Helicobacter pylori infection in Turkish children: comparison of diagnostic tests, evaluation of eradication rate, and changes in symptoms after eradication

BACKGROUND: Helicobacter pylori infection is most frequently acquired in childhood. After this organism is eradicated, the rate of reinfection is low. Thus, it is very important to diagnose and treat the disease appropriately in childhood, and to be able to assess eradication with certainty. Eradication of H. pylori infection is reported to reduce or eliminate abdominal pain and dyspeptic symptoms in children. PATIENTS AND METHODS: The study involved 102 children who had already been diagnosed with symptomatic H. pylori infection based on gastric histopathological examination, urea breath test, rapid urease test, serology and culture. Each patient's symptoms and family history of gastrointestinal problems were recorded. Using histology as the gold standard for identifying H. pylori infection, we determined the diagnostic sensitivity of each of the other methods. Omeprazole or lansoprazole, amoxicillin and clarithromycin were administered as eradication treatment, and each patient was re-evaluated by urea breath test 8 weeks later. Each child was re-interviewed about symptoms after treatment. These answers and the results of drug sensitivity testing were recorded. Cases of failed eradication were re-treated with a quadruple-drug regimen of tetracycline, metronidazole, bismuth subsalicylate and omeprazole. RESULTS: The most frequent symptom was abdominal pain (89.2%). Fifty-four per cent of the subjects had a family history of dyspeptic symptoms. Sixty-six patients (64.7%) exhibited nodularity in the antral mucosa. The sensitivities of the diagnostic tests in histologically proven cases were as follows: urea breath test 100%, rapid urease test 89.2%, serology 71.9%, and culture 54.9%. Metronidazole had the highest frequency of resistance (36.4%) and the rate of clarithromycin resistance was 18.2%. The eradication rate after first-line therapy was 75.5%, and abdominal pain and dyspeptic symptoms were reduced or completely resolved in 75.7% of the successful-eradication cases. The proportion of failed-eradication cases that responded well to quadruple-drug therapy was 93.8%. CONCLUSION: Symptomatic H. pylori infection in a child should always be treated. The urea breath test is an accurate and reliable way to identify H. pylori-positive patients and to determine the response to treatment. Triple-agent therapy is effective for eradicating H. pylori infection in children and usually helps reduce or eliminate dyspeptic symptoms. The level of H. pylori resistance to metronidazole is high in our region. The significant rate of resistance to clarithromycin (18.1%) may explain the treatment failure observed in this study.     

Immune response to CagA protein is associated with improved platelet count after Helicobacter pylori eradication in patients with idiopathic thrombocytopenic purpura

BACKGROUND: Improvement in platelet counts has been reported after eradication of Helicobacter pylori in patients with idiopathic thrombocytopenic purpura (ITP). We examined the levels of serum markers of gastritis and anti-CagA (cytotoxin-associated gene A) IgG antibody in patients with ITP to investigate whether these factors are associated with the platelet response after H. pylori eradication therapy. MATERIALS AND METHODS: One hundred and sixteen consecutive patients with ITP were assessed for H. pylori infection by (13)C-urea breath test and serum H. pylori antibody test. Patients with H. pylori infection received eradication therapy. Before and after eradication therapy, we evaluated serum levels of gastrin, pepsinogen (PG)-I, and PG-II and the anti-CagA IgG antibody titer. RESULTS: H. pylori infection was found in 67 (58%) of the 116 patients with ITP. Fifty-two infected patients received eradication therapy, which was successful in 44 patients (85%). Twenty-seven patients (62%) showed an increased platelet count and were identified as responders. The duration of ITP was shorter in responders than in nonresponders (p = .017). There was no difference of the levels of gastrin and PGs between responders and nonresponders. Before eradication therapy, the serum anti-CagA antibody titer did not differ significantly between responders and nonresponders. However, reduction in the anti-CagA antibody titer after eradication therapy was significantly greater in responders than in nonresponders (p = .013). CONCLUSIONS: H. pylori eradication therapy improves the platelet count in H. pylori-positive patients with ITP of short duration. Immune response of hosts to CagA protein of H. pylori may play a role in the pathogenesis of ITP.     

