Eradication of Helicobacter pyloriin clinical situations

Abstract. Helicobacter pylori is prevalent worldwide, especially in developing countries, and is associated with several upper gastrointestinal diseases. Since it is present in over 90% of duodenal ulcer patients, empirical eradication in these patients is often recommended. In gastric ulcer patients, eradication is indicated only after the infection is confirmed. Testing for H. pylori infection should be carried out in patients with peptic ulcer hemorrhage, because eradication has been shown to reduce recurrent bleeding. Both H. pylori and NSAIDs are risk factors for peptic ulceration, and it is reasonable to screen for and eradicate H. pylori infection in peptic ulcer patients taking NSAIDs. H. pylori is a group I carcinogen for gastric adenocarcinoma, and should be eradicated for the primary prevention of this cancer. Eradication of this organism has been reported to result in regression of early low-grade mucosa-associated lymphoid tissue lymphoma. The role of H. pylori infection in the causation of gastroesophageal reflux and non-ulcer dyspepsia is not clearly established. Several tests are available for the diagnosis of H. pylori infection. These include invasive tests, such as histology, culture and urease test, and non-invasive tests, such as serology, urea breath test and stool antigen test. The choice of test is determined by clinical indication, pretest probability of infection, as well as the availability, cost, sensitivity and specificity of the test. H. pylori eradication therapy using proton pump inhibitor with clarithromycin and amoxycillin for 7 days has a success rate of 85–90%. Improved living standard and sanitation are vital in the control of H. pylori transmission and infection. Future development may include the use of vaccines against H. pylori, and therapies specifically targeting cagA strains of the bacteria.     

Helicobacter pylori & gastric disease

Since the discovery of Helicobacter pylori(H. pylori), causal linkage between H. pylori infection and some of gastric disease has been generally accepted from the results of many studies. Indeed the usefulness of H. pylori eradication therapy for acute gastritis, peptic ulcer, gastric polyp and MALT lymphoma etc. has been reported. In the low grade MALT lymphoma, the regression rate by this therapy is about 70%. On the other hand, we should pay the caution to several adverse effects, such as drug resistance and GERD, of H. pylori eradication therapy. However, based on the several results of comparative studies between antibiotic therapy and the other one, the antibiotic therapy for peptic ulcer is only covered by national health insurance at present. The reversibility of gastric precancerous conditions such as mucosal atrophy, intestinal metaplasia and dysplasia by antibiotic therapy has been studied, but its significance is not clear yet. In animal experiment, H. pylori infection induced gastric adenocarcinoma in Mongolian Gerbils. However, this phenomenon is limited to this kind of animal only. To proof the causal link between H. pylori infection and genesis of gastric cancer in human being, clinical intervention trials are ongoing in the world. If these trials can clarify it, the H. pylori eradication therapy will be established as preventive measure for gastric carcinogenesis.     

Interleukin-6 polymorphism and Helicobacter pylori infection in Brazilian adult patients with chronic gastritis

Helicobacter pylori is recognised as the most common cause of chronic active gastritis and this bacterium is also an important pathogenic factor in peptic ulcer disease. The biological factors that influence clinical outcome in H. pylori infection have been extensively studied. In addition to immunological factors in the host, bacterial virulence determinants in H. pylori strains are likely to play a crucial role in gastric cancer development. Singlenucleotide polymorphisms at the 5' flanking region of the interleukin (IL)-6 gene promoter (G or C at -174 base) have been identified and individuals with the G allele at position -174 have been shown to produce higher levels of IL-6 than those with the C/C genotype. The mucosal levels of IL-6 were reported to be increased in H. pylori-associated gastritis. The present study was conducted to examine any relationship between inflammatory cytokine polymorphisms and the inflammatory process in mucosa infected by H. pylori. In our study we did not find any association between the C and G alleles in adult patients with chronic gastritis and inflammatory process in gastric mucosa.     

