Campylobacter pylori, duodenal ulcer, and gastric metaplasia: possible role of functional heterotopic tissue in ulcerogenesis.

Multiple pinch biopsies were taken from the duodenum and antrum of 137 subjects (46 active duodenal ulceration; 44 healed ulcers; 47 'normal'), and examined for the presence and grade of gastritis, gastric metaplasia, and Campylobacter pylori. These factors, as well as age, sex, cigarette, and anti-inflammatory agent intake were evaluated as possible risk factors for duodenal ulceration. Pentagastrin induced Congo Red staining of the duodenal bulb was performed in an additional 43 cases, to determine the presence of functioning parietal cells in the duodenum. Ninety eight per cent of patients with duodenal infection with C pylori had active or healed duodenal ulcers. Bacteria were confined to areas of gastric metaplasia which was always infiltrated with inflammatory cells. The metaplastic tissue was usually superficial in type, although patients had C pylori associated with heterotopic tissue: this has not been previously described. Congo Red staining of the duodenal bulb showed that functioning endogenous acid producing tissue could be found most often at the edges of duodenal ulcers, but also in non-ulcer subjects. Cigarette smoking, age, sex, and ingestion of non-steroidal anti-inflammatory agents were not to be found to be significant risk factors for duodenal ulceration. In contrast, the presence of duodenal infection with C pylori proved to be a strong risk factor for duodenal ulceration (RR = 51), together with gastric metaplasia (RR = 6.2), and antral C pylori infection (RR = 7.6). These data identify duodenal infection with C pylori as the strongest risk factor for development of duodenal ulceration. Our finding of endogenous acid production around the edges of duodenal ulcers suggests an active role for parietal cells in the duodenum. We postulate a synergistic role for duodenal C pylori and endogenous acid production in the development of duodenal ulceration.     

Campylobacter pylori infection: Experience in a multiracial population

Over a 15-month period, 399 patients with dyspepsia were investigated for the presence of Campylobacter pylori infection. Half of the patients (50.6%) had Campylobacter organisms in the antrum of the stomach. C. pylori was found in 96.1% of patients with histological changes of chronic active gastritis in the antrum. Of patients with duodenal and gastric ulcers, 87.8% and 87.5%, respectively, had Campylobacter organisms, as did 39.3% of patients with non-ulcer dyspepsia. C. pylori infection was most commonly found in Chinese and Indians. Although the prevalence of infection appeared to increase with age, there was an equal distribution amongst the sexes.     

Increased incidence of Campylobacter pylori infection in gastroenterologists: further evidence to support person-to-person transmission of C. pylori

The mode transmission of Campylobacter pylori is still unknown, although several studies have suggested person-to-person transmission. In this study the incidence of active C. pylori infection in an endoscopy staff was compared with that in general practitioners and normal blood donors. Since endoscopy workers are in close contact with patients, many of whom would be likely to have active C. pylori infection, it was likely that there would be an increased incidence of active C. pylori infection in endoscopists if the organism can spread from person to person. The incidence of active C. pylori infection in the group of gastroenterologists was 52%, compared with 21% in an age-matched group of blood donors. This finding was statistically significant (p less than 0.01). In comparison, the incidence of active C. pylori infection in the endoscopy nurses and general practitioners was not statistically different from that in the normal population.     

Duodenal ulcer, Helicobacter pylori, and gastric secretion.

Patients with chronic dyspepsia were categorised by macroscopic appearance at oesophagogastroduodenoscopy as having duodenal ulceration (DU), other diagnosed lesions such as reflux oesophagitis, carcinoma of stomach, etc, or no organic lesion (non-ulcer dyspepsia, NUD). Material was collected to identify gastric infection with Helicobacter pylori (H pylori) by CP urease test, culture, and histological examination and to make the microscopic diagnosis of active chronic gastritis. Each patient in the DU and NUD categories was then invited to volunteer for a gastric secretion study in which maximal gastric secretion in response to histamine was measured. Sixty two gastric secretion tests were performed (31 DU, 31 NUD). The presence of H pylori was associated with active chronic gastritis (100%). DU patients secreted more acid than the NUD patients. H pylori positivity was associated with decreased maximal gastric secretion in both groups. There was a positive correlation between smoking and maximal acid output shown only in H pylori negative but not in H pylori positive patients. These findings were clear cut when all corrections of maximal gastric secretion were made for pyloric loss, duodenogastric reflux, and stature. This study failed to show any aetiological link between H pylori and DU by increased maximal gastric secretion.     

