaling 557 patients/years. Recurrence did not occur in the first year. In the second year, two patients were reinfected; in the third, four patients; in the fourth, three patients; and in the fifth, one patient. The total of reinfected patients was 10. The annual reinfection rate was 1.8%.
Conclusion:  Brazil presents a low prevalence of H. pylori reinfection, similar to the developed countries.     

Helicobacter pylori: an invading microorganism? A review

In this review we evaluate the pros and cons of Helicobacter pylori invasion of epithelial cells as part of the natural history of H. pylori infection. H. pylori is generally considered an extracellular microorganism. However, a growing body of evidence supports the controversial hypothesis that at least a subset of H. pylori microorganisms has an intracellular (intraepithelial) location. Most significant is the fact that H. pylori invades cultured epithelial cells with invasion frequencies similar to Yersinia enterocolitica and better than Shigella flexneri; furthermore, studies of invasion mechanisms suggest that H. pylori invasion of and survival within epithelial cells is not merely a passive event, but requires active participation of the microorganism. Although many studies of human gastric biopsy specimens have failed to demonstrate any intracellular H. pylori, some studies have revealed a minor fraction of H. pylori inside gastric epithelial cells, with possible linkage to peptic ulceration and epithelial cell damage. In conclusion, these data encourage further research to establish whether intracellular H. pylori does play a role in H. pylori colonization of the human stomach and in peptic ulcer pathogenesis.     

The Ideal Therapy Must Be Def ined in Each Geographical Area: Experience with a Quadruple Therapy in Spain

Background. Multiple therapeutic combinations have been tested to determine the optimal regimen(s) for Helicobacter pylori eradication, leading to very different results depending on the geographical area. Our goal was to evaluate the efficacy of a "quadruple" therapy with omeprazole, tetracycline, bismuth and metronidazole in our area.
Materials and Methods. We investigate 106 consecutive patients with active peptic ulcer disease (duodenal, gastric or both) and Helicobacter pylori infection. One-week therapy with omeprazole 20 mg b.i.d., tetracycline hydrochloride 500 mg q.i.d., colloidal bismuth subcitrate 120 mg q.i.d., and metronidazole 250 mg t.i.d was prescribed. Between the days 30 and 40 after treatment ended follow-up endoscopy was performed. Eradication was defined as both negative urease test and histology. Between days 90 and 360 a ¹³C urea breath test was performed in 100 patients.
Results. Of the 106 patients in the study, 91 had duodenal ulcer, 12 had gastric ulcer, and 3 had both. Side effects were observed in 25% of the cases. Eradication was achieved in 87.7% (93/106; CI 79.9–93.3). Healing was obtained in 95.2% (100/105; CI 89.2–98.4); 97.8% (CI 92.4–99.7) in those eradicated and 75% (CI 42.8–94.5) in non-eradicated ( p < .01).
Conclusions. Quadruple therapy with omeprazole, tetracycline, bismuth subcitrate and metronidazole achieves healing rates up to 95–100%. The 87.7% eradication rate obtained suggests that the regimen we used is a reasonable therapeutic alternative in our area.     

Comparative Treatment of Helicobacter pylori–Positive Duodenal Ulcer Using Pantoprazole at Low and High Doses Versus Omeprazole in Triple Therapy

Background. Helicobacter pylori eradication has become the standard treatment for peptic ulcer disease. H. pylori –eradicating triple therapy with omeprazole plus two antibiotics has been used until recently; however, the efficacy of pantoprazole and antibiotics for H. pylori eradication has not been researched thoroughly until now. The aim of this randomized clinical trial was to verify the efficacy of triple oral therapy comparing the effects of pantoprazole using two different doses versus omeprazole twice daily in H. pylori eradication, in ulcer healing and relapses, and in gastritis improvement.
Materials and Methods. We enrolled 243 patients with H. pylori– positive duodenal ulcer and randomized them into three treatment groups: 84 patients (group Ome40) were assigned to receive omeprazole, 20 mg twice daily, plus amoxicillin, 1 gm twice daily, and clarithromycin, 500 mg twice daily for 10 days; 79 patients (group Pan40) were treated with pantoprazole, 40 mg daily, plus amoxicillin and clarithromycin at the same doses as those of group Ome40; and 80 patients (group Pan80) were treated with pantoprazole, 40 mg twice daily, plus amoxicillin and clarithromycin at the same doses as those of group Ome40.
Results. Ulcer healing was observed in 81 of 84 patients (96.4%) in group Ome40; in 66 of 79 patients (83.5%) in group Pan40; and in 77 of 80 patients (96.2%) in group Pan80. H. pylori was eradicated in 79 of 84 patients (94%) in group Ome40; in 63 of 79 patients (79.7%) in group Pan40; and in 75 of 80 patients (93.7%) in group Pan80.
Conclusions. We found that 10-day triple therapy with amoxicillin, clarithromycin, and either pantoprazole, 80 mg daily, or omeprazole, 40 mg daily, is highly effective in ulcer healing and is very well tolerated, achieving the 90% cure recommended for an ideal first-line anti– H. pylori positive duodenal ulcer treatment regimen.     

Helicobacter pylori stool antigen test in patients with bleeding peptic ulcers

BACKGROUND: Helicobacter pylori has been linked to chronic gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma. Invasive tests are less sensitive than noninvasive tests in diagnosing H. pylori infection in patients with bleeding peptic ulcers. The H. pylori stool antigen test has been useful in diagnosing H. pylori in patients with peptic ulcers before and after eradication of H. pylori. The aim of this study was to evaluate the H. pylori stool antigen test in patients with bleeding peptic ulcers. METHODS: Patients with bleeding and nonbleeding peptic ulcers underwent a rapid urease test, histology, bacterial culture and H. pylori stool antigen test. Positive H. pylori infection was defined as a positive culture or both a positive histology and a positive rapid urease test. Helicobacter pylori stool antigen was assessed with a commercial kit (Diagnostec H. pylori antigen EIA Kit, Hong Kong). RESULTS: Between October 2000 and April 2002, 93 patients with bleeding peptic ulcers (men/women: 78/15, gastric ulcer/duodenal ulcer: 58/35) and 59 patients with nonbleeding peptic ulcers (men/women: 47/12, gastric ulcer/duodenal ulcer: 30/29) were enrolled in this study. Forty-seven (50.5%) patients with bleeding peptic ulcers and 30 (50.8%) patients with nonbleeding peptic ulcers, were found to be infected with H. pylori (p > .1). Helicobacter pylori stool antigen tests were positive in 54 (58.1%) and 30 (50.8%) patients with bleeding peptic ulcers and nonbleeding peptic ulcers, respectively (p > .1). The sensitivity (82% vs. 93%), specificity (68% vs. 93%), positive predictive value (74% vs. 93%), negative predictive value (77% vs. 93%) and diagnostic accuracy (75% vs. 93%) were all lower in patients with bleeding vs. nonbleeding peptic ulcers. The specificity, positive predictive value, and diagnostic accuracy of the H. pylori stool antigen test in patients with bleeding peptic ulcers were significantly lower than those in patients with nonbleeding peptic ulcers (p = .01, p = .02 and p = .003, respectively). CONCLUSION: The H. pylori stool antigen test is not reliable for diagnosing H. pylori infection in patients with bleeding peptic ulcers.