Proof of an association between Helicobacter pylori and idiopathic thrombocytopenic purpura in Latin America

BACKGROUND: Association between Helicobacter pylori and idiopathic thrombocytopenic purpura (ITP) has been found in Japan and in some European countries. It has also been shown that eradication of H. pylori can increase platelet counts in patients with ITP. The aims of this study were to determine the prevalence of H. pylori infection in patients with ITP in Colombia, and the effect of bacterial eradication on their platelet counts. MATERIALS AND METHODS: Between December 1998 and April 2006, a total of 32 patients diagnosed with ITP were included in the study. Controls were age and sex matched. RESULTS: H. pylori infection in patients with ITP was significantly higher (p = .00006) than in control individuals (90.6% and 43.8%, respectively), as determined by (13)C-urea breath test. A significant association between H. pylori infection and ITP was found (p < .0003), with an odds ratio (OR) of 13.15 (95%CI: 3.24-53.29). Multivariate analysis for the association between H. pylori and ITP showed an OR of 20.44 (95%CI: 3.88-107.49) for women and 19.28 (95%CI: 2.03-183.42) for individuals over 50 years. All 29 H. pylori-positive patients with ITP received eradication treatment. After a median follow up of 12.2 months, 80.8% had a recovery in platelet counts. CONCLUSIONS: According to these results and others from different countries where H. pylori infection rates are high, patients with ITP should be initially tested for H. pylori status, and if present, infection should be eradicated before initiating a drastic conventional ITP treatment. An algorithm for the study and management of patients with ITP in the post-Helicobacter era is presented.     

Hereditary Angioedema Attacks Resolve Faster and Are Shorter after Early Icatibant Treatment

Background

Attacks of hereditary angioedema (HAE) are unpredictable and, if affecting the upper airway, can be lethal. Icatibant is used for physician- or patient self-administered symptomatic treatment of HAE attacks in adults. Its mode of action includes disruption of the bradykinin pathway via blockade of the bradykinin B₂ receptor. Early treatment is believed to shorten attack duration and prevent severe outcomes; however, evidence to support these benefits is lacking.

Objective

To examine the impact of timing of icatibant administration on the duration and resolution of HAE type I and II attacks.

Methods

The Icatibant Outcome Survey is an international, prospective, observational study for patients treated with icatibant. Data on timings and outcomes of icatibant treatment for HAE attacks were collected between July 2009–February 2012. A mixed-model of repeated measures was performed for 426 attacks in 136 HAE type I and II patients.

Results

Attack duration was significantly shorter in patients treated <1 hour of attack onset compared with those treated ≥1 hour (6.1 hours versus 16.8 hours [p<0.001]). Similar significant effects were observed for <2 hours versus ≥2 hours (7.2 hours versus 20.2 hours [p<0.001]) and <5 hours versus ≥5 hours (8.0 hours versus 23.5 hours [p<0.001]). Treatment within 1 hour of attack onset also significantly reduced time to attack resolution (5.8 hours versus 8.8 hours [p<0.05]). Self-administrators were more likely to treat early and experience shorter attacks than those treated by a healthcare professional.

Conclusion

Early blockade of the bradykinin B₂ receptor with icatibant, particularly within the first hour of attack onset, significantly reduced attack duration and time to attack resolution.     

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 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.     

肝硬化患者幽门螺杆菌感染与血氨的关系

目的 :探讨幽门螺杆菌 (Hp)感染对肝硬化患者血氨浓度的影响。 方法 :35例肝硬化患者及 2 5例消化性溃疡患者分别测定Hp感染情况及空腹血氨浓度 ,对于Hp阳性病人口服质子泵抑制剂三联方案1周后测定空腹血氨。结果 :Hp阳性的肝硬化患者空腹血氨较Hp阴性的肝硬化患者空腹血氨显著升高(P <0 0 1)。根除Hp后 ,肝硬化患者空腹血氨浓度显著下降 (P <0 0 5 )。 结论 :Hp感染可引起肝硬化患者血氨浓度升高 ,对此类患者采用Hp根除治疗 ,可显著降低血氨浓度。抗Hp治疗可能有助于预防及治疗肝硬化患者的高氨血症及由此诱发的肝性脑病及亚临床肝性脑病。     

Reversal of migraine symptoms by Helicobacter pylori eradication therapy in patients with hepatitis-B-related liver cirrhosis

Helicobacter pylori infection might be associated with vascular diseases, such as primary Raynaud phenomenon and coronary heart diseases. The possible mechanism might be due to H. pylori antigens causing intermittent vasospasm of arterioles, which also played roles in the development of liver cirrhosis. Migraine, a functional vascular disease, was observed in many patients with cirrhosis in the clinic. This study aimed to assess the effects of H. pylori eradication on migraine symptoms in patients with hepatitis-B-virus-related cirrhosis. The results clearly showed that the intensity, duration, and frequency of attacks of migraine were significantly reduced in all the patients in whom H. pylori has been eradicated. Thus, the study pushed further insight into the mechanisms of migraine pathogenesis.     