Campylobacter pylori in gastric, duodenal and jejunal juices and mucosae of patients with duodenal ulcer

The presence of Campylobacter pylori was investigated in biopsies and fluids obtained in the antrum, duodenal bulb and jejunum during jejunoscopy in 20 patients with an active duodenal ulcer. C. pylori was present in cultured antral biopsies in all patients, in the bulb of most patients (16/20), but was unusual in jejunal mucosa (2/20). Using a non-contaminated sampling method of fluid, C. pylori was found in only two samples at each level. In conclusion, C. pylori is frequent in bulbar mucosa of duodenal ulcer patients, rare in jejunal mucosa and in fluid at each level, thus confirming the ecological mucosal niche of C. pylori.     

Relationship between endoscopic nodular gastritis and Helicobacter pylori infection in children.

INTRODUCTION: The specificity of relationship of endoscopic evidence of nodular gastritis with Helicobacter pylori infection is unclear. AIM: To assess the relationship of endoscopic nodular gastritis and H. pylori infection among children. METHODS: 124 children (median age 8.2 years, range 1-15) undergoing upper GI endoscopy for abdominal pain underwent urease test and histological examination of gastric mucosa to determine the presence and density of H. pylori infection, and presence and severity of gastritis. RESULTS: H. pylori infection was detected in 57 (46%) children. Endoscopic nodular gastritis was present in 46 of these 57 patients (81%) and in 24 of 67 (36%) H. pylori-negative patients (36%). The frequency of endoscopic nodular gastritis was related to increasing age (p< 0.0001), presence of H. pylori, grade of histologic gastritis, and H. pylori density (p< 0.0001). CONCLUSION: Endoscopic finding of nodular gastritis is associated with presence of H. pylori infection and active chronic gastritis in children.     

Patterns of colonisation of Campylobacter pylori in the oesophagus, stomach and duodenum.

Thirty five subjects underwent upper gastrointestinal endoscopy and multiple biopsy (30 patients, five normal subjects). A total of 11 biopsies per subject from four sites (oesophagus (three), gastric body (two), antrum (three), duodenum (three] were examined for inflammation and the presence of Campylobacter pylori and using standard methods of culture and by light (LM) and electron microscopy (EM). The organism was cultured from oesophageal biopsies in eight of 30 (27%) patients but could not be identified at this site by LM or EM. There was evidence of oesophageal inflammation in 20 patients which was associated with the local finding of C pylori in five (25%) including two of seven (29%) with Barrett's mucosa. Antral C pylori was present in 22 of 23 (96%) patients with chronic active gastritis. The organism was found in the antrum and oesophagus in four of 22 patients (18%), in the antrum and duodenum in four of 22 patients (18%) and in all three sites in a further two of 22 patients (9%). Antral C pylori was found in five of six patients with peptic ulceration. C pylori was cultured from the duodenum in six patients with confirmation by LN and EM in three, but only on areas of gastric metaplasia. The organism was not found in the normal group. This study indicates that C pylori may be irregularly isolated from the oesophagus and duodenum in patients with antral C pylori and chronic active gastritis. The role of C pylori in the oesophagus is most likely that of a commensal or contaminant.     

Campylobacter pylori-Associated Gastritis and Immune Response in a Population at Increased Risk of Gastric Carcinoma

