Study on the relationship between Helicobacter pylori in the dental plaque and the occurrence of dental caries or oral hygiene index

Background: The aims of our study were to determine the presence of Helicobacter pylori DNA in the dental plaque of Chinese children aged 3–6 years by nested polymerase chain reaction (PCR) and to investigate the relationship between this infection and the occurrence of dental caries or oral hygiene index.
Methods: Two hundred and fourteen children from a kindergarten in Guangzhou City of China were evaluated. The children's plaques were assessed by plaque indices of Quigley–Hein. Dental plaque was analyzed using nested PCR for two sets of primers directed to the 860-bp fragment of H. pylori genomic DNA, which have been reported to be highly sensitive and specific by other researchers.
Results: H. pylori was detected in dental plaque samples from 126 children, and 70 children with dental caries carried H. pylori in dental plaque. Of these children without infection, only 36 of 88 suffered dental caries. Besides, the average dental plaque index of 126 H. pylori -positive children was higher than that of 88 children without infection. In the present study, there was a significant correlation between H. pylori infection and dental caries or dental hygiene.
Conclusion: The oral cavity may be a reservoir for H. pylori infection in children. H. pylori in dental plaque may play a role in the occurrence of dental caries, and poor oral hygiene may represent a risk factor for H. pylori in the oral cavity.     

Effect of Helicobacter pylori eradication on peptic ulcer disease complicated with outlet obstruction

Background. At present, the prevalence of Helicobacter pylori ( H. pylori ) in complicated peptic ulcer and the effect of H. pylori eradication on complicated peptic ulcer have not been fully established. In this study, we report the prevalence of H. pylori in peptic ulcer patients complicated with gastric outlet obstruction, effectiveness of oral eradication therapy on these patients, and their long-term follow up.
Patients and Methods. Ten consecutive patients presenting with clinically and endoscopically significant obstructed peptic ulcers were included in this study. During each endoscopy, seven gastric biopsy specimens were obtained and analyzed for H. pylori colonization.
Results. The antral mucosal biopsy specimens were positive for H. pylori in nine patients. H. pylori infection was eradicated and complete ulcer healing was observed in all patients. The mean follow-up period was 14 (7–24) months. One patient had duodenal perforation and underwent surgical intervention following medical treatment, despite the eradication of H. pylori. Ulcer recurrence was noted in two (22.2%) of nine patients, and in one of them the recurrent ulcer was complicated with obstruction (11.1%). The mean time to ulcer recurrence was 17 months (range, 10–24 months). The biopsies and CLOtests were H. pylori negative at the time of ulcer or erosion recurrence in two patients.
Conclusion. We suggest that H. pylori eradication may improve the resolution in obstructive ulcer cases with colonization.     

Role of Helicobacter pylori Infection in the Treatment and Outcome of Chronic Urticaria

Introduction:  Chronic urticaria is thought to have numerous causative factors including a large variety of infectious conditions, food intake, and drugs. The impact of Helicobacter pylori infection has been studied with ambiguous results. The aim of this study was to investigate the course of chronic urticaria in H. pylori -positive patients undergoing eradication compared to H. pylori -negative urticaria patients.
Patients and Methods:  We included 74 urticaria patients with positive H. pylori breath test and 74 age- and sex-matched H. pylori -negative controls. All urticaria patients underwent an extensive diagnostic work-up to search for trigger foci. H. pylori -infected patients were submitted to eradication therapy. Mean follow-up time was 58 months.
Results:  Neither the prevalence of H. pylori nor the eradication therapy had an influence on the clinical course of chronic urticaria. In 81.1% of H. pylori -infected patients at least one additional infectious focus was found. Nevertheless, it could be shown that individuals that described any kind of symptom relief presented with higher serum IgE levels at diagnosis (198.1 vs 115.7 kU/L, p = .027) but this effect was independent of H. pylori infection.
Conclusions:  In conclusion there is no evidence that eradication of H. pylori improves the outcome in patients with chronic urticaria. The high rate of spontaneous remission and the coexisistance of multiple foci will always obscure the evaluation of any specific antimicrobial therapy.     