Indications for treatment of Helicobacter pylori infection: a systematic overview.

OBJECTIVE: To determine (a) the advantages and disadvantages of treatment options for the eradication of Helicobacter pylori and (b) whether eradication of H. pylori is indicated in patients with duodenal ulcer, nonucler dyspepsia and gastric cancer. DATA SOURCES: A MEDLINE search for articles published in English between January 1983 and December 1992 with the use of MeSH terms Helicobacter pylori (called Campylobacter pylori before 1990) and duodenal ulcer, gastric cancer, dyspepsia and clinical trial. Six journals and Current Contents were searched manually for pertinent articles published in that time frame. STUDY SELECTION: For duodenal ulcer the search was limited to studies involving adults, studies of H. pylori eradication and randomized clinical trials comparing anti-H. pylori therapy with conventional ulcer treatment. For nonulcer dyspepsia with H. pylori infection the search was limited to placebo-controlled randomized clinical trials. DATA EXTRACTION: The quality of each study was rated independently on a four-point scale by each author. For the studies of duodenal ulcer the outcome measures assessed were acute ulcer healing and time required for healing, H. pylori eradication and ulcer relapse. For the studies of nonulcer dyspepsia with H. pylori infection the authors assessed H. pylori eradication, the symptoms used as outcome measures and whether validated outcome measures had been used. DATA SYNTHESIS: Eight trials involving duodenal ulcer met our inclusion criteria: five were considered high quality, two were of reasonable quality, and one was weak. Six trials involving nonulcer dyspepsia met the criteria, but all were rated as weak. Among treatment options triple therapy with a bismuth compound, metronidazole and either amoxicillin or tetracycline achieved the highest eradication rates (73% to 94%). Results concerning treatment indications for duodenal ulcer were consistent among all of the studies: when anti-H. pylori therapy was added to conventional ulcer treatment acute ulcers healed more rapidly. Ulcer relapse rates were dramatically reduced after H. pylori eradication. All of the studies involving nonulcer dyspepsia assessed clearance rather than eradication of H. pylori. No study used validated outcome measures. A consistent decrease in symptom severity was no more prevalent in patients in whom the organism had been cleared than in those taking a placebo. Of the studies concerning gastric cancer none investigated the effect of eradication of H. pylori on subsequent risk of gastric cancer. CONCLUSIONS: There is sufficient evidence to support the use of anti-H. pylori therapy in patients with duodenal ulcers who have H. pylori infection, triple therapy achieving the best results. There is no current evidence to support such therapy for nonulcer dyspepsia in patients with H. pylori infection. Much more attention must be paid to the design of nonulcer dyspepsia studies. Also, studies are needed to determine whether H. pylori eradication in patients with gastritis will prevent gastric cancer.     

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.     

Eradication of Helicobacter pylori infection equally improves chronic urticaria with positive and negative autologous serum skin test

BACKGROUND: The aim of the study was to examine effects of Helicobacter pylori eradication on chronic idiopathic urticaria (CU) with and without positive aulogous serum skin test (ASST). METHODS: Seventy-eight patients with CU were checked for the positivity ASST and H. pylori urea (13)C-urea breath test ((13)C-UBT). Twenty-one patients were with both positive ASST and positive (13)C-UBT (group A), and 24 patients were with negative ASST and positive (13)C-UBT (group B). All patients with positive (13)C-UBT received a 14-day, open treatment with amoxicillin 1 g b.i.d., clarithromycin 500 mg b.i.d., and omeprazole 20 mg b.i.d. H. pylori eradication was assessed by a second (13)C-UBT after 8 weeks. In control group, 33 patients with CU were included. The effect of H. pylori eradication on CU was evaluated by urticaria activity score (UAS), measured at study entry and at 8 and 16 weeks. RESULTS: At week 8, baseline UAS reduced from 4.7 +/- 1.1 to 2.4 +/- 1.4 (p = .027) in group A and from 4.3 +/- 1.5 to 2.3 +/- 1.2 (p = .008) in group B, without statistically significant difference between the two groups. In control group and in six patients with H. pylori eradication failure, no changes of UAS were noted. CONCLUSION: Eradication of H. pylori infection by triple therapy significantly and equally reduces UAS in CU patients with positive and negative ASST.     

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.     