A series of 169 consecutive patients from low socioeconomic strata attending the gastroenterology clinic of Charity Hospital in New Orleans were evaluated clinically and endoscopically. This general New Orleans population is known to be at increased risk of developing gastric carcinoma. The type of gastritis was identified histologically, and the presence of Campylobacter pylori was determined by culture and/or histology. The overall prevalence of C. pylori infection in this patient population was 71% (126/169). These findings were correlated with serum IgG antibody to C. pylori using an ELISA. Fifteen patients with neither demonstrable gastritis nor C. pylori served as negative controls and had low levels of IgG antibody to C. pylori. A strong correlation was found between Campylobacter detection by morphologic and/or culture technique and the presence of serum IgG antibody. For all patients examined, the sensitivity of the ELISA was 94.2% and the specificity 75.5%. The highest ELISA values for IgG antibody (sensitivity = 89%, specificity = 75%) were detected in patients positive for C. pylori, who also had diffuse antral gastritis with prominent lymphoid follicles. For patients with chronic atrophic gastritis and intestinal metaplasia, the sensitivity of the ELISA was 96% and the specificity 67%. The latter number may indicate underrepresentation of foveolar epithelium in biopsies with extreme intestinal metaplasia. Results suggest a high prevalence of chronic infection of C. pylori in this clinic population. The possible role of C. pylori in the development of precursor lesions of gastric cancer is discussed.     

Identification and eradication of Helicobacter pylori infection in haemophilic patients

The aim of this study was to identify and eradicate H. pylori infection in patients with haemophilia. Patients were screened for IgG antibodies against H. pylori ; active infection was determined using a ¹³C-urea breath test and infected patients were given combination therapy with antibiotics to eradicate infection. Seventy-eight of 219 (36%) patients with haemophilia were found to have an elevated serum antibody titre against H. pylori ; of 36 antibody-positive patients with confirmatory testing, 14 were found to have active H. pylori infection. H. pylori infection was successfully eradicated in every infectedpatient using acombination of ranitidine plus two antibiotics (usually amoxycillin and metronidazole). It is concluded that eradication of H. pylori infection is likely to be a cost-effective screening strategy in patients with haemophilia, to prevent complications of peptic ulcer disease.     

Prevalence of Campylobacter pylori in esophagitis, gastritis, and duodenal disease

The relationship between the presence of Campylobacter pylori and esophagitis was studied in patients undergoing paired biopsies of distal esophagus and gastric antrum during esophagogastroduodenoscopy. Biopsy specimens were examined for urease activity and for the presence of C pylori by culture and by histologic examination of hematoxylin-eosin- and Warthin-Starry-stained sections. Sixty-two patients were entered into the study. All esophageal biopsy specimens, regardless of histologic findings, were negative for the presence of C pylori by urease test, culture, and histologic examination. Of 35 patients with normal esophageal biopsy specimens, 11 (31%) had antral specimens that were positive for C pylori, while 11 (41%) of the 27 patients with esophagitis had antral specimens that were positive for the organism. Campylobacter pylori was detected in 14 (70%) of 20 patients with chronic gastritis, in 8 (67%) of 12 patients with endoscopically documented duodenal ulcers and erosions, but in only 3 (33%) of 9 patients with endoscopically defined duodenitis. We conclude that histologic esophagitis is not associated with increased prevalence of either gastric or esophageal C pylori. The well-described association of chronic gastritis and duodenal ulcers with C pylori was present in our study population.     

Sofalcone, a mucoprotective agent, increases the cure rate of Helicobacter pylori infection when combined with rabeprazole, amoxicillin and clarithromycin

AIM: The mucoprotective agents, sofalcone and polaprezinc have anti-Helicobacter pylori (H pylori) activities. We determined the therapeutic effects of sofalcone and polaprezinc when combined with rabeprazole, amoxicillin and clarithromycin for Helicobacter pylori infection. METHODS: One hundred and sixty-five consecutive outpatients with peptic ulcer and H pylori infection were randomly assigned to one of the following three groups and medicated for 7 d. Group A: triple therapy with rabeprazole (10 mg twice daily), clarithromycin (200 mg twice daily) and amoxicillin (750 mg twice daily). Group B: sofalcone (100 mg thrice daily) plus the triple therapy. Group C: polaprezinc (150 mg twice daily) plus the triple therapy. Eradication was considered successful if 13C-urea breath test was negative at least 4 wk after cessation of eradication regimens or successive famotidine in the cases of active peptic ulcer. RESULTS: On intention-to-treat basis, H pylori cure was achieved in 43 of 55 (78.2%) patients, 47 of 54 (87.0%) and 45 of 56 (80.4%) for the groups A, B and C respectively. Using per protocol analysis, the eradication rates were 81.1% (43/53), 94.0% (47/50) and 84.9% (45/53) respectively. There was a significant difference in the cure rates between group A and B. Adverse events occurred in 10, 12 and 11 patients, from groups A, B and C respectively, but the events were generally mild. CONCLUSION: The addition of sofalcone, but not polaprezinc, significantly increased the cure rate of H pylori infection when combined with the rabeprazole-amoxicillin-clarithromycin regimen.     

Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: the role of Helicobacter pylori infection and portal hypertensive gastropathy.

BACKGROUND & AIM: The relationship between Helicobacter pylori infection and peptic ulcer disease in cirrhosis remains controversial. The purpose of the present study was to investigate the role of H pylori infection and portal hypertension gastropathy in the prevalence of active peptic ulcer among dyspeptic patients with compensated hepatitis C virus (HCV)-related cirrhosis. METHODS: Patients undergoing upper endoscopy with compensated HCV-related cirrhosis were enrolled. Child-Pugh's score was determined at the entry. Variceal size was measured endoscopically and the severity of portal hypertensive gastropathy was graded. H pylori infection status was determined by urea breath testing and/or histology. RESULTS: A total of 178 patients positive for HCV (A and B Child-Pugh's score) were prospectively included. The prevalence of H pylori infection was 43%. An active peptic ulcer was found in 14 patients (8%) and was significantly more common among those with H pylori infection (16% versus 2% in H pylori uninfected patients, odds ratio: 8.0). No association was observed between H pylori infection and variceal size, or hypertensive gastropathy. CONCLUSIONS: Patients with compensated cirrhosis and H pylori infection showed higher risk of developing a peptic ulcer. Clinical relevance of this result would be that dyspeptic patients with HCV-related cirrhosis may benefit from preventive screening and eradication of H pylori, especially those with features of insufficient hemostasis.     

Gastroduodenal mucosal vitamin-C levels in Helicobacter pylori infection.

BACKGROUND: Vitamin C is an important endogenous antioxidant, and epidemiologic evidence suggests that it may protect against the development of gastric cancer. We therefore determined mucosal vitamin-C levels in the stomach and duodenum of subjects with and without Helicobacter pylori infection. METHODS: The patients were 30 subjects undergoing routine gastroscopy for investigation of dyspepsia. High-performance liquid chromatography with electrochemical detection was used to determine mucosal ascorbic acid and total vitamin-C levels. RESULTS: In H. pylori-negative subjects with normal gastroduodenal histology the antrum contained significantly higher levels of ascorbic acid and total vitamin C than the corpus or duodenum (P < 0.05). No significant changes were seen in gastric mucosal ascorbic acid or total vitamin-C levels in the presence of H. pylori infection and related inflammation. The presence of gastric atrophy did not affect mucosal ascorbic acid or total vitamin C levels. Duodenal ascorbic acid and total vitamin-C levels did not change significantly in the presence of gastric H. pylori or duodenal inflammation. CONCLUSIONS: Although high levels of vitamin C are present in the gastroduodenal mucosa, these are not altered in the presence of H. pylori infection and inflammation. These observations suggest that the mucosal antioxidant potential of vitamin C is not impaired by H. pylori infection.     

Mucosal changes in the gastric remnant: long-term effects of bile reflux diversion and Helicobacter pylori infection

OBJECTIVE: Bile reflux is thought to be responsible for reflux gastritis and stump carcinoma occurring after partial gastrectomy for peptic ulcer. Gastritis and gastric carcinoma are also correlated with Helicobacter pylori. The aim of this study was to investigate whether diversion of enteric reflux and the presence of H. pylori infection alter long-term histological developments in the gastric remnant. METHODS: Twenty-nine patients partially gastrectomized for peptic ulcer were reoperated on with re-resection and a Roux-en-Y reconstruction because of reflux gastritis (12 patients) or severe dysplasia/early gastric cancer (17 patients). The resected specimens and subsequent biopsies from the new anastomotic region taken at endoscopies 5-17 years after reoperation were evaluated regarding the presence of H. pylori, the grade of active and non-active chronic gastritis, and the premalignant changes--atrophy, intestinal metaplasia and dysplasia. RESULTS: A progression of active chronic gastritis, atrophy, intestinal metaplasia and dysplasia was seen after re-resection and Roux-en-Y reconstruction. Non-active chronic gastritis remained unchanged. The development was, in general, independent of H. pylori infection. CONCLUSIONS: Enteric reflux may perhaps induce a histological transformation of the gastric mucosa that cannot be reversed, even if the reflux is diverted. In our study, H. pylori infection had no impact on the histological development. Factors other than enteric reflux and H. pylori infection might also be of importance.     