Helicobacter pylori and associated gastroduodenal diseases. Review article

Helicobacter pylori is a microaerophilic, Gram-negative, spiral rod, the role of which in different gastric diseases has been investigated worldwide since the beginning of the 1980s. H. pylori has been shown to be the causative agent in active chronic gastritis, and it is regularly found in patients endoscopied for duodenal ulcer. The bacterium is also frequently isolated from persons with gastric ulcer, gastric carcinoma and non-ulcer dyspepsia. Apart from cultivation of the bacterium, other diagnostic procedures include various staining methods and urease tests of gastric biopsy samples. The application of non-invasive diagnostic methods, serology and urea breath tests, is rapidly increasing. H. pylori is susceptible to several antimicrobials in vitro, but eradication of the bacterium from the gastric mucosa is not always achieved. The best results until now have been obtained with the combined use of bismuth salts and two antibiotics. In active chronic gastritis and duodenal ulcer patients, eradication of the bacteria has resulted in healing of the disease with permanent decrease of circulating antibodies and negative urease tests. H. pylori has been found worldwide and the infection shows an age-dependent increase. Man, apparently, is the reservoir of the bacterium, but the exact mechanisms of interhuman transmission are still not defined.     

Peptic ulceration may be a hormonal deficiency disease

Evidence is reviewed that Helicobacter pylori infection may cause a deficiency of the hormone secretin that allows peptic ulcer disease to develop by impairing the body's defenses to gastric acid. Secretin is released into the circulation from the S-cells of the duodenal crypts in response to gastric acid entering the duodenum. Once in the circulation, secretin has five well-documented effects that protect the upper intestine from gastric acid: it stimulates secretion of bicarbonate rich exocrine pancreatic juice; it stimulates secretion of alkaline bile; it stimulates secretion of alkaline mucus from the duodenal submucosal glands of Brunner; it inhibits the humoral phase of gastric secretion; and it inhibits gastric motility, thereby delaying gastric emptying. Impaired secretin release and reduced duodenal S-cells have been documented in peptic ulcer patients compared with control patients. Clinical evidence that patients with H. pylori infection and peptic ulceration have increased gastric secretion and motility and decreased duodenal bicarbonate response to gastric acid, all of which normalize after eradication of the infection, could be explained by reversible impairment of the secretin mechanism. Gastric metaplasia in the duodenum with H. pylori infection is known to reduce the S-cell population. The fact that not all patients with H. pylori infection develop peptic ulceration suggests that degree of secretin deficiency determined by extent of the infection must reach a critical level for peptic ulceration to occur. Peptic ulceration may be a hormonal deficiency disease, a result of secretin deficiency caused by H. pylori infection. It may be the first example of a specific hormonal deficiency disease caused by a specific bacterial infection.     

Impact of Helicobacter pylori eradication on morphological changes in gastric mucosa

The purpose of the study was to examine gastric mucosal morphological changes in patients with gastroduodenal pathology after eradication therapy for Helicobacter pylori (H. pylori). A hundred and thirty-eight patients (40 females and 98 males) were examined. Of them, there were 122 patients with duodenal peptic ulcer, 8 with gastric peptic ulcer, 5 with erosive gastritis, 2 with chronic atrophic antral gastritis, and 1 with non-atrophic gastritis. Two months and a year after therapy, manifestations of gastric mucosal atrophy, the degree of inflammation, and its activity significantly diminished in patients with complete H. pylori eradication. Positive changes were observed mainly in the antral portion of the stomach. In patients with partial eradication, chronic inflammation and its activity became less. Two months and a year following therapy, positive changes in the gastric mucosa were absent in patients without H. pylori eradication.     

Role of Helicobacter pylori in gastrointestinal disease: implications for primary care of a revolution in management of dyspepsia.