Curing Helicobacter pylori infection in patients with duodenal ulcer does not provoke gastroesophageal reflux disease

Background. It has been suggested that the incidence of gastroesophageal reflux disease (GERD) increases after successful eradication of Helicobacter pylori infection. We present data on development of GERD from a controlled study of H. pylori eradication in 165 duodenal ulcer patients.
Methods. Patients (mean age, 55 years; 102 men; current smokers; n = 74) were randomly assigned 2 : 1 to receive omeprazole, 40 mg twice daily, in combination with either amoxicillin, 750 mg twice daily, or placebo. Endoscopy and dyspeptic symptoms, including heartburn, were assessed at inclusion and at 6, 12, and 24 months after treatment. In addition, symptoms were assessed at 18 months. Patients with erosive esophagitis or reflux symptoms requiring treatment at inclusion were not included in the study.
Results. Fifty-one of 145 (35%) evaluable patients developed heartburn, and 13 of 145 (9%) developed esophagitis during follow-up. The life-table analysis of the cumulated risk of developing heartburn showed that patients whose H. pylori infection was eradicated had a significantly lower risk for developing heartburn than those with persistent H. pylori infection. The groups did not show any difference in cumulative risk of developing esophagitis.
Conclusion. Our data show that successful eradication of H. pylori infection does not increase the incidence of GERD in duodenal ulcer patients.     

The influence of cholecystokinin on gastric myoelectrical activity in duodenal ulcer following Helicobacter pylori eradication--an electrogastrographic study.

Cholecystokinin (CCK) plays an important role in the regulation of postprandial gastric motor activity which was found to be abnormal in duodenal ulcer patients. This study was designed to compare the influence of CCK on gastric myoelectrical function in duodenal ulcer patients and healthy controls. Fifteen patients with active duodenal ulcer and Helicobacterpylori (H. pylori) infection and 15 healthy controls were included into this study. Electrogastrography (EGG) was performed before and 4 weeks after the eradication of H. pylori in ulcer patients and in healthy controls. We compared EGG parameters in the fasting and postprandial period and during intravenous infusion of caerulein, an analog of CCK with or without addition of loxiglumide, a specific CCK-1 receptor antagonist. The amplitude of fasting EGG in duodenal ulcer patients was similar to that in control subjects and was not affected by H. pylori eradication. In contrast, the amplitude of postprandial EGG was markedly increased in duodenal ulcer patients when compared to that in healthy controls and it was significantly reduced following the eradication of H. pylori. The blockade of CCK-1 receptors with loxiglumide in healthy controls or H. pylori eradicated ulcer patients significantly enhanced postprandial EGG amplitude almost to the level observed in the infected duodenal ulcer patients, but failed to affect this amplitude in ulcer patients. Exogenous caerulein, an analog of CCK, failed to affect EGG amplitude in duodenal ulcer patients with H. pylori infection, but it reduced significantly EGG amplitude in these patients after H. pylori eradication and in control subjects. This inhibitory effect of caerulein in H. pylori negative ulcer patients and healthy controls was abolished by the addition of loxiglumide. Ulcer patients showed significant dysrhythmia with tachygastria up to 20% of the recording time both under basal conditions and postprandially and H. pylori eradication was followed by a significant decrease in tachygastria to about 5%, the value being similar to that in healthy controls. We conclude that the amplitude and frequency of gastric myoelectrical activity are enhanced in duodenal ulcer patients and impaired in response to CCK but these changes can be normalized by successful H. pylori eradication.     

Assessing the therapeutic use of Lafoensia pacari St. Hil. extract (mangava-brava) in the eradication of Helicobacter pylori: double-blind randomized clinical trial

BACKGROUND: The eradication of Helicobacter pylori is easily achieved by combining antisecretory agents and antibiotics; however, the cost of these associations is very high for the population of Third World countries, where the prevalence of the infection is even higher and leads to markedly reduced treatment effectiveness. We tested a plant (Lafoensia pacari) that is used in the central region of Brazil. According to previous studies, this plant has high concentrations of ellagic acid, which presents gastric antisecretory and antibacterial actions. MATERIAL AND METHODS: One hundred dyspeptic, urease-positive patients were randomized to receive 500 mg of methanolic extract of L. pacari (n = 55) or placebo (n = 45), for 14 days, in a double-blind clinical trial. The main variables assessed were the eradication of H. pylori 8 weeks after the intervention and complete symptom relief at the end of the treatment. RESULTS: The examinations (urease and histology) showed persistence of H. pylori in 100% of participants. Complete symptom relief was experienced by 42.5% of patients (95% CI: 29.4-55.8) in the intervention group and by 21% (95% CI: 8.8-33.1) in the control group, p = .020. The side-effects were minimal and similar in both groups. CONCLUSIONS: The extract of L. pacari as a single agent was not effective to eradicate H. pylori. However, it was well tolerated and many participants reported relief of symptoms. Future studies may test the agent using larger doses and longer periods, in monotherapy or in combination with antibiotics.     

