Once-daily gentamicin therapy for experimental Escherichia coli meningitis

BACKGROUND: Eradication of Helicobacter pylori by antibiotics in combination with gastric acid inhibition can result in overgrowth of non-H. pylori bacterial flora. This may confound the histological detection of H. pylori at eradication control if non-specific staining methods are used. OBJECTIVE AND METHODS: In 18 patients treated with amoxycillin (2 weeks) and omeprazole (6 weeks), endoscopically obtained gastric juice was cultured and two biopsies of corpus, antrum and duodenum were taken before and after eradication therapy (with gastric acid inhibition still going on) for culture and for histology to assess the intragastric bacterial flora. By histology, modified Giemsa (MG) and an H. pylori-specific immunohistochemical stain (IMM) were evaluated. RESULTS: Median pH of gastric juice was 1.5 (n = 18) before and 7 (n = 17) after eradication therapy, when patients were still on omeprazole. After therapy, culture showed a significant decrease (P < 0.05) in mean amount of H. pylori in corpus, antral and duodenal biopsies and a significant increase of non-H. pylori flora (P < 0.05) in gastric juice, corpus, antral and duodenal mucosa. With culture as a standard, 16 and 4 biopsy specimens were scored falsely positive for H. pylori by MG and IMM, respectively, and H. pylori was not detected in 23 and 13 biopsy specimens when culture was H. pylori-positive. CONCLUSION: Because of the possible presence of non-H. pylori flora after eradication therapy, the use of IMM is recommended in this situation for the histological detection of H. pylori, especially in those patients with ongoing gastric acid inhibitory therapy.     

Helicobacter pylori does not migrate from the antrum to the corpus in response to omeprazole

BACKGROUND: Omeprazole is known to have an effect on Helicobacter pylori in vivo. One opinion is that H. pylori "migrates" from the antrum to the corpus in response to omeprazole therapy. METHODS: To determine whether H. pylori migrates in response to omeprazole, we assessed the presence of H. pylori in the antrum and corpus in duodenal ulcer patients receiving omeprazole for 4 wk. Culture and histological examination of antral biopsies (Genta stain) were performed before patients received omeprazole, at the end of therapy, and 4-6 wk later. The end points were presence or absence of H. pylori and the number of H. pylori colonies per biopsy. RESULTS: Seventy-two patients had H. pylori in both the antrum and corpus at entry and 4-6 wk after ending therapy. Three general patterns were prevalent at the end of omeprazole therapy: antrum- and corpus-positive (54%), antrum-negative and corpus-positive (24%), both antrum- and corpus-negative (21%), and one patient had antrum-positive with corpus-negative (1%). Evaluation of the number of colonies per biopsy in those who remained H. pylori-positive in both the antrum and corpus throughout showed that the number of H. pylori decreased in both the antrum and corpus during therapy (507 +/- 60 vs. 225 +/- 51, p < 0.01 and 415 +/- 58 vs. 290 +/- 46 0.1) for antrum and corpus, respectively, and tended to return to pre-therapy levels 4-6 wk later. The number of H. pylori in the corpus also decreased in the antrum-negative and corpus-positive group during therapy with omeprazole (433 +/- 87 vs. 185 +/- 61, p < 0.05). In most of the patients studied, the number of H. pylori in the corpus was less posttreatment than it was pretreatment. The decrease in H. pylori load was also reflected in the development of false-negative urea breath tests. CONCLUSIONS: Omeprazole is detrimental to H. pylori in both the antrum and the corpus; migration from the antrum to the corpus in response to omeprazole is a myth.     

Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.     

The importance of increasing the number of gastric biopsies in the diagnosis of Helicobacter pylori