Effect of Helicobacter pylori Eradication on Incidence of Gastric Cancer in Human and Animal Models: Underlying Biochemical and Molecular Events

Background:  Gastric cancer remains one of the most common cancers worldwide. A strong association exists between Helicobacter pylori infection and the risk of developing noncardia gastric cancer. H. pylori eradication by antibiotic treatment is regarded as a primary chemoprevention strategy to reduce gastric cancer incidence.
Aim:  To analyze the efficacy of H. pylori eradication in preventing gastric cancer in human and animal models, and to discuss whether biochemical, genetic, and epigenetic changes associated with H. pylori infection are reversible after curing the infection.
Results:  Several intervention trials have indicated that in some patients, H. pylori eradication leads to regression and prevents the progression of precancerous lesions. The eradication therapy reduces gastric cancer incidence in patients without any precancerous lesions at the baseline and is most effective before the development of atrophic gastritis. A few recent intervention studies in Japan have demonstrated significant prophylactic effects of eradication therapy on the development of gastric cancer, suggesting the use of eradication therapy in high-risk populations as a gastric cancer reduction strategy. However, gastric cancer may still develop despite successful eradication therapy. Studies in animal models have confirmed the use of eradication therapy at an early point of infection to prevent gastric cancer development.
Conclusion:  H. pylori eradication may not completely abolish the risk of gastric cancer. However, eradication therapy may be used in high-risk populations to reduce gastric cancer incidence. It can reverse many biochemical, genetic, and epigenetic changes that H. pylori infection induces in the stomach.     

Mixed Infection with cagA-Positive and cagA-Negative Strains of Helicobacter pylori

Background Helicobacter pylori infection has been implicated strongly in the pathogenesis of gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric lymphoma, but the reasons for these widely different clinical outcomes are unknown. The aim of this study was to determine whether these differences could be due in part to mixed infection in the same individual, with bacteria having differences in pathogenic factors associated with ulcers.
Materials and Methods. The cagA gene of H. pylori was used to test for mixed infection because it is present in only some strains, and its presence has been associated with ulcers. Polymerase chain reaction (PCR) assays for the cagA gene were applied to H. pylori culture isolates and endoscopic gastric aspirates. Individual bacterial clones were tested for genetic similarity by random primer amplification and restriction endonuclease digestion of urease gene PCR products.
Results. The majority of H. pylori -positive patients had strongly cagA -positive culture isolates and endoscopic samples (62.5% and 69.6%, respectively). However, many of these patients had evidence of mixed infection with cagA negative and cagA positive strais in cultures isolates and endoscopic samples (25% and 17.4%, respectively). Mixed infection was found to be due to genetically unrelated strains in two patients in whom genetic analysis was performed.
Conclusion. Mixed infection with differences in substrain pathogenic factors might occur in H. pylori infection and might contribute to differences in clinical outcome.     

Guidelines for the Management of Helicobacter pylori Infection in Japan: 2009 Revised Edition

Background:  Over the past few years, the profile of Helicobacter pylori infection has changed in Japan. In particular, the relationship between H. pylori and gastric cancer has been demonstrated more clearly. Accordingly, the committee of the Japanese Society for Helicobacter Research has revised the guidelines for diagnosis and treatment of H. pylori infection in Japan.
Materials and Methods:  Four meetings of guidelines preparation committee were held from July 2007 to December 2008. In the new guidelines, recommendations for treatment have been classified into five grades according to the Minds Recommendation Grades, while the level of evidence has been classified into six grades. The Japanese national health insurance system was not taken into consideration when preparing these guidelines.
Results:  Helicobacter pylori eradication therapy achieved a Grade A recommendation, being useful for the treatment of gastric or duodenal ulcer, for the treatment and prevention of H. pylori -associated diseases such as gastric cancer, and for inhibiting the spread of H. pylori infection. Levels of evidence were determined for each disease associated with H. pylori infection. For the diagnosis of H. pylori infection, measurement of H. pylori antigen in the feces was added to the tests not requiring biopsy. One week of proton-pump inhibitor-based triple therapy (including amoxicillin and metronidazole) was recommended as second-line therapy after failure of first-line eradication therapy.
Conclusion:  The revised Japanese guidelines for H. pylori are based on scientific evidence and avoid the administrative restraints that applied to earlier versions .     