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.     

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.     

Helicobacter pylori and Non-malignant Diseases

In 2007 Helicobacter pylori research continued to deal with some controversies raised in the last decade. The main problems remain unsolved: peptic ulcer disease negative for H. pylori , synergism of H. pylori infection and aspirin and other nonsteroidal anti-inflammatory drugs or cyclooxygenase 2 specific inhibitors, the role of H. pylori eradication in uninvestigated and nonulcer dyspepsia, and the possible protective effect of H. pylori infection against gastroesophageal reflux disease and its complications such as Barrett's esophagus and adenocarcinoma. The incidence and prevalence of peptic ulcer disease as well as ulcer-related mortality are continuing to decline all over the world. The increasing consumption of anti-inflammatory and antisecretory drugs was not found to change the trend over the last period and therefore H. pylori was considered the key factor in causing ulcer-related mortality. Some progress has been achieved in understanding H. pylori -induced immunological processes, and attack mechanisms, as well as specific pathogenesis in uremic and cirrhotic patients. There is still a lot to learn about the bacterium and host factors related to H. pylori infection and its complications.     

Double-dose, new-generation proton pump inhibitors do not improve Helicobacter pylori eradication rate

BACKGROUND: Up to present, omeprazole plus two antibiotics are used for Helicobacter pylori eradication therapy . Few studies have compared double-dose new-generation, proton pump inhibitors (PPI) with omeprazole. Therefore, we conducted a randomized, prospective study to evaluate differences in H. pylori eradication rates by PPI type. MATERIAL AND METHODS: Between January 2006 and December 2006, 576 consecutive patients with proven H. pylori infection were enrolled prospectively. Four different PPIs [omeprazole 20 mg b.i.d. (old generation), or pantoprazole 40 mg b.i.d., rabeprazole 20 mg b.i.d., or esomeprazole 40 mg b.i.d. (new generation)] were added to clarithromycin (500 mg b.i.d.) and amoxicillin (1 g b.i.d.) for 1 week. RESULTS: By intention-to-treat analysis, no difference was found between the eradication rates of these four PPIs: 64.9% (omeprazole, n = 148), 69.3% (pantoprazole, n = 140), 69.3% (rabeprazole, n = 140), and 72.9% (esomoprazole, n = 148). When eradication rates were analyzed according to whether patients had an ulcer or not on a per-protocol basis, no difference was found between the eradication rates of the four PPIs. However, side-effects were more common in the esomeprazole-based triple therapy group than in the other groups (p < .05). CONCLUSIONS: No convincing evidence was obtained that double-dose new-generation PPIs have better H. pylori eradication rates and tolerability than omeprazole.     

High rate of Helicobacter pylori reinfection in children and adolescents

AIMS: Primary Helicobacter pylori infection occurs predominantly in childhood. The aims of this study were to establish the rate of H. pylori reinfection after successful eradication in children and adolescents and to determine the risk factors associated with reinfection. PATIENTS AND METHODS: This retrospective study involved 45 children (20 girls, 25 boys) who met the following criteria: eradication of H. pylori confirmed at least 4 weeks after the completion of therapy, and the search for reinfection at least one year after control of eradication of H. pylori. Demographic data, socioeconomic status and living conditions were recorded. RESULTS: Forty-five children aged 1.2-17.6 years (median, 10.9 years) at the time of H. pylori treatment were reviewed 1 to 9 years after H. pylori eradication. Eight children (18%) had been reinfected (5.4% to 6% per patient-year). Six of 25 (24%) children older than 10 years at the time of diagnosis became reinfected. None of the studied risk factors was associated with reinfection. However, having a sibling younger than 5 years was found in four of seven (57%) reinfected children versus five of 24 (21%) nonreinfected children (p = .08). CONCLUSION: Children become reinfected more frequently than adults. Adolescents become reinfected, whereas acquisition of primary H. pylori infection occurs predominantly in early childhood. Close contact with young children, especially siblings, younger than 5 years could be a more important risk factor than the age of the patient at the time of treatment for the high rate of reinfection in childhood.