"Campylobacter pyloridis" and epigastric pain: endoscopic, histological, and bacteriological correlations

Campylobacter pyloridis is a newly discovered bacterium which has been implicated in gastric pathology. C. pyloridis was looked for by hematoxylin and eosin staining and culture (chocolate and brucella blood agar) in gastric antral biopsies in 136 unselected patients suffering from epigastric pain. The distribution of C. pyloridis positive cases according to the endoscopic diagnosis was as follows: duodenal ulcer (19 positive/21 tested), duodenitis (6/10), gastric ulcer (9/21), gastritis (13/26), and normal endoscopy (21/58). The association was statistically significant for duodenal ulcers (p less than 0.001). All of the 68 C. pyloridis positive patients showed histologic signs of gastritis as compared to 29 of the 68 C. pyloridis negative patients. The two techniques detection were comparable in sensitivity: 57 were detected by culture only and 63 by microscopy only. We also looked for C. pyloridis in biopsies of the body of the stomach in 71 patients. Bacteria were found in 33 of 36 cases with C. pyloridis positive antral biopsies (15 had histologic lesions) but only in 2 of 35 C. pyloridis antrum negative cases. Therefore, C. pyloridis was tightly associated with histologic signs of antral gastritis and with duodenal ulcers when diagnosed by endoscopy.     

Campylobacter pyloridis in peptic ulcer disease: microbiology, pathology, and scanning electron microscopy.

After the recent successful isolation of spiral organisms from the stomach this paper presents the bacteriological and pathological correlation of gastric antral biopsies from 51 patients endoscopied for upper gastrointestinal symptoms. Campylobacter pyloridis was cultured from 29 patients and seen by either silver staining of the biopsy or scanning electron microscopy in an additional three. The organism was cultured from 23 of the 33 (69%) patients with peptic ulcer disease and from within this group 17 (80%) of the 21 patients with duodenal ulceration. It was cultured only once from the 12 normal biopsies in the series but from 27 of the 38 (71%) biopsies showing gastritis. C pyloridis was also cultured from five out of seven of the 14 endoscopically normal patients, who despite this had biopsy evidence of gastritis. It was the sole organism cultured from 65% of the positive biopsies and scanning electron microscopy invariably revealed it deep to the surface mucus layer. C pyloridis persisted in the three patients with duodenal ulcers after treatment and healing. The findings support the hypothesis that C pyloridis is aetiologically related to gastritis and peptic ulceration though its precise role still remains to be defined.     

Campylobacter pyloridis in peptic ulcer disease. I. Gastric and duodenal infection caused by C. pyloridis: histopathologic and microbiologic findings

In this study 153 patients with dyspepsia were biopsied in the gastric antrum and duodenum. All specimens were investigated histopathologically and microbiologically for the presence of Campylobacter pyloridis, and the type of inflammation was recorded in accordance with Morson's criteria. C. pyloridis was found beneath the mucus close to the epithelial cells and mostly in connection with granulocytic infiltration (active gastritis). C. pyloridis was cultured from all of 10 patients with histologically active gastritis and active duodenitis, in 86% of 64 patients with active gastritis and morphologically normal duodenum, and in only 5% of 79 patients without morphologic gastric and duodenal changes. The close relation between active gastritis and C. pyloridis shows that C. pyloridis plays an important role in gastric inflammation, as it fulfils the criterion for a localized bacterial infection.     

Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment

To determine the clinical importance of Campylobacter pyloridis infection, its association with gastric inflammation, and the response to drug therapy, patients with a duodenal or gastric ulcer (n = 63), patients with nonulcer dyspepsia (n = 240), and asymptomatic volunteers (n = 34) were studied. In a prospective longitudinal study, the type, intensity, and distribution of inflammation in antral biopsy specimens were correlated with the presence of C. pyloridis. Campylobacter pyloridis was cultured from antral biopsy specimens in 98% of the ulcer patients, 70% of the nonulcer dyspepsia patients, and 20% of the asymptomatic volunteers. The dependency of chronic active gastritis on the presence of C. pyloridis was shown by an association of gastritis with positive culture and healing of gastritis with negative culture after various therapeutic regimens. Spontaneous disappearance of C. pyloridis never occurred. Colloidal bismuth subcitrate, amoxicillin, and the combination of colloidal bismuth subcitrate and amoxicillin were effective therapies in eradicating C. pyloridis. Recolonization with the same bacterial subtype and recurrence of gastritis frequently occurred within 1 mo after initial eradication. In this study we demonstrate ultimate normalization of gastric mucosa after successful eradication of C. pyloridis. Especially complete normalization of gastric mucosa after amoxicillin monotherapy provides additional strong evidence for a true cause-effect relationship between C. pyloridis colonization and gastritis.     