Randomized Placebo-Controlled Trial of Helicobacter pylori Eradication for Iron-Deficiency Anemia in Preadolescent Children and Adolescents

Background. A few cases relating H. pylori infection to iron-deficiency anemia have been described recently. We investigated the role of H. pylori infection in iron-deficiency anemia in preadolescent children and adolescents.
Patients and Methods. We conducted a double-blind, placebo-controlled therapeutic trial in 43 subjects (mean age, 15.4 years) with iron-deficiency anemia. Endoscopy was performed, and biopsy specimens were examined by urease test and histological analysis. Twenty-two of 25 H. pylori –positive patients were assigned randomly to three groups. Group A patients were given oral ferrous sulfate and a 2-week course of bismuth subcitrate, amoxicillin, and metronidazole. Group B patients were given placebo for iron and a 2-week course of triple therapy. Group C patients were given oral ferrous sulfate and a 2-week course of placebo. Iron status was reassessed 4 weeks and 8 weeks after the 2-week regimen ended.
Results. Of the 43 subjects with iron-deficiency anemia, 25 (58.1%) had H. pylori in the antrum. Group A and B subjects, who received eradication therapy, showed a significant increase in hemoglobin level as compared with group C subjects at 8 weeks after therapy ( p = .0086).
Conclusions. Treatment of H. pylori infection was associated with more rapid response to oral iron therapy as compared with the use of iron therapy alone. Such treatment also led to enhanced iron absorption even in those subjects who did not receive oral iron therapy.     

Helicobacter pylori Infection, Gastritis, and the Temperature of Choice for Hot Drinks

Background. The role of the temperature of the diet as a potential etiological factor for gastritis or peptic ulcer disease has been postulated since the beginning of the century. Animal studies have demonstrated damage to gastric mucosa caused by hot water at 60 to 80°C. In the pre- Helicobacter pylori era it was reported that the majority of ulcer patients preferred hot drinks. It also was reported that the temperature of choice for drinks increased with severity of histological grade of gastritis. We evaluated the association between the preferred temperature of hot drinks and the presence of H. pylori infection.
Methods. We tested the temperature of choice for hot drinking liquids among 12 H. pylori -negative and 43 H. pylori -positive volunteers. We also compared the effect of H. pylori therapy on hot drink temperature preference and, in 32 individuals, whether there was a relation between temperature and the degree of gastric atrophy.
Results. There was no difference in the preferred temperature for hot drinks between those volunteers with and without H. pylori infection (63.4°± 6°C compared to 61.3°± 7°C, respectively) (mean ± 1 SD, p =.3) There was no change in preferred temperature after successful therapy of the H. pylori infection compared to unsuccessful H. pylori therapy, nor was there a correlation between the preferred temperature and the presence, absence, or degree of gastric atrophy ( r ² < 0.001).
Conclusion. The temperature of preference for hot drinks was not influenced by H. pylori infection or by the presence of atrophic gastritis.     