The majority of patients with dyspepsia are managed in general practice. However, most of the literature on Helicobacter pylori and its association with gastrointestinal disease has originated from secondary care. This review summarizes the role of H pylori in dyspepsia from the perspective of primary care and suggests a new strategy for the management of dyspeptic patients in this setting. Recent meta-analyses and consensus statements have supported the use of eradication therapy as first-line treatment of peptic ulceration. Studies from primary care have supported the use of eradication therapy in patients who have H pylori related peptic ulcer disease and require long-term H2-antagonist medication, on both clinical benefit and cost-effectiveness grounds. Of the many regimens proposed for the eradication of H pylori, the best evidence supports a triple combination of bismuth, metronidazole and tetracycline. Regimens using proton pump inhibitors may be more acceptable to patients but lack good evidence from trials. Use of a positive serum enzyme-linked immunoabsorbent assay for H pylori antibodies as a criterion for endoscopic investigation has been shown to result in a 23% reduction in endoscopic workload. Further research should answer questions of importance to general practitioners, such as the role of eradication therapy in patients with nonulcer dyspepsia and the effectiveness of eradication of H pylori in the prevention of gastric cancer.     

Helicobacter pylori.

Helicobacter pylori is a gram-negative bacterium which causes chronic gastritis and plays important roles in peptic ulcer disease, gastric carcinoma, and gastric lymphoma. H. pylori has been found in the stomachs of humans in all parts of the world. In developing countries, 70 to 90% of the population carries H. pylori. In developed countries, the prevalence of infection is lower. There appears to be no substantial reservoir of H. pylori aside from the human stomach. Transmission can occur by iatrogenic, fecal-oral, and oral-oral routes. H. pylori is able to colonize and persist in a unique biological niche within the gastric lumen. All fresh isolates of H. pylori express significant urease activity, which appears essential to the survival and pathogenesis of the bacterium. A variety of tests to diagnose H. pylori infection are now available. Histological examination of gastric tissue, culture, rapid urease testing, DNA probes, and PCR analysis, when used to test gastric tissue, all require endoscopy. In contrast, breath tests, serology, gastric juice PCR, and urinary excretion of [15N]ammonia are noninvasive tests that do not require endoscopy. In this review, we highlight advances in the detection of the presence of the organism and methods of differentiating among types of H. pylori, and we provide a background for appropriate chemotherapy of the infection.     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis> and <Emphasis Type="Italic">cagA</Emphasis> and <Emphasis Type="Italic">vacA</Emphasis> gene status in children from Brazil with chronic gastritis

Helicobacter pylori has been shown to be strongly associated with chronic gastritis, gastric and duodenal ulceration, and is a risk factor for gastric carcinoma. Histology, urease, culture, and polymerase chain reaction have been employed as for H. pylori diagnostic methods, pre and post treatment or during follow-up of dyspeptic adult individuals referred for endoscopy. In order to obtain a more-sensitive and specific method for H. pylori detection, we evaluated gastric body and antrum biopsies of 134 consecutive Brazilian consecutive dyspeptic children aged 1-16 years by rapid urease test, histology and polymerase chain reaction using two pairs of oligonucleotides. Our results indicated that polymerase chain reaction with Southern blotting and hybridization with specific chemiluminescent probes increased the number of positive H. pylori patients by 35%. The genotyping of H. pylori strains directly from gastric biopsy using the same nucleic acid methodology revealed that there is no association of chronic gastritis in our infant patients with vacA s1 and the presence of the cagA gene. These data suggest an initial infection of children with normal mucosa and probably others factors than vacA s1 genotype or the presence of the cagA gene are associated with the onset of gastric disease. Altogether, our results reinforce the need for using more sensitive diagnostic methods in order to understand the role of H. pylori in the genesis of gastric disease in children and its progression in adults.     