A study on the correlation of duodenal-ulcer healing with campylobacter-like organisms

Abstract Campylobacter-like organisms (CLOS) occur frequently in the antrum of patients with duodenal ulcer, but their pathogenetic role has remained uncertain. This study examined prospectively endoscopic biopsies of the antrum of 109 patients with duodenal ulcer, taken before and after 4–12 weeks of treatment with either a prostaglandin E₁ or its placebo, for the density of campylobacter-like organisms and the severity of antral gastritis. Antral biopsies from 30 non-ulcer dyspeptic patients were used as controls. Active chronic antral gastritis and CLOS respectively occurred in 98% and 99% of patients with duodenal ulcer, and in 50% and 57% of the controls ( P < 0.005). CLOS occurred in 97% of all subjects with active chronic gastritis and in 14% of those with normal gastric mucosa ( P < 0.0005). The density of CLOS correlated with the severity of gastritis. After treatment with prostaglandin E₁ and placebo, 89% and 51% respectively of ulcers healed, and 42% and 6% respectively of gastritis improved from a moderate to a mild grade, but bacteria remained positive and persisted in the same density as before treatment. The conclusion was that CLOS, antral gastritis and duodenal ulcer are closely associated, but that healing of duodenal ulcer and improvement of antral gastritis are unaffected by CLOS.     

Pernicious anaemia and Campylobacter like organisms; is the gastric antrum resistant to colonisation?

Gastric biopsies from 86 patients with pernicious anaemia were examined for Campylobacter like organisms with particular attention to those showing an antral gastritis in addition to the usual pattern of body gastritis. All the patients had chronic atrophic gastritis in the body but Campylobacter like organisms were found at this site in only three patients. Thus the Type A pattern of gastritis (autoimmune) seen in patients with pernicious anaemia is only rarely associated with Campylobacter like organisms. Forty four of these patients had biopsies from body and antrum, 16 showed an antral gastritis of whom only one had Campylobacter like organism present. Twenty five of this latter group of patients were rebiopsied after five years. There was no change in the pattern of gastritis, and the same single patient remained colonised. The frequency of an antral gastritis in patients with pernicious anaemia was 36% yet the frequency of antral colonisation by Campylobacter like organisms was very low (6%). These results show that, as in the body, Campylobacter like organisms are not associated with gastritis when it occurs at this site in pernicious anaemia. The antral gastritis that may accompany body gastritis in pernicious anaemia seems more likely therefore to be an extension of primary type A body gastritis (autoimmune) rather than a secondary type B (chronic) gastritis and, it is argued, the antrum may exhibit resistance to colonisation.     

Histological appearances of oesophagus, antrum and duodenum and their correlation with symptoms in patients with a duodenal ulcer.

Clinical data and histology from the oesophagus, gastric antrum, and duodenum were collected from 36 patients undergoing surgery for duodenal ulcer. Gastritis was present in 94% of the patients (25% of atrophic type), oesophagitis in 72% and duodenitis in 39%. Abnormal biopsies were present from all three sites in 33% of the patients. Only one patient showed three normal biopsies. The low incidence of duodenitis does not support the theory that duodenitis is part of the same spectrum as duodenal ulcer. Heartburn was related to the presence of gastritis (100%) and oesophagitis (76%) but not to duodenitis (52%). No relationship was found between the length of history, severity of pain, and histological abnormalities.     

Occurrence of Campylobacter pylori in patients with gastritis and peptic ulcer

Endoscopic biopsies from the gastric antrum and margin of peptic ulcers (gastric and duodenal) were obtained from 56 patients for histologic and microbiologic studies in order to establish the occurrence of Campylobacter pylori. Thirty nine of them had antral gastritis and in 37 (94.8%) the bacteria was detected. In 17 cases with normal mucosa the culture was positive in only 2 of them (p less than 0.01). Patients with duodenal and gastric ulcer had a 100% and 88.8%, respectively, of positivity to C. pylori at samples from the margin of the lesions. Bacteriologic findings were similar to those described in the literature. At the electronic microscopy bacilli were found near or adhering to the cellular surface without signs of intraepithelial penetration. This study confirms the association between C. pylori and gastritis and peptic gastroduodenal ulcer.     