BACKGROUND/AIMS: The role of Helicobacter pylori in various gastroduodenal diseases is universally accepted. In this study, we aimed to determine the proper number and sites of the gastric biopsies in order to achieve the highest diagnostic yield through the use of a urease test and histopathology. We also compared the histological findings encountered in patients who had Helicobacter pylori (H. pylori) colonization. METHODOLOGY: Fifty patients referred for upper gastrointestinal endoscopy for dyspeptic complaints were included in the study. Our mapping protocol included 2 biopsies from antrum and 2 biopsies from corpus. We obtained 2 biopsies from each biopsy site for urease test and histopathological assessment. Golden standard positivity for the presence of H. pylori colonization was defined as concomitantly positive urease test and histologically detected bacteria found at the same biopsy site. RESULTS: Forty-three patients had H. pylori colonization. Colonization rates of H. pylori, sensitivities of urease testing, and histopathology in 4 biopsy sites were not statistically different. Sensitivity of urease testing was 81.4% for 1 biopsy and 100% for 4 cumulative biopsies. Sensitivities of histological assessment were 93% and 100% for 1 and 4 biopsies, respectively. CONCLUSIONS: Results of this study suggest that 2 biopsies for urease testing and 1 biopsy for histopathology obtained from the antrum or corpus of the stomach were sufficient to obtain the highest statistically significant diagnostic sensitivity.     

Oral health status of an industrial population in Romania

BACKGROUND: We investigated whether addition of bismuth subcitrate (BSC, 4 x 120 mg) to a two week therapy scheme of omeprazole (OME, 2 x 40 mg)/amoxicillin (AMO, 4 x 500 mg) increases Helicobacter pylori eradication. MATERIALS AND METHODS: Patients with dyspepsia underwent upper endoscopy. H. pylori positive patients were randomized to treatment A (OME/AMO, 83 patients) or treatment B (OME/AMO/BSC, 84 patients). RESULTS: In 65 patients of group A (78%) H. pylori was eradicated as determined from the histological assessment (Sydney classification) of antrum and corpus biopsies. In comparison, in 68 patients of group B (81%) H. pylori was eradicated (p = NS between groups). H. pylori eradication in both groups was associated similarly with a decrease of inflammation and activity whereas atrophy and intestinal metaplasia were not affected. A positive association was revealed between the decrease of H. pylori score and the decrease of both inflammation and activity scores for antrum as well as corpus biopsies. CONCLUSIONS: Addition of BSC to OME/AMO does not increase H. pylori eradication in patients with dyspepsia. Eradication of H. pylori is associated with disappearance of epithelial damage (inflammation and activity) in antral and corpus mucosa.     

Management of febrile infants under 3 years old

BACKGROUND: Rapid ureas tests (RUTs) provide a simple, sensitive method of detecting Helicobacter pylori infection. OBJECTIVES: Our aim, therefore, was to determine whether the yield of detecting H. pylori infection by RUT varied depending on the site of gastric biopsy. MATERIALS AND METHODS: Gastric biopsies were obtained from 50 patients for RUT by use of hpfast (GI Supply, Camp Hill, PA). Biopsies were taken from the prepyloric greater curve antrum, from the gastric angle, and from the greater curve in mid-corpus. One biopsy specimen was placed in the RUT gel, and the biopsy from the adjacent mucosa was placed in formalin for subsequent histological evaluation by using the Genta stain. RUTs were examined and scored at intervals of 5, 10, 15, 30, and 45 minutes and after 1, 2, 4, and 24 hours. RESULTS: Fifty patients were entered in the rest (150 RUTs), 32 having H. pylori infection. There were no false-positive RUTs (specificity, 100%). The gastric angle site was positive in 100%. The prepyloric site was positive in 87%, and the corpus site was positive in 84.4% (p < .052 for angle or prepyloric antrum versus corpus). The most common pattern was for all to be positive (74%). The median time to positivity was similar with angle and prepyloric sites (37.5 and 60 minutes, respectively, p = not significant) and shorter than the corpus biopsy (180 minutes); (p < .05 for angle or prepyloric antrum versus corpus). CONCLUSION: The maximum probability for detecting H. pylori infection using a RUT is to obtain a biopsy from the gastric angle. To prevent missing a positive result when intestinal metaplasia is present, we recommend that (at a minimum) biopsies be taken from both the angle and the corpus.     