PCR detection of Helicobacter pylori in string-absorbed gastric juice

Molecular methods for detection of Helicobacter pylori infection have been shown to be highly sensitive in gastric biopsies and cultures. The objective of this work was to compare PCR detection of H. pylori DNA in string-absorbed gastric juice and in gastric biopsies. The study was performed in 47 dyspeptic adult patients undergoing endoscopy, and infection was detected by amplification of a segment of H. pylori ureA gene. Of the 29 patients positive in biopsy analysis, 23 (79%) were also positive in the gastric string. PCR analysis of gastric strings is a sensitive and safe procedure to detect H. pylori when endoscopy is not indicated, and may be of great clinical and epidemiological usefulness in determining effectiveness of eradication therapies, typing virulence genes and detecting antibiotic resistance mutations.     

Impact of Quadruple Regimen of Clarithromycin Added to Metronidazole-Containing Triple Therapy Against Helicobacter pylori Infection Following Clarithromycin-Containing Triple-Therapy Failure

Background: The establishment of an optimal second-line regimen for Helicobacter pylori infection is required. Although quadruple therapy should overcome resistance to either clarithromycin or metronidazole, the effects of a quadruple regimen in second-line therapy are unknown. This study aims to evaluate the efficacy of triple therapy composed of proton pump inhibitor/amoxicillin plus metronidazole with the combined additive effects of clarithromycin as a second-line quadruple therapy against H. pylori infection.
Materials and Methods: Participants were 104 patients in whom first-line therapy containing proton pump inhibitor-amoxicillin-clarithromycin failed. Before starting second-line therapy, patients underwent endoscopy to obtain H. pylori strain for antibiotic susceptibility tests. Patients were randomized to receive rabeprazole (10 mg), amoxicillin (750 mg), and metronidazole (250 mg), either with clarithromycin (200 mg; RAMC group) or without (RAM group); all treatments were administered twice daily for 7 days. H. pylori eradication was confirmed by ¹³C-urea breath tests performed 2 to 3 months post-therapy.
Results: As shown by intention-to-treat/per-protocol analyses, the cure rates for H. pylori infection were 88.5%/93.9% and 82.7%/84.3% for the RAMC and RAM groups. Although the study probably had an insufficient power to show a significant difference between the cure rates of the two regimens, the eradication rates showed a clear trend in favor of the RAMC group. There were no severe side-effects in any group.
Conclusions: In Japan, the RAMC regimen is thought to be a promising alternative strategy for second-line eradication of H. pylori infection.     

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 Helicobacter pylori infection on the expression of DNA mismatch repair protein

BACKGROUND: Helicobacer pylori infection is a major gastric cancer risk factor. Deficient DNA mismatch repair (MMR) caused by H. pylori may underlie microsatellite instability (MSI) in the gastric epithelium and may represent a major mechanism of mutation accumulation in the gastric mucosa during the early stages of H. pylori-associated gastric carcinogenesis. In this study, we examined the expression of DNA MMR protein (hMLH1 and hMSH2) in patients with chronic H. pylori infection before and after eradication of the infection. MATERIALS AND METHODS: Gastric tissue samples were collected from 60 patients with H. pylori gastritis and peptic ulcer disease before and after eradication of the infection. The DNA MMR protein expression (hMLH1 and hMSH2) was determined by immunohistochemical staining in 60 patients before and after H. pylori eradication. The percentage of epithelial cell nuclei and intensity of staining were then compared in gastric biopsies before and after eradication. RESULTS: The percentage of hMLH1 (76.60 +/- 20.27, 84.82 +/- 12.73, p=.01) and hMSH2 (82.36 +/- 12.86, 88.11 +/- 9.27, p<.05) positive epithelial cells significantly increased in 53 patients who became H. pylori-negative after eradication therapy. However, the intensity of hMLH1 and hMSH2 staining was not significantly different. In those 7 patients, who did not respond to the eradication therapy and were still H. pylori-positive, the percent positivity and intensity of hMLH1 and hMSH2 staining did not change. CONCLUSIONS: The expression of DNA MMR proteins increased in the gastric mucosa after H. pylori eradication, indicating that H. pylori gastritis may be associated with a reduced DNA MMR system during infection. The effect of H. pylori infection on MMR protein expression appears to be at least partially reversible after H. pylori eradication. These data suggest that H. pylori gastritis might lead to a deficiency of DNA MMR in gastric epithelium that may increase the risk of mutation accumulation in the gastric mucosa cells during chronic H. pylori infection.     