Screening for Campylobacter pyloridis in patients with upper dyspepsia and the relation to inflammation of the human gastric antrum

Campylobacter pyloridis, a recently detected microorganism, was isolated from gastric antral mucosa in 58% of 119 consecutive patients with upper dyspepsia. There was a highly significant correlation between the presence of Campylobacter pyloridis and antral inflammation and a close relation to prepyloric and duodenal ulcer. There was no significant correlation with the severity or type of inflammation. This microorganism, which seems to be as common in Denmark as in other parts of the world, is considered a possible cause of gastroduodenal disease.     

Campylobacter pyloridis in the upper gastrointestinal tract: a Brazilian study

The successful isolation of C. pyloridis from human gastric mucosa has renewed interest in these bacteria and their role as a causative agent for gastritis, and possible causal relationship between chronic gastritis and peptic ulceration. To determine the incidence of C. pyloridis in gastric biopsies we studied 51 consecutive Brazilian patients with a wide range of alimentary disorders presenting for endoscopy. At least three biopsies were taken from each site: antrum, any ulcer or cancer. Microbiological and histological studies were performed to identify the bacteria. The organism was found in 40/51 (78%) of patients. These was a close correlation between culture (100%), Gram (90%) and Gimenez staining (80%) in identifying the bacteria. All C. pyloridis positive patients had histological evidence of antral chronic gastritis (active or quiescent) even if the endoscopic appearance looked normal. All peptic ulcer patients (n = 17) showed C. pyloridis in the antrum. In the duodenum the bacteria were mainly seen in gastric type of mucosa. Our findings support the hypothesis that C. pyloridis is etiologically related to gastritis and possibly peptic ulceration.     

Pathogenetic role of Campylobacter pyloridis in gastric ulcer

Recent reports of the occurrence of Campylobacter pyloridis in the stomach of patients with gastric ulcer have revived interest in the possible aetiological role of bacteria in this condition. To study the pathogenetic role of C. pyloridis in gastric ulcer, endoscopic biopsies, at least four from antrum, four from fundus and four, where appropriate, from the ulcer site, were taken from 28 non-ulcer controls and 67 patients with gastric ulcer before and after complete healing of ulcer, following treatment with either enprostil or cimetidine for up to 8 weeks. The activity of gastritis as assessed by the degree of polymorph infiltration was graded blindly, by two independent pathologists, as nil, mild, moderate or severe. The presence of C. pyloridis was determined by smear and culture, and by Warthin Starry stain, and the bacterial density after staining was scored. The occurrence of C. pyloridis in the gastric antrum was not significantly different in gastric ulcer than in controls but was significantly (P < 0.005) more frequent in gastritic than in non-gastritic mucosa. With gastric ulcer healing the activity of antral gastritis improved significantly (P < 0.05). Despite ulcer healing and improvement of gastritis, the frequency of occurrence and the density of C. pyloridis remained unchanged. It seems that C. pyloridis occurs frequently in gastritic mucosa, and does not affect the healing of gastric ulcer or improvement of gastritis, suggesting that it is unlikely to play a major pathogenetic role.     

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.     

Rapid Urease Test in the Management of Campylobacter pyloridis-Associated Gastritis

Campylobacter pyloridis colonization of the stomach may be an etiological factor in gastritis and peptic ulceration. Campylobacter pyloridis produces large amounts of urease, and the presence of this enzyme in gastric mucosa usually indicates infection with the organism. In this paper we describe the use of a rapid urease test (CLOtest) to detect C. pyloridis infection in gastric mucosal biopsies. In 141 consecutive endoscopy cases, antral biopsies were taken for culture and histology, and an extra biopsy was inserted into the CLOtest gel. There were 79 patients infected with C. pyloridis, 78 of whom were detected by CLOtest: 75% were positive at 20 min, 92% at 3 h, and 98% at 24 h. There were no false positive results. Eighteen infected patients were rebiopsied after a course of amoxycillin and bismuth subcitrate. Active chronic gastritis resolved in eight of nine who were cleared of the organism, but histological gastritis was unchanged in nine patients who were still infected. CLOtest is a simple, sensitive, and highly specific test that enables the endoscopist to diagnose C. pyloridis infection in the endoscopy room. A negative test after antibiotic therapy correlates with clearance of the bacteria and healing of active gastritis.     