Evaluation of a new urease reagent strip for detection of Helicobacter pylori in gastric biopsy specimens

OBJECTIVES: Determine sensitivity and specificity of a new urease reagent strip (URS) test for detection of Helicobacter pylori in gastric biopsy specimens. METHODS: Six paired biopsy specimens were obtained from the greater curvature of the distal antrum, the lesser curvature near the incisura, and the corpus along the greater curvature during 66 procedures on 59 patients with endoscopic findings of gastric antral mucosal erythema or erosions, or gastric or duodenal ulcers. One biopsy from each site was tested with the URS. The second was evaluated with histology. A final antral biopsy was evaluated with a urea/gel test. RESULTS: Twenty-eight of the 66 cases were histologically positive, with H. pylori observed in at least one of the three biopsy sites. The URS test correctly identified all 28. Of 193 individual biopsy specimens, 78 were positive for H. pylori. The URS correctly identified 77. Sensitivity was 0.99, specificity 0.95, positive predictive value 0.93, negative predictive value 0.99, and kappa 0.92. Average time to positive was 20 min. Twenty-seven antral biopsies were histologically positive for H. pylori. The URS test correctly identified all 27, whereas the urea/gel test correctly identified 21. For antral sites, URS sensitivity was 1.00 and specificity 0.95 versus urea/gel test sensitivity of 0.75 and specificity of 1.00. CONCLUSIONS: In this sample, the URS test is as accurate as histology in diagnosing H. pylori infections, and it provides results in less time and at a lower cost than histology.     

Free and total bupivacaine plasma concentrations after continuous epidural anaesthesia in infants and children

OBJECTIVES: The aim of this study was to elucidate the prevalence of Helicobacter pylori and its distribution in order to clarify the frequency of H. pylori infection and the most appropriate site of endoscopic biopsy for studies of H. pylori infection associated with different gastric diseases. DESIGNS AND METHODS: Swiss role mucosal strips from 275 resected stomachs, which included the greater curvature, anterior wall and lesser curvature of the antrum, incisura and corpus, were stained with haematoxylin-eosin and H. pylori antibody. RESULTS: The prevalence of H. pylori infection was 97% in duodenal ulcers, 98% in gastric ulcers, 98% in intestinal-type carcinomas and 99% in diffuse-type carcinomas. H. pylori was present at a rate of 100% in any site in cases of duodenal ulcer, but was diffusely distributed in the antrum and patchily distributed in the corpus. The detection rate of H. pylori was 50-100% in gastric ulcers, 30-100% in intestinal-type adenocarcinomas and 63-100% in diffuse-type adenocarcinomas depending on the site of the stomach examined. CONCLUSIONS: The prevalence of H. pylori infection was very high in peptic ulcers of the duodenum and stomach and gastric carcinomas of Japanese patients. Biopsy specimens for evaluation of H. pylori infection should be taken routinely from both the greater curvature of the antrum and corpus. Immunohistochemical staining should be used to assay for H. pylori when few organisms are present or eradication therapy has been used.     

Helicobacter pylori infections in children in the tropical zone. Endoscopic and histological aspects

AIMS: To assess the endoscopic and histological aspects of Helicobacter pylori (H. pylori) infection in children in a prospective study. PATIENTS AND METHODS: One hundred and four children (6 months-15 years old), with digestive symptoms admitted to the Pediatric Department of the National Hospital of Ouagadougou between February Ist and October 31 1996, underwent upper digestive endoscopy with fundic and antral biopsies for histological and bacteriological analysis. RESULTS: Endoscopy was normal in 80 cases (77%). No lesion was specific of H. pylori infection. Nodular gastritis was observed in 3% of the cases only. Duodenal ulcers were seen in 3 children (3%). 83% of the children had chronic antral gastritis, associates with H. pylori in 95% of the cases. The lesions were follicular gastritis (45%), mild atrophic gastritis (38.5%) and lymphocytic gastritis (1%). Follicular gastritis was more pronounced in the antrum than in the fundus. CONCLUSION: The high prevalence of early H. pylori infection and chronic gastritis in children contrasts with the rarity of gastric cancer in black Africa. Protective factors or peculiar strains should be searched for.     

Carbohydrate-deficient transferrin: marker of actual alcohol consumption or chronic alcohol misuse?