Diagnosis and treatment of Helicobacter pylori infection

National Danish guidelines for the diagnosis and treatment of Helicobacter pylori (Hp) infection have been approved by the Danish Society for Gastroenterology. All patients with peptic ulcer disease, gastric cancer, and MALT lymphoma should be tested for Hp. We also recommend testing in first degree relatives to patients with gastric cancer, in NSAID-naive patients, who need long-term NSAID therapy, and in patients presenting with dyspepsia and no alarm symptoms. Non-endoscoped patients can be tested with a urea-breath test or a faecal antigen test. Endoscoped patients can be tested with a rapid urease test. Proton pump inhibitor therapy should be stopped at least 1 week prior to Hp testing. All infected patients should be offered Hp eradication therapy. First-line treatment is 7-day triple therapy with a proton pump inhibitor and clarithromycine in combination with metronidazole or amoxicilline. Quadruple therapy for 2 weeks with bismuthsubsalicylate, tetracycline, metronidazole and a proton pump inhibitor is recommended in case of treatment failure. Hp testing should be offered to all patients after eradication therapy but is mandatory in patients with ulcer disease, noninvasive gastric cancer or MALT lymphoma. Testing after eradication should not be done before 4 weeks after treatment has ended.     

Helicobacter pylori test and medical reimbursement

There are an estimated 60 million people with Helicobacter pylori(H. pylori) infection who occupied 50% of the population of Japan. In Japanese medical reimbursement H. pylori tests were introduced on November 1, 2000 and they are able to use only to patients with gastric and duodenal ulcer. H. pylori tests were composed of rapid urease test, urea breath test, antibody test, bacterial culture and pathologic test. Payment of each test is 700 Yen. Classification and cost of H. pylori tests are shown. Usage of laboratory tests for H. pylori infection is mentioned. Those particular tests are useful to decrease the number of gastric and duodenal ulcer in Japan.     

Eradication therapy of Helicobacter pylori infection

Helicobacter pylori(H. pylori) infection is recognized to be a pathogen of various gastro-duodenal diseases. Eradication therapy of H. pylori reduces the recurrence of gastro-duodenal ulcer, and improves gastritis histologically. Recently, proton pump inhibitor(PPI) based triple therapy, that combining PPI, clarithromycin, amoxicillin is widely accepted throughout the world, and shows high eradication rate which ranged about 80-90%. In Japan, one week triple therapy is recommended for the treatment of gastro-duodenal ulcer, though it is expected the improvement of recurrent peptic ulcer. In the present studies, the rate of clarithromycin resistant strains has been increased gradually, and this fact may lead to the development of failure of PPI based triple therapy. Another problem is suggested by several studies that gastro-esophageal reflux disease(GERD) may increase after successful eradication of H. pylori. Reflux esophagitis and Barrett's esophagus are recognized as precancerous lesion of esophageal adenocarcinoma, but the association of newly occurrence of GERD after H. pylori eradication and increase of esophageal adenocarcinoma is not clear. Merits and demerits of H. pylori eradication need to be observed carefully over a long term.     

Histopathological changes in gastric mucosa colonized by H. pylori

Helicobacter pylori (H. pylori), infection has been linked to acute and chronic gastritis, non-ulcer-dyspepsia, peptic ulcer, gastric adenocarcinoma and gastric non-Hodgkin's lymphoma of mucosa-associated lymphoid tissue (MALT). The epithelial changes in H. pylori colonized gastric mucosa are easy to recognize in routine Haematoxylin & Eosin stained sections and are so distinctive that they can serve as a helpful histological indicator for the presence of H. pylori in gastric biopsies. The histopathology of seventy-five gastric biopsies showing colonization by H. pylori was studied. Histologically, the H. pylori colonized gastric epithelium showed characteristic changes that were topographically related to the bacteria. These changes included irregular surface, epithelial pits, individual cell dropout and microerosion, which were specific for H. pylori colonization. These were absent in areas not colonized by H. pylori and in 20 consecutive H. pylori negative gastric biopsies seen during the same study period. As specific treatment for H. pylori infection is available, identification of H. pylori colonization in gastric biopsies should be attempted in all cases of gastritis, peptic ulcers and non-ulcer-dyspepsia.     