Is Duodenal Gastric Metaplasia a Consequence of Helicobacter pylori Infection in Children?

Background: Duodenal gastric metaplasia (DGM) is commonly found in association with Helicobacter pylori (Hp)-associated gastritis in adults. DGM is also considered a risk factor for duodenal ulcer development. The prevalence of DGM in children and its association with gastritis, duodenitis, or the presence of Hp organisms is not clear. We investigated the prevalence of DGM in children and explore its association with several possible risk factors, including age, gender, gastritis, duodenitis, or Hp presence in the gastric antrum. Methods : A retrospective analysis of 173 upper endoscopy procedures performed between 1993 and 1995 at Cabell Huntington Hospital, Huntington, WV, was done. Gastric and duodenal biopsies were stained with Giemsa for Hp detection, periodic acid-Schiff for DGM, and hematoxylin and eosin for histologic assessment. Gastric mucosal inflammation was graded according to Sydney criteria. Results : Duodenal gastric metaplasia was identified in 23 of 173 (13%) patients. Duodenitis hut not age, gender, gastritis, or the presence of Hp in the gastric antrum was associated with DGM development. In 4 of 23 DGM foci, Hp was identified. Conclusions : In children, DGM is not the consequence of Hp infection.     

Low-dose cimetidine in the acute treatment of duodenal ulcer. Comparison of a single nocturnal dose regimen with a twice daily regimen

A 0.5 g daily dose of cimetidine was as effective as a 1 g dose in the acute treatment of duodenal ulcer patients in Hong Kong. The aims of the present study were, first, to determine whether low-dose cimetidine treatment was as effective as standard doses in acute duodenal ulcer treatment of patients in Singapore, and second, to compare a single nocturnal dosage regimen with a twice daily regimen. In this single centre, double-blind, controlled trial, 282 patients with endoscopically proven duodenal ulcer were randomized to receive four weeks' treatment with cimetidine using one of three dosage regimens: (A) 800 mg at night; (B) 400 mg at night; or (C) 400 mg twice daily. Two hundred and forty-seven patients were evaluated. The incidences of healing at four weeks were: (A) 40/80 (50%), (B) 39/88 (44%); and (C) 48/79 (61%); (B vs C: P less than 0.05; A vs C: NS; 95% confidence limits: -5% to 27%; A vs B: NS, 95% confidence limits: -6% to 21%). Of 183 patients who had antral biopsies taken, 176 (96%) had histological gastritis, while 167 (91%) were positive for Helicobacter-like organisms. The occurrence of gastritis or Helicobacter-like organisms had no influence on ulcer healing. A 400 mg dose of cimetidine is therefore suboptimal for the treatment of duodenal ulcer in patients in Singapore. A single nocturnal dosage regimen may be less effective than a twice daily regimen.     

Helicobacter pylori and chronic active inflammation of the duodenum and stomach in duodenal ulcer patients treated with ranitidine, misoprostol, or an acid-neutralizing agent

Biopsy specimens from the stomach and duodenum of 45 duodenal ulcer patients treated with ranitidine, misoprostol, or an antacid were examined. During 4 weeks of treatment the duodenal ulcer healed in 31 patients. The treatment regimens showed no significant effect on the amount of Helicobacter-like structures (HLS) or the presence of active inflammation, either in the stomach or in the duodenum. All patients had chronic active antral gastritis before and after treatment. HLS were found histologically in 91.7% of all antral specimens, in 94.2% of the gastric corpus specimens, in 15.9% of the duodenal bulb specimens, and in 0.9% from the lower duodenal knee. The frequency of chronic active gastritis was clearly lower in the gastric corpus than in the antrum, whereas the occurrence of HLS was about the same. This may indicate a higher resistance of the gastric corpus mucosa to H. pylori.     