In this randomized, multicenter trial, we evaluated the effectiveness and side effect profile of a modified omeprazole-based triple therapy to cure Helicobacter pylori infection. The control group consisted of patients treated with standard dual therapy comprising omeprazole and amoxicillin. One hundred and fifty-seven H. pylori infected patients with duodenal ulcers were randomly assigned to receive either a combination of omeprazole 10 mg, clarithromycin 250 mg and metronidazole 400 mg (OCM) given three times daily for 10 days (n = 81), or a combination of omeprazole 20 mg and amoxicillin 1 g (OA) given twice daily for 14 days (n = 76). Prior to treatment and after 2 and 6 weeks, gastric biopsies from the antrum and corpus were obtained for histology and H. pylori culture. H. pylori infection was cured in 97.4% after OCM and in 65.8% after OA in the per-protocol analysis (p < 0.001) (intention-to-treat analysis: 93.4% and 63.2%, respectively). H. pylori was successfully cultured in 122 patients (77%). The overall rate of metronidazole resistance was 19.7% (24/122), no primary resistance to clarithromycin or amoxicillin was found. In the OCM group, all patients infected with metronidazole-sensitive H. pylori strains (n = 51) and those infected with strains of unknown susceptibility to metronidazole (n = 14) were cured (100%), while 77% (10/13) of those harboring metronidazole-resistant strains were cured of the infection (p = 0.36). Side effects leading to premature termination of treatment occurred in 2.5% of the patients in the OCM group and in 1.4% of the OA group. We conclude that combined treatment with omeprazole, clarithromycin and a higher dose of metronidazole is highly effective in curing H. pylori infection, and that this regimen remains very effective in the presence of metronidazole-resistant strains.     

Helicobacter pylori and gastroduodenal lesions in 547 symptomatic young adults

OBJECTIVES: Helicobacter pylori (H. pylori) is involved in the pathogenesis of gastric inflammatory disorders. Both antral chronic gastritis and H. pylori infection prevalence increase with age. The aim of the study was to assess the prevalence of H. pylori infection in young adults and to study the relationship between endoscopical and histological features and H. pylori infection. METHODS: The study concerned 547 young patients (age: 18-25 years), undergoing endoscopy for upper gastrointestinal symptoms. The severity and the activity of chronic gastritis was graded by histological examination of antral biopsies. The diagnosis of H. pylori infection was based on histology and culture or urease test. RESULTS: Fifty-three percent of the patients had a normal endoscopy; 44 ulcers were found: 34 duodenal ulcers and 10 gastric ulcers. H. pylori infection was detected in 34% of cases. The prevalence of H. pylori infection was 29.8% in non-ulcer patients, 50% in gastric ulcers and 91% in duodenal ulcers (P < 0.01). Duodenal ulcer, aspect of antral mosaic mucosa and nodular gastritis, were closely related to the presence of H. pylori. There was a significant relationship between H. pylori infection and both the severity (P < 0.01) and the activity (P < 0.01) of the antral chronic gastritis. The prevalence of follicular gastritis was 22% : it was present in 60% of H. pylori positive patients and 2.4% of H. pylori negative patients. H. pylori infection was more frequent in patients from Africa than in Europeans (P < 0.01). There was no significant association between H. pylori infection and different types of diets, settlements (rural vs urban) or symptoms. CONCLUSION: These results show that in the young population studied, duodenal ulcer, nodular gastritis, antral mosaic mucosa, active chronic gastric and follicular gastritis are closely related to H. pylori infection. They suggest that in the subgroup of non ulcer symptomatic patients, H. pylori prevalence is higher than in the general population.     

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

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

Antibody-secreting cells in the stomachs of symptomatic and asymptomatic Helicobacter pylori-infected subjects