Treatment of Helicobacter pylori infections

The treatment of Helicobacter pylori (H.p.) infection is based on the recommendations of the Maastricht consensus conference 1996. The main indications for eradication of H.p. are peptic ulcer disease, gastritis with severe histological abnormalities, low grade gastric MALT lymphoma and a history of resection for gastric cancer. The results of recent studies demonstrate that the symptoms of non-ulcer dyspepsia are not improved by H.p. eradication. A family history of gastric cancer and an earlier operation for peptic ulcer are considered advisable indications for the treatment of H.p. infection. Triple therapies consisting of a proton pump inhibitor (PPI) or ranitidine bismuth citrate plus 2 antibiotics are established as effective and well-tolerated first line regimens. The most important antibiotics are clarithromycin and amoxicillin. The efficacy of metronidazole is impaired by an increasing rate of resistant strains. Only few new antibiotics are currently tested in clinical trials. After the failure of a first anti-H.p. treatment it is advisable to change antibiotics according to the probability of resistance, to increase dosage and duration of treatment and to include bismuth compounds in the second line regimen. An alternative option after failed triple therapies may be a high dosage and prolonged dual regimen with a PPI and amoxicillin or quadruple therapy consisting of a PPI, bismuth subcitrate, tetracycline and metronidazole.     

Topographic expression of MUC5AC and MUC6 in the gastric mucosa infected by Helicobacter pylori and in associated diseases

We investigated the topographic expression of MUC5AC and MUC6 in relationship with gastric diseases. The immunoexpression of MUC5AC and MUC6 was evaluated in 75 adults presenting Helicobacter pylori gastritis (n = 22; 11 cagA positive), duodenal ulcer (DU, n = 11), gastric ulcer (GU, n = 9), gastric carcinoma (GC, n = 20), and normal mucosa (H. pylori negative, n = 13). Five gastric areas (antral and corporeal lesser and greater curvatures and incisura) were studied. H. pylori was detected by carbolfuchsin, urease, and culture; cagA was determined by PCR. All patients with DU (eight with GU and 13 with GC) were H. pylori-positive. In H. pylori gastritis, MUC5AC expression was higher in the antrum than in the corpus; no difference was observed with respect to cagA status. MUC5AC expression was higher in the antrum of gastritis than in DU, and it was lower in the incisura among GU patients compared to DU. MUC6 expression was higher in the antrum of H. pylori gastritis compared to DU and to uninfected patients. No difference was observed in the topographic pattern of expression of MUC5AC and MUC6 among GC cases. The topographic over- and under-expression of mucins in H. pylori-associated gastritis and peptic disease suggest a role for these mucins in the pathogenesis of H. pylori infection and associated diseases.     

Factors associated with gastro-duodenal disease in patients undergoing upper GI endoscopy at the Korle-Bu Teaching Hospital,Accra, Ghana

BackgroundThere is a high prevalence of gastro-duodenal disease in sub-Saharan Africa. Peptic ulcer disease in dyspeptic patients, 24.5%, was comparable to prevalence of gastro-duodenal disease among symptomatic individuals in developed countries (12 — 25%). Limited data exists regarding its associated risk factors despite accumulating evidence indicating that gastroduodenal disease is common in Ghana.ObjectivesThis study investigates risk factors associated with gastro-duodenal disease at the Korle-Bu Teaching Hospital, Accra, Ghana.MethodsThis study utilized a cross-sectional design to consecutively recruit patients referred with upper gastro-intestinal symptoms for endoscopy. The study questionnaire was administered to study participants. Helicobacter pylori infection was confirmed by rapid-urease examination at endoscopy.ResultsOf 242 patients sampled; 64 had duodenal ulcer, 66 gastric ulcer, 27gastric cancer and 64 non-ulcer dyspepsia. Nineteen (19) had duodenal and gastric ulcer while 2 had gastric ulcer and cancer. A third (32.6%) of patients had history of NSAID-use. H. pyloriwas associated with gastric ulcer (p=0.033) and duodenal ulcer (p=0.001). There was an increased prevalence of duodenal ulcer in H. pylori-infected patients taking NSAIDs, P=0.003.ConclusionH. pylori was a major risk factor for peptic ulcer disease. However, NSAID-related gastro-duodenal injury has been shown to be common in H. pylori infected patients. It highlights the need for awareness of the adverse gastro-intestinal effects in a H. pylori endemic area.     