Ingestion of Campylobacter pyloridis Causes Gastritis and Raised Fasting Gastric pH

Campylobacter pyloridis was ingested by a volunteer who had a histologically normal gastric mucosa and fasting gastric pH recordings of less than 2. Three days later he developed moderate to severe attacks of epigastric pain. On the 5th day after ingestion C. pyloridis was cultured from antral biopsies which showed histological acute gastritis. However, fundal histology and fasting gastric pH were normal. On the 8th day fasting gastric pH rose to 7.6. On day 11 C. pyloridis was cultured from both antral and fundal biopsies which showed histological gastritis. Doxycycline was taken for 28 days but infection and gastritis persisted. Bismuth subsalicylate was taken for 28 days and final biopsies, taken 1 wk after stopping therapy, were culture negative. Histology showed a minimal residual chronic gastritis. C. pyloridis can cause an acute upper gastrointestinal illness associated with histological gastritis and an increase in fasting gastric pH.     

The Effects of Short-Term Lansoprazole Therapy on Helicobacter pylori Infection and Antral Gastritis in Duodenal Ulcer Patients

Background/Aims: Lansoprazole is a new potent proton pump inhibitor that exhibits activity against Helicobacter pylori in vitro . This study endeavored to determine the effects of 4 wk of lansoprazole therapy upon H. pylori infection and antral gastritis in duodenal ulcer patients and to determine the relationship of the gastritis with Helicobacter infection and with ulcer activity.
Methods: Satisfactory antral biopsies were obtained from 119 duodenal ulcer patients before and after 4 wk of therapy with lansoprazole, ranitidine, or placebo. Sections were scored blindly for degree of active and chronic inflammation and extent of H. pylori infection.
Results: Four weeks of lansoprazole (30 mg daily) or ranitidine (300 mg daily) therapy produced a significant decrease in H. pylori infection. The reduction of H. pylori infection, but not ulcer healing per se , correlated with the decrease in active and chronic antral inflammation. Reduction of H . pylori infection, however, did not improve the good ulcer-healing rates already achieved at 4 wk by potent acid inhibition.
Conclusions: Lansoprazole exhibits activity against H. pylori in vivo . Short-term improvement in antral gastritis is affected by reduction of H. pylori infection but not by ulcer healing.     

Campylobacter pylori: Associations with Antral and Fundic Mucosal Histology and Diagnosis by Serology in Patients with Upper Gastrointestinal Symptoms

We obtained a sample of serum and mucosal biopsies from the antrum and usually from the corpus of the stomach from 35 symptomatic patients during routine endoscopy to analyze for the relationship between Campylobacter pylori infection, inflammation, and the diagnostic utility of a C. pylori IgG antibody assay. C. pylori was identified prospectively by culture and/or silver stain in gastric biopsies from 24 patients, and the antibody was detected in 19 (79%) of these patients. The antibody assay was positive in three other patients, two of whom had C. pylori, on reexamination of their biopsies. The accuracy of the antibody assay was 83%. Inflammation was detected in all C. pylori-positive antral biopsies (N = 19). However, five (71%) of seven antral biopsies from patients in whom all tests were C. pylori negative, also had inflammation, constituting 17% of all patients with antral gastritis (N = 30). Both antral and fundic mucosa were obtained from 26 patients and, in this group, C. pylori was detected in fundic mucosa from all patients in whom the organism also was present in the antrum (N = 15). In significant (p less than 0.001) contrast to C. pylori-positive antral histology, fundic mucosal histology was normal in 6 (40%) of 15 C. pylori-positive biopsies, all from patients with peptic ulcer disease. We conclude that C. pylori antibody assays will be useful for epidemiological studies and initial screening of the C. pylori status of individual patients. In addition, there is a high concordance rate between antral and fundic mucosa for the prevalence of C. pylori, but in contrast to the probable etiological role of C. pylori in antral gastritis, the organism appears to be only a commensal of fundic mucosa. Moreover, C. pylori infection is not evident in all patients with type B gastritis.     

Campylobacter like organisms in duodenal and antral endoscopic biopsies: relationship to inflammation.

In 66 endoscopic duodenal biopsies studied retrospectively and in 84 paired duodenal and antral biopsies assessed prospectively campylobacter like organisms were seen in 22 (33%) of the retrospectively examined duodenal biopsies and in 61 (73%) examined prospectively, and in 70 (83%) of antral biopsies. In the duodenum the organisms were mostly confined to the surface epithelium in areas showing gastric metaplasia, while in the antrum they were also found within superficial glands. A strong association was shown between the presence of campylobacter like organisms and histological active duodenal inflammation.