Reactive Nitrogen Species Mediate DNA Damage in Helicobacter pylori-Infected Gastric Mucosa

Background:  Reactive oxygen species (ROS) and reactive nitrogen species (RNS) can play an important role in cellular injury and carcinogenesis of gastric epithelial cells infected with Helicobacter pylori . 8-OH-deoxy guanosine (8-OHdG) and 8-nitroguanine (8-NG) are markers for ROS- and RNS-mediated DNA oxidation, respectively. In this study, RNS-mediated DNA damage in gastric mucosa was observed directly using a newly developed antibody to 8-NG to clarify how H. pylori infection causes nitrative DNA damage to gastric epithelial cells.
Methods:  Immunohistochemistry with anti-8-OHdG and anti-8-NG antibodies was performed on gastric tissue samples from 45 patients (25 men and 20 women) with H. pylori -positive gastritis and 19 patients (11 men and 8 women) exhibiting successful H. pylori eradication. Histologic factors for gastric mucosal inflammation were graded according to the guidelines of the Updated Sydney system.
Results:  In corpus mucosa, 8-OHdG and 8-NG production were significantly associated with the degree of glandular atrophy, infiltration of chronic inflammatory cells and intestinal metaplasia in the glandular epithelial cells. Successful H. pylori eradication resulted in a significant reduction of chronic inflammatory cell infiltration and neutrophilic activity. Mean 8-OHdG production was lower after H. pylori eradication in both corpus and antral mucosa ( p  = .022 and .049, respectively). However, the reduction in 8-NG exhibited was more pronounced than the reduction of 8-OhdG ( p  = .004 and .007, respectively).
Conclusions:  Helicobacter pylori infection can induce inflammatory cells infiltration, which evokes DNA damage of gastric epithelial cells through ROS and RNS production. 8-NG might be a more sensitive biomarker than 8-OHdG for H. pylori -induced DNA damage in gastric mucosa.     

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.     

Comparative study of Helicobacter pylori eradication rates of twice-versus four-times-daily amoxicillin administered with proton pump inhibitor and clarithromycin: a randomized study

Background: Proton pump inhibitor (PPI)-containing triple therapy with clarithromycin and amoxicillin is now a standard regimen for Helicobacter pylori eradication in Korea. Amoxicillin has time-dependent bactericidal activity against H. pylori ; we therefore assumed a dosing schedule of amoxicillin would affect the eradication rate of H. pylori . The purpose of this study was to evaluate and compare the efficacy of different amoxicillin dosing schedules for the eradication of H. pylori .
Materials and Methods: One hundred and eighty-six patients with H. pylori infection were eligible for this study. Patients were randomly assigned to one of two regimens: amoxicillin 1000 mg with clarithromycin 500 mg and omeprazole 20 mg twice daily for 2 weeks (BID group, n = 93), or amoxicillin 500 mg four times daily with clarithromycin 500 mg and omeprazole 20 mg twice daily for 2 weeks (QID group, n = 93). The success of H. pylori eradication was evaluated 4–5 weeks after completing treatment.
Results: Overall eradication rate was 90.3%, and eradication rates were 91.4% in the BID group and 89.2% in the QID group ( p  = 0.62). Compliances was 95.7% in the BID group and 93.5% in the QID group ( p  = 0.516); this was the only factor that significantly affected H. pylori eradication in this study. Side effects in both groups were generally mild.
Conclusions: Amoxicillin regimens with PPI and clarithromycin are found to be equally effective and safe in both the BID and QID groups for H. pylori eradication. Therefore, considering patient's comfort, we recommend a twice daily amoxicillin regimen.     