The role of apoptosis and proliferation of epitheliocytes in morphogenesis of Helicobacter pylori-associated gastritis

77 patients with chronic Helicobacter gastritis verified endoscopically and exacerbation of duodenal ulcer were examined. H. pylori infection was identified by the rapid ureasa test (CLO-test) and Giemza staining. The patients received 7-day three-component therapy for eradication of H. pylori. Apoptosis and proliferation were studied in 16 patients in serial sections with the use of monoclonal antibodies. Eradication of H. pylori resulted in relief of inflammation and transformation of active gastritis in inactive one. H. pylori-associated gastritis is associated with activation of apoptosis of gastric mucosa epithelial cells and epitheliocytes proliferation. H. pylori eradication alters correlation between apoptosis of epitheliocytes and their proliferation: successful eradication of the infection decreases apoptosis, high proliferative activity of epitheliocytes persists reflecting enhancement of regeneration in gastric mucosa.     

Helicobacter pylori infection affects eosinophilic cationic protein in the gastric juice of patients with idiopathic chronic urticaria

BACKGROUND: Helicobacter pylori, the main cause of gastritis and peptic ulcer, has been associated with idiopathic chronic urticaria (ICU), an immunological skin disorder of unknown origin. Eosinophilic cationic protein (ECP) is a cytotoxic molecule secreted by the activated eosinophils involved in the pathogenesis of ICU. We assessed serum/gastric juice ECP levels and gastric mucosal eosinophil infiltration in ICU patients infected or not with H. pylori and evaluated the modification after bacterium eradication. METHODS: 33 patients with ICU and 25 dyspeptic controls underwent upper gastrointestinal endoscopy for histological evaluation and assessment of H. pylori infection. One-week triple therapy was given to H. pylori-positive patients. Serum and gastric juice ECP levels, eosinophil infiltration from gastric mucosal sections and urticaria symptoms were evaluated in all patients at enrollment and 8 weeks after eradication. RESULTS: 19 of 33 (57%) ICU patients and 16 of 25 (64%) controls were found to be infected with H. pylori. Serum ECP was significantly higher in ICU patients compared to controls, regardless of infectious status. Gastric juice ECP and gastric eosinophil infiltration were significantly higher in infected ICU patients when compared both to uninfected ICU patients and controls. H. pylori eradication determined a significant decrease in gastric juice ECP and gastric eosinophil infiltration only in ICU patients. Moreover, a total or partial remission of urticaria symptoms was observed only in ICU patients in whom the bacterium was eradicated. CONCLUSIONS: Although H. pylori infection affects gastric juice ECP and eosinophil infiltration of ICU patients, the role of the bacterium in the pathogenesis of this skin disorder still remains uncertain.     

The role of screening for Helicobacter pylori in patients with duodenal ulceration in the primary health care setting.