Effect of Helicobacter pylori Infection on Gastric Emptying and Gastrointestinal Hormones in Dyspeptic and Healthy Subjects

There is no general agreement as regards the effect of Helicobacter pylori infection on gastric emptying in patients with functional dyspepsia. Food releases several gastrointestinal hormones, and some of these are known to contribute to the regulation of gastric emptying. The aim of this study was to investigate the influence of H. pylori on gastric emptying in dyspeptic and healthy subjects and to verify whether different hormone secretion patterns are affected by the presence of the bacterium. Twenty-seven patients affected by functional dyspepsia and 30 asymptomatic healthy subjects entered the study. H. pylori presence was assessed in controls by IgG antibodies to H. pylori and [¹³C] urea breath test, and that in patients by Warthin-Starry stain on gastric biopsies. After ingesting a standard solid-liquid meal, an ultrasound examination of gastric emptying was performed. Plasma concentrations of gastrin, cholecystokinin, and pancreatic polypeptide were measured in the fasting and postprandial period for 4 hours. The incidence of H. pylori infection was not higher in functional dyspepsia patients than in controls. As regards gastric emptying, no difference was detected between patients and controls with and without H. pylori infection. On the contrary, the presence of H. pylori infection determined alterations in gastrin levels, which were higher in controls than in patients. Basal CCK levels were higher in the H. pylori-negative patients than H. pylori-positive patients and controls. In conclusion, H. pylori infection seems not to cause alterations in gastric emptying, but rather alterations in gastrin levels. In contrast, the altered levels of CCK account for its involvement in the pathophysiology of H. pylori-negative dyspepsia.     

A comparative study on Helicobacter pylori infection in peptic ulcer disease patients with or without previous eradication therapy

BACKGROUND/AIMS: Although H. pyloric eradication therapy is indicated for peptic ulcer patients, the prevalence of H. pylori infection may be different between patients with active or chronic (scarred) peptic ulcers. This study aimed to compare the prevalence of H. pylori infection in active and chronic peptic ulcer patients with or without previous H. pyloric eradication therapy. METHODOLOGY: Both non-invasive (13C or 14C urea breath test) and invasive methods (rapid urease test and histology) were used to detect H. pylori. From Dec. 2002 to Jan. 2003, 153 patients with 63% male were enrolled in this study. Fifty-six patients who previously received H. pyloric eradication therapy were enrolled as treated patients, and 97 patients who did not receive therapy were enrolled as untreated patients. RESULTS: H. pylori infection rate was still high in untreated patients even when duodenal ulcer had been scarred (96% in active duodenal ulcer and 63% in scarred duodenal ulcer). In treated patients, H. pyloric infected rates were very low when peptic ulcers were scarred (0% in scarred gastric ulcer, 4% in scarred duodenal ulcer and 0% in both scarred ulcers). CONCLUSIONS: H. pyloric eradication therapy is indicated for untreated patients even when endoscopic examination revealed chronic scarred duodenal ulcer.     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM： To compare the prevalence of H pylori infection, peptic ulcer, cytomegalovirus （CNV） infection and Candida esophagitis in human immunodeficiency virus （HIV）- positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.
METHODS： A total of 151 patients （122 HIV-positive and 29 HIV-negative） with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of Hpylori infection, CMV, candida esophagitis and histologic chronic gastritis.
RESULTS： The prevalence of Hpylori was less common in HIV-positive patients （22.1%） than in HIV-negative controls （44.8%; P 〈 0.05）, and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer （20.7% vs 4.1%; P 〈 0.01）, but a higher prevalence of chronic atrophy gastritis （6.9% vs 24.6%; P 〈 0.05）, Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis （P 〈 0.05）. In HIV-positive patients, chronic active gastritis was not significantly different between those with Hpylori infection and those without.
CONCLUSION： The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to Hpylori infection.     