Pantoprazole suppresses Helicobacter pylori without affecting cure

Background. Short-term, low-dose triple regimens composed of proton-pump inhibitors (PPI) and two antibiotics are the current gold standard therapy for cure of Helicobacter pylori infection. To date, the effect of PPI pretreatment on eradication outcome is not known. The aim of this study was to evaluate the influence of pretreatment with pantoprazole on the efficacy of an ensuing triple therapy.
Methods. In this open, randomized, monocenter, parallel group comparison, 107 patients with duodenal ulcer or functional dyspepsia were assigned to receive one of the following treatment regimens: a 7-day triple therapy with pantoprazole, 40 mg bid; clarithromycin, 250 mg bid; and metronidazole, 400 mg bid, which was either preceded or followed by a 7-day therapy with pantoprazole, 40 mg (P-PCM or PCM-P). Assessment of H. pylori status was performed by a biopsy urease test and ¹³C urea breath test at the initial visit and ¹³C urea breath test at all follow-up visits.
Results. The 7-day pantoprazole pretreatment resulted in a significant decline of the δ values of the ¹³C urea breath test. H. pylori infection was cured in 47 of 52 intention-to-treat patients of the P-PCM group (90%; 95% confidence interval, 79–97%) and in 46 of 53 of the PCM-P group (87%; 95% confidence interval, 75–95%).
Conclusions. Pretreatment with pantoprazole suppresses H. pylori but does not impair the efficacy of a consecutive short-term, low-dose triple therapy.     

Controlled trial of the effect of cinnamon extract on Helicobacter pylori

Background. Helicobacter pylori has been associated with the pathogenesis of antral gastritis, duodenal ulcer, and gastric lymphoma. Eradication of H. pylori has been shown to reverse or prevent relapse of these diseases. Antimicrobials employed in the eradication of H. pylori are not without adverse effects. Newer treatment modalities, therefore, are required. In vitro studies have shown the effectiveness of cinnamon extract against H. pylori and its urease. In this pilot study, we tested the activity of an alcoholic extract of cinnamon in a group of patients infected with H. pylori.
Materials and Methods. Fifteen patients (11 women, 4 men) aged 16 to 79 years were given 40 mg of an alcoholic cinnamon extract twice daily for 4 weeks; eight patients aged 35 to 79 (7 women, 1 man) received placebo. The amount of H. pylori colonization was measured by the ¹³C urea breath test before and after therapy.
Results. The mean urea breath test counts in the study and control groups before and after therapy were 22.1 and 23.9 versus 24.4 and 25.9, respectively. The cinnamon extract was well tolerated, and side effects were minimal.
Conclusions. We concluded that cinnamon extract, at a concentration of 80 mg /day as a single agent, is ineffective in eradicating H. pylori. Combination of cinnamon with other antimicrobials, or cinnamon extract at a higher concentration, however, may prove useful.     

Miconazole Gel Increases the Cure Rate of Helicobacter pylori Infection When Added to Lansoprazole and Amoxicillin in a Randomized Trial

Background. Miconazole is an antimycotic agent with bacteriocidal activity against Helicobacter pylori in vitro. Its role in the clinical eradication of H. pylori has not been studied. The objective of this study was to investigate the efficacy and side effect profile of miconazole for the treatment of H. pylori.
Materials and Methods. We studied 65 patients with gastritis or peptic ulcer disease in whom H. pylori infection was confirmed by a rapid urease test and microbiologic assessment. In vitro miconazole sensitivity was assessed for the H. pylori strains isolated from the enrolled patients. All patients were randomized to receive either dual therapy consisting of lansoprazole 30 mg daily and amoxicillin 500 mg three times a day for 14 days (LA, n = 33) or triple therapy using the LA regimen plus miconazole gel 100 mg three times a day for 14 days (LAM, n = 32). At least 8 weeks after the treatment, successful therapy was validated by the histological and microbiologic assessment. Adverse effects and drug adherence were monitored by direct questioning.
Results. The minimum inhibitory concentrations of miconazole ranged from 3.13 to 6.25 mg/L. H. pylori was eradicated in 16 of 33 patients (48%, 95% CI = 31% to 67%) after LA therapy, and 24 of 32 patients (75%, 95% CI = 59% to 91%) after LAM therapy ( p < .03). There was no significant difference in the occurrence of adverse events between the two groups.
Conclusion. The addition of miconazole gel to the LA regimen significantly improved the cure rate of H. pylori without an increase in adverse effects.     