BACKGROUND: It is known that at least 90% of duodenal ulcers are caused by infection with the bacterium Helicobacter pylori. Eradicating this organism usually results in complete resolution of the disease. Testing for H pylori was introduced relatively recently, and thus, many patients known to have uncomplicated peptic ulcer disease who continue to need long-term treatment with ulcer-healing drugs have never been tested for the infection or offered eradication therapy. In modern computerized practices, this subgroup of patients can readily be identified by reference to morbidity and repeat prescribing data. Eradication of H pylori infection in this group of patients has great potential benefit for the individuals concerned as well as cost-saving benefit for the National Health Service. AIM: The aim of this prospective study was to determine whether it is worthwhile screening for and treating H pylori infection in patients in a general practice population with previously diagnosed duodenal ulcer disease taking ulcer-healing drugs long term. METHOD: In 1994, in a practice of 7100 patients, morbidity and repeat prescribing data were used to identify 40 patients (0.6%) with proven duodenal ulcer disease taking ulcer-healing medication long term and with uncertain H pylori status. Twenty-nine of the 40 subjects agreed to undergo serology testing for H pylori antibodies. Of 20 (69%) who were positive, 18 (eight women, median age 63.8 years) were given eradication therapy. Seventeen patients received omeprazole 40 mg once daily and amoxycillin 500 mg three times daily for 14 days with metronidazole 400 mg three times daily for the first 7 days; for the remaining patient metronidazole was inadvertently omitted. [13C]Urea breath testing was carried out at the local hospital at least one month after therapy to determine whether eradication treatment had been successful. Subjects were also personally followed up by telephone after 1 and 4 months to assess the success of treatment subjectively. RESULTS: [13C]Urea breath testing showed that H pylori eradication was successful in all 17 patients (100%) who received the intended eradication regimen. Helicobacter pylori was not eradicated in the patient who received only omeprazole and amoxycillin. Four months after successful H pylori eradication, 13 of the 17 (76%) patients remained completely asymptomatic. Two of the four patients who had some recurrent dyspepsia had known gastro-oesophageal reflux and their ongoing symptoms after eradication therapy seemed, on close questioning, to be more attributable to this than to duodenal ulcer disease. CONCLUSION: Testing for and eradication of H pylori is worthwhile in general practice in those patients with previous proven duodenal ulceration who need long-term ulcer-healing medication. The high rate of eradication of H pylori achieved with the regimen used in this study compares very favourably with that of other treatment regimens. However, in patients with duodenal ulcers there may be coexisting pathology, and H pylori eradication does not necessarily result in complete disappearance of dyspeptic symptoms. Thus, when monitoring the outcome of treatment it is important to assess improvement of symptoms as well as objective evidence of eradication.     

CagA antibodies in Japanese children with nodular gastritis or peptic ulcer disease

cagA(+) Helicobacter pylori strains have been linked to more severe gastric inflammation, peptic ulcer disease, and gastric cancer in adults, but there have been few studies of cagA in children. We examined the relationship between H. pylori cagA status and clinical status in Japanese children. Forty H. pylori-positive children were studied: 15 with nodular gastritis, 5 with gastric ulcers, and 20 with duodenal ulcers. H. pylori status was confirmed by biopsy-based tests and serum anti-H. pylori immunoglobulin G (IgG) antibody. As controls, 77 asymptomatic children with sera positive for anti-H. pylori IgG were enrolled. Levels of IgG antibodies to CagA in serum were measured by an antigen-specific enzyme-linked immunosorbent assay. In 16 patients with successful H. pylori eradication, posttreatment levels of CagA and H. pylori IgG antibodies also were studied. The CagA antibody seropositivities of asymptomatic controls (81.8%) and patients with nodular gastritis, gastric ulcers, and duodenal ulcers (80.0 to 95.0%) were not significantly different. Compared with pretreatment levels of CagA antibodies, posttreatment levels decreased progressively and significantly. We conclude that, as in Japanese adults, a high prevalence of cagA(+) H. pylori strains was found in Japanese children, and that there was no association with nodular gastritis or peptic ulcer disease. In the assessment of eradicative therapies, monitoring of serum anti-CagA antibodies does not appear to offer any direct benefit over monitoring of anti-H. pylori antibodies.