In this study we analyzed whether infection with Helicobacter pylori gives rise to specific B-cell responses against a number of putative virulence factors of H. pylori, e.g., urease, flagellin, and different bacterial surface antigens, locally in the gastric mucosa. This was studied in antrum and corpus biopsies collected from 11 H. pylori-infected patients with duodenal ulcers, 11 asymptomatic H. pylori carriers, and 13 noninfected, healthy controls. Mononuclear cells were isolated from the biopsies and assayed for frequencies of total and H. pylori-specific antibody-secreting cells (ASCs) by means of the enzyme-linked immunospot technique. The H. pylori-infected subjects had remarkably higher frequencies of total immunoglobulin A (IgA)- and IgM-secreting cells than the noninfected subjects, while the frequencies of IgG-secreting cells were virtually the same in the different groups. In addition, most of the infected subjects had IgA ASCs reacting with H. pylori membrane proteins, flagellin, and urease, while none of the noninfected subjects had any detectable H. pylori-reactive ASCs. Furthermore, half of the infected subjects also had ASCs reacting with a Helicobacter-specific 26-kDa protein, while only a few of them had ASCs reacting with neutrophil-activating protein, the neuraminyllactose-binding hemagglutinin HpaA, or lipopolysaccharides purified from different H. pylori strains. The frequencies of H. pylori-specific ASCs in the antrum and corpus were almost identical, and no differences in either antigen specificity or magnitude of the B-cell response in the stomach could be detected between the ulcer patients and the asymptomatic H. pylori carriers. This study demonstrates that H. pylori infection induces strong antibody responses in the human gastric mucosa, both in asymptomatic carriers and in duodenal ulcer patients. However, the outcome of infection could not be explained by differences in the local B-cell response to any of the antigens used in this study.     

Somatostatin receptor imaging of olfactory neuroblastoma

BACKGROUND: Cure of H. pylori infection in peptic ulcer patients significantly reduces the risk of ulcer recurrence. Since data on the rate of H. pylori reinfection in patients undergoing successful anti-H. pylori therapy are sparse, this study was conducted with the aim of determining the H. pylori reinfection rate in peptic ulcer patients receiving antibacterial treatment to heal their ulcer and cure H. pylori infection. METHODS: A total of 217 patients with H. pylori-associated duodenal or gastric ulcer were followed up after treatment with various antibacterial regimens resulting in histologically documented cure of H. pylori infection. Endoscopic and histological examinations were performed 4 weeks after completion of treatment and after 1, 2 and 5 years, or whenever dyspeptic symptoms occurred. To assess the H. pylori status two antral and two corpus biopsies were obtained for histological examination. RESULTS: Out of 217 patients with initially cured H. pylori infection 175 were available for endoscopic follow-up. At the time of analysis, 44 patients were re-examined after 1 year, 113 patients after 2 years and 18 patients after 5 years, giving a total of 360 patient years of follow-up. The mean duration of follow-up was 24.7 months. H. pylori reinfection was confirmed histologically in eight patients, three of whom becoming H. pylori-positive again within the first year of follow-up. Six of the eight patients with H. pylori reinfection also suffered an ulcer relapse. Eight cases of reinfection in 360 patient years represents an overall reinfection rate of 2.2%. Within the first 2 years of follow-up the reinfection rate was 0.8% per year. CONCLUSION: Our data suggest that H. pylori reinfection is rare in peptic ulcer patients receiving successful anti-H. pylori therapy. H. pylori reinfection frequently coincides with ulcer recurrence. Cure of H. pylori infection results in cure of peptic ulcer disease, provided H. pylori reinfection does not occur.     

High-dose proton pump inhibitor plus amoxycillin for the treatment or retreatment of Helicobacter pylori infection

BACKGROUND: The combination of 120 mg of omeprazole (40 mg t.d.s.) and amoxycillin has been reported to be effective for treating H. pylori infections. METHODS: Normal volunteers with H. pylori infection received high-dose omeprazole (40 mg t.d.s.) or lansoprazole (60 mg t.d.s.) plus amoxycillin 750 mg t.d.s. for 14 days. The studies were open label and not randomized as those receiving omeprazole plus amoxycillin had previously failed lower dose omeprazole (20 mg b.d.) plus amoxycillin therapy more than 6 months previously. Those receiving lansoprazole plus amoxycillin had not been previously treated. Four to 6 weeks after ending antimicrobial therapy, H. pylori status was determined by Genta stain of gastric mucosal biopsies. RESULTS: Forty-three volunteers entered the study and 41 completed it. The overall success with high-dose proton pump inhibitor plus amoxycillin was 34.9%. For the individual regimens the per-protocol results were 48% (95% CI = 28-69%) with lansoprazole and 12.5% (95% CI = 2-38%) with omeprazole. Compliance was > 95% for both regimens. Side-effects were experienced by four lansoprazole and three omeprazole subjects, and caused two omeprazole subjects to withdraw. Cure rates were similar among different races and ethnic groups, between men and women, and between smokers and non-smokers. The level of the pre-treatment urea breath test also did not predict outcome. CONCLUSION: High-dose proton pump inhibitor plus amoxycillin combinations for treatment of H. pylori infection yielded unacceptable results, as the 95% confidence intervals did not include an 80% cure rate. These combinations do not yield consistent results worldwide and cannot be recommended as primary therapy.     