Comparison of seven and fourteen days of lansoprazole, clarithromycin, and amoxicillin therapy for eradication of Helicobacter pylori: a report from India

Background. In developed countries, a 1-week regimen of combined proton pump inhibitors and two antibiotics is considered adequate for Helicobacter pylori eradication. However, there is a paucity of reports from developing countries on treatment duration of less than 14 days. We compared efficacy of 7 and 14 days of lansoprazole (L), clarithromycin (C), and amoxicillin (A) combinations for eradication of H. pylori.
Patients and Methods. Forty-six consecutive patients who presented with upper gastrointestinal symptoms and tested positive for H. pylori infection were included in the study. In every patient, after performance of upper gastrointestinal endoscopy, antral biopsies were obtained. H. pylori infection was diagnosed by positive rapid urease test and identification of organisms on antral histology. Patients were randomly selected to receive lansoprazole, 30 mg once daily, plus clarithromycin, 250 mg twice daily, plus amoxicillin, 500 mg three times daily for 2 weeks ( group 1; n = 24; age , 36 ± 12 years ; 18 men ) or 1 week ( group 2; n = 22; age , 45 ± 15 years ; 12 men ). One month after completion of treatment, repeat upper gastrointestinal endoscopy was performed. H. pylori eradication was defined as absence of organism on histopathological examination of both antrum and body of stomach and negative rapid urease test.
Results. Eradication rate was higher in group 1 (23 of 24; 96%) as compared to group 2 (12 of 22; 54%; p < .05). One patient in group 1 had diarrhea, and one patient in group two had skin rash and itching.
Conclusions. Fourteen-day therapy with lansoprazole, clarithromycin, and amoxicillin is highly effective in eradication of H. pylori. Reducing duration of therapy to 7 days significantly lowers eradication rates.     

Evidence that the degree and duration of acid suppression are related to Helicobacter pylori eradication by triple therapy

BACKGROUNDS AND AIMS: Eradication rates of Helicobacter pylori by a proton pump inhibitor-based triple therapy depend on CYP2C19 genotype status. We investigated whether gastric acid inhibition during an eradication therapy would influence the eradication rates attained by the triple therapy. METHODS: Thirty-two patients with H. pylori infection underwent the first-line triple therapy with lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 400 mg b.i.d. for 1 week. In all 32 patients, the 24-hour intragastric pH monitoring was performed on day 6 during the treatment period. RESULTS: The intention-to-treat-based eradication rate by the first-line therapy was 75.0% (24/32, 95%CI: 56.60-88.54%). In patients with successful eradication, the median 24-hour pH was 6.4 (range; 5.0-7.6), which was significantly higher than that in patients without eradication [5.2 (2.2-6.2), p = .0131]. The median percentage time of pH < 4.0 during 24-hour postdose in patients with eradication [0.5% (0.0-31.6%)] was significantly shorter than that in patients without eradication [26.7% (6.0-72.2%), p = .0017]. These parameters for acid inhibition significantly differed among the different CYP2C19 genotype groups. When the percentage time of pH < 4.0 and 24-hour pH were attained < 10% and > 6.0, respectively, during the eradication treatment, the majority of patients could eradicate H. pylori infection, irrespective of the bacterial susceptibility to clarithromycin. CONCLUSIONS: The sustained intragastric pH > 4.0 for a longer postdose time appears to be required for a successful eradication of H. pylori with lansoprazole and acid-labile antibiotics.