Helicobacter pylori infection in healthy people: a dynamic process?

Epidemiological studies using serological tests have shown that a large proportion of healthy people have antibodies against Helicobacter pylori (anti-Hp). It is uncertain whether the presence of anti-Hp indicates active infection or only past exposure to the micro-organism. In this study we determined anti-Hp with a specific enzyme linked immunosorbent assay in 100 healthy volunteers who were at the same time investigated for active H pylori infection by means of the 13C-urea breath test. Forty nine per cent had a high anti-Hp titre, but only 24% had active H pylori infection. Our study suggests that a considerable number of healthy people previously infected with H pylori have spontaneously eliminated this microorganism. We suggest that the inability of ulcer patients to eliminate H pylori may be important in the pathogenesis of peptic ulcer disease.     

Comparison of 13C- urea blood test to 13C-breath test and rapid urease test for the diagnosis of Helicobacter pylori infection

At present, the available methods to diagnose active H. pylori infection are endoscopy with biopsy for histology, culture, rapid urease tests, 13C or 14C urea breath test, urine antibody and the stool antigen test. The aims of this study were to simplify the 13C urea test by measuring 13C in blood rather than breath, and to evaluate the usefulness of the 13C urea blood test for the diagnosis of H. pylori infection. Patients who underwent upper endoscopy for standard clinical indications (e.g. dyspepsia, abdominal pain) were enrolled. A total of 161 patients (93F, 68M, mean age 47 +/- 14.2) were evaluated; 50 (31%) of them were H. pylori positive, and 111(69%) were H. pylori negative. H. pylori infection was diagnosed with a rapid urease test (CLO-test) and 13C urea breath test (UBT). Performance characteristics for the 13C urea blood test for diagnosis and evaluation of H. pylori eradication were calculated using UBT and CLO as gold standards. The fifty H. pylori-positive patients were treated with triple antibiotic therapy for two weeks. Four weeks after finishing antibiotic therapy patients were retested with a commercial UBT and urea blood test. The 13C blood test had sensitivities of 92 and 98% and specificities of 96 and 100% as compared with urea breath test and CLO, respectively. We conclude that the 13C urea blood test is highly sensitive and specific for the initial diagnosis and control of eradication of H. pylori infection.     

Campylobacter pylori antibodies in humans

STUDY OBJECTIVE: To determine the diagnostic value of assays to measure serum antibodies to Campylobacter pylori, and to use these assays to determine the prevalence of C. pylori infection in a healthy population. DESIGN: A survey of patients having endoscopies for upper gastrointestinal symptoms, patients with other gastrointestinal illnesses, and healthy controls. SETTING: Outpatients attending endoscopy suites in two university-affiliated medical centers. PATIENTS: One hundred and twenty patients who had gastroduodenoscopies, 61 patients with lower intestinal illnesses, and 166 healthy controls. INTERVENTION: Assay to detect serum IgA, IgG, and IgM antibodies specific for C. pylori. MEASUREMENTS AND MAIN RESULTS: Absorption with other gram-negative pathogens showed that IgG and IgA assays, but not IgM assays, were specific for C. pylori. In patients in whom C. pylori had been isolated and who had gastritis diagnosed by histologic methods, significantly higher mean IgA and IgG levels were seen compared with patients without demonstrable C. pylori or gastritis. The sensitivity and specificity of a positive value in both IgA and IgG assays were more than 93%. Among healthy persons, IgG and IgA antibodies were rarely seen in patients less than 20 years old, but antibody prevalence progressed with age, reaching 50% in patients more than 60 years old. High IgA and IgG levels to C. pylori in five persons tested remained stable for more than 1 year, suggesting the organism persists for at least that period. In 61 patients with acute bacterial enteritis, acute pancreatitis, Crohn disease, or ulcerative colitis, prevalence of antibodies to C. pylori was consistent with age and unrelated to current disease. CONCLUSIONS: Campylobacter pylori infection, which is highly associated with active gastritis, may be diagnosed by serologic assay. Acquisition of infection begins in adult life, and prevalence increases with age.