Comparison of diagnostic methods for detection of Helicobacter pylori

Of two hundred Ethiopian patients with dyspepsia, multiple biopsies were taken from the antrum of the stomach. Helicobacter pylori was cultured from 85% of duodenal ulcer and in 75% of chronic antral gastritis patients. The overall Helicobacter pylori positivity was 70%. The sensitivity, specificity, positive and negative predictive values of the tests as compared to culture were as follows, respectively: direct urease test 100%/87%/95%/100%, direct gram stain 60%/98%/99%/51%, histological gram stain 66%/97%/98%/56%, Giemsa stain 100%/97%/99%/100% and Gimenez stain 100%/87%/95%/100%. It is concluded that gram staining of direct tissue smear or histology is an insensitive method in the diagnosis of Helicobacter pylori. All the other tests, are shown to be valid. Urease test is an excellent test for provision of presumptive diagnosis of Helicobacter pylori while awaiting confirmation either by culture of histology.     

Safety and efficacy of rabeprazole in combination with four antibiotic regimens for the eradication of Helicobacter pylori in patients with chronic gastritis with or without peptic ulceration

OBJECTIVES: Rabeprazole is a new fast acting proton pump inhibitor that has recently been proven to be effective in the treatment of peptic ulceration and reflux esophagitis. The aim of this study was to evaluate rabeprazole in combination with antibiotics for the eradication of Helicobacter pylori (H. pylori) in patients with chronic active gastritis with or without peptic ulcer disease. METHODS: Seventy-five H. pylori-infected patients were randomized in a double-blind fashion to receive a 7-day treatment regimen consisting of: RAC, RAM, RCM, or RC (R=rabeprazole 20 mg b.d., A=amoxycillin 1 g b.d., C=clarithromycin 500 mg b.d., M=metronidazole 400 mg b.d.). Randomized patients were H. pylori-positive by gastric biopsy urease test, histology and 13C urea breath test (13C-UBT). H. pylori eradication was assessed by 13C-UBT, 4 and 8 wk after finishing treatment. Endoscopy with histology and culture for antibiotic sensitivity testing was performed pretreatment and if treatment failed. RESULTS: On an intention-to-treat analysis, treatment success was: RCM 100%, RAC 95%, RAM 90%, and RC 63%. The most common side effects were loose stools, headache, and taste disturbance, but there were no serious adverse events related to the study medication. The two patients failing RAM treatment had metronidazole-resistant strains before and after treatment. None of the pretreatment H. pylori isolates from six patients failing RC were clarithromycin resistant, but three of five successfully cultured posttreatment had developed clarithromycin resistance. CONCLUSION: Rabeprazole-based triple therapy with two antibiotics for 1 wk is safe and effective in eradicating H. pylori. Dual therapy with clarithromycin is less successful, and the majority of treatment failures develop clarithromycin resistance.     

Factors influencing Helicobacter pylori eradication with 2 week combination therapy of lansoprazole and amoxycillin: intragastric distribution of colonization and gastric mucosal atrophy

In Japan, gastric ulcers are often accompanied by marked gastric mucosal atrophy. We evaluated the dual therapy of double-dose lansoprazole and amoxycillin for Helicobacter pylori eradication in Japanese ulcer patients and investigated the effects of intragastric distribution of H. pylori colonization and gastric mucosal atrophy on eradication with this combination therapy. Seventy-six H. pylori-positive ulcer patients received lansoprazole (30 mg) plus amoxycillin (500 mg) twice daily for 2 weeks (LA-60 group), lansoprazole (30 mg once daily) plus amoxycillin (500 mg twice daily) for 2 weeks (LA-30 group) or lansoprazole (30 mg once daily) for 6 or 8 weeks (LPZ group). Infection was evaluated by light microscopy, culture and biopsy urease tests. Helicobacter pylori colonization was classified as localized to the corpus (localized type) or involving the antrum and corpus (whole type). Fundic mucosal atrophy was graded according to endoscopic and histological features. Eradication was achieved in 67.6% in the LA-60 group, 31.6% in the LA-30 group, and 0% in the LPZ group, and moderate or severe histological gastritis was improved in the LA-60 group. Eradication was better in localized-type colonization (92%) than whole-type (56%), and better with fundic mucosal atrophy (84%) than without, but poor in both whole-type colonization and scanty mucosal atrophy (47%). The LA-60 therapy achieves better eradication in Japanese ulcer patients with localized H. pylori colonization and/or gastric mucosal atrophy, which are likely to be important predictors for the successful eradication with dual therapy.     

The effect of H. pylori in perforation of duodenal ulcer

BACKGROUND/AIMS: H. pylori has been described as an opportunistic pathogen attracted by changes in the gastric mucosa caused by inflammation and ulceration. However, the role of H. pylori infection in the perforation of duodenal ulcers has not yet been clearly determined. The aim of this study was to assess the prevalence of H. pylori infection in patients undergoing laparotomy for repair of a perforated duodenal ulcer. METHODOLOGY: Patients who underwent surgery for a perforated duodenal ulcer in our Surgical Unit between January 1994 and July 1996 were included in this study. The study population consisted of eighteen patients with a mean age of 32.7 (21-48) years. All of the patients were male. Patients with chronic duodenal ulcer perforation and with no contraindications for definitive surgery, such as peritonitis, shock (blood pressure <90 mm Hg), age >60 years, or more than a 12-hour elapse from the time of perforation, were treated by bilateral truncal vagotomy and Weinberg pyloroplasty. The ulcer was excised with the pyloric ring. The cut was then extented by about 2 cm on both the gastric and duodenal sides. Two biopsies were taken from the antral mucosa by endoscopic biopsy forceps. The defect was closed transversely. The ulcer specimen and the antral biopsies were fixed separately in 10% formalin solution and sent to the department of Histopathology. The specimens were stained with Hematoxylin-Eosin and examined for H. pylori . Sections of the ulcer specimen were especially investigated for the presence of H. pylori through all layers of the ulcer. RESULTS: H. pylori was found in the antral biopsies of 16 patients (88.8%). In seven of the ulcer specimens (38.8%), H. pylori was present in the mucosa and also extended through the wall of the ulcer. H. pylori was positive in the antral biopsies of all patients with H. pylori present in the ulcer wall. CONCLUSIONS: In our study, H. pylori was present at a high ratio in the antral biopsies of patients with duodenal ulcer perforation. The presence of H. pylori throughout the ulcer wall to a considerable extent emphasizes the fact that eradication of H. pylori is important in the treatment of perforated duodenal ulcer.     

Prognostic factors and scoring systems in myelodysplastic syndromes

The treatment of peptic ulcers has been revolutionized by the discovery that Helicobacter pylori (H. pylori) bacteria is a causative agent for ulcer formation. However, when patients present with dyspepsia or epigastric discomfort, more than 80% of patients will not have ulcer disease and empiric treatment of H. pylori is not recommended for these patients. Eradication of H. pylori has not been demonstrated to improve the symptoms of non-ulcer dyspepsia compared with non-ulcer dyspepsia patients treated with placebo. Therefore, we recommend that patients should first be evaluated for peptic ulcers with endoscopy or upper gastrointestinal series before the diagnosis and treatment of H. pylori. Generally, the treatment of H. pylori should be limited to patients with peptic ulcers, mucosal-associated lymphoid tissue lymphomas, and gastric cancers. Most diagnostic tests for H. pylori, including quantitative IgG antibody, urea breath tests, rapid urease tests (CLO), tests of gastric mucosal biopsies, and staining of gastric mucosal biopsies, have equivalent diagnostic characteristics. Therefore, the choice of diagnostic test for H. pylori should be based on cost, ease of use, and lack of complications. Multiple antibiotic regimens are available for the treatment of H. pylori. Triple antibiotic therapy is the least expensive but has the highest rate of side effects and the least compliance. Combining a proton pump inhibitor with clarithromycin and another antibiotic will eradicate H. pylori with fewer side effects and better compliance but this is the most expensive antibiotic regimen.