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PubMed1990

[Deficiency syndrome of chronic gastritis].

161 cases of chronic gastritis (including 59 superficial gastritis, 86 atrophic gastritis, 16 superficial gastritis combined with atrophic gastritis) typed in deficiency syndrome (including 64 Spleen-deficiency syndrome, 97 Spleen-Kidney-deficiency syndrome) were studied clinically with modern medicinal multiple-index. The gastroscope image, pathologic changes of gastric mucosa, stomach barium meal examination, gastric acid, serum gastrin, urine pepsinogen, urine 17-ketosteroid, vegetative nerve function, peripheral blood picture, etc. were selected as observation indices. The preliminary findings showed that in Spleen-deficiency patients, the superficial gastritis constituted the majority, the asthenic stomach constituted the minority, the gastric secretion and the serum gastrin were on the high side, the urine pepsinogen, the adrenocortical function and the hemoglobin were on the low side, but the white blood cell was rather normal; otherwise, in Spleen-Kidney deficiency patients, the atrophic gastritis and the asthenic stomach constituted the majority, the gastric secretion decreased, the serum gastrin level was higher, while the urine pepsinogen, the adrenocortical function, white blood cell and the hemoglobin were on the low side. It was also found that in certain same inflammation changes, the gastric secretion of the Spleen-Kidney-deficiency syndrome was markedly than that of Spleen-deficiency syndrome. With the treatment method of invigorating the Spleen and reinforcing the Spleen-Kidney, each index was relatively improved. The degree of seriousness to inflammation changes of gastric mucosa and the disturbance or imbalance of gastric secretion function were reflected from the Spleen-deficiency and the Spleen-Kidney-deficiency syndromes of chronic gastritis. It is suggested that hemopoiesis and hypothalamo-adenohypophysial-adrenal cortical axis be influenced.

Adult↗
PubMed1988

Effect of sofalcone on gastric mucous glycoprotein in experimental gastritis induced by sodium taurocholate.

Changes in gastric mucous glycoprotein (GP) and effects of the anti-ulcer agent, sofalcone, on experimental gastritis induced by 3 or 6 months administration of sodium taurocholate (TCA) were investigated. Macromolecular mucous GP determined as the hexose content, which was fractionated by gel filtration, was decreased with the development of gastritis. This was also demonstrated by the histochemical observations. Soluble mucus, which is easily released into the incubation medium, was significantly decreased, and the insoluble mucus remaining in the gastric mucosa was not changed in 3-month-old gastritis. On the other hand, insoluble mucus was significantly decreased in 6-month-old gastritis. Synthetic activity of mucous GP, which was determined by incorporation of [3H]-glucosamine and [35S]-sulfate, was not changed in 3-month-old gastritis, but, it was markedly decreased in 6-month-old gastritis. The decrease in the content and the synthetic activity of macromolecular mucous GP in 6-month-old gastritis were significantly normalized by 3 weeks administration of sofalcone. The histochemical study also supported the therapeutic effect of sofalcone. These findings suggest that the therapeutic effect of sofalcone on experimental gastritis is closely associated with increased mucus synthesis.

Animals↗
PubMed1996

Distribution of inflammation and atrophy in the stomach of Helicobacter pylori-positive and -negative patients with chronic gastritis.

OBJECTIVES: To investigate the extent of inflammation and atrophy in the stomach of Helicobacter pylori-positive and -negative patients with chronic gastritis. METHODS: Endoscopy with biopsies from the lesser curvatures of the antrum, angulus, middle body, and the greater curvature of the middle body of the stomach was performed in 59 patients with histologically confirmed chronic gastritis. The extent of atrophic gastritis was assessed endoscopically as well histologically. H. pylori status was assessed by histology as well as enzyme-linked immunosorbent assay. The histological severity of chronic and acute inflammation, glandular atrophy, and intestinal metaplasia was assessed according to the Sydney system. RESULTS: In H. pylori-positive patients, H. pylori was evenly distributed throughout the stomach when the extent of atrophic gastritis was limited to the antrum and the lesser curvature of the body, but disappeared from the antrum of patients with more extensive atrophic gastritis. The severity of acute and chronic inflammation at the greater curvature of the body increased with the extension of atrophic gastritis. In H. pylori-negative patients, the severity of chronic inflammation at the greater curvature of the body was significantly higher in patients with extensive atrophic gastritis than in those with a lesser extent of atrophic gastritis. CONCLUSION: At the greater curvature of the body, the development of atrophy is closely associated with the increase in the severity of inflammation, which is more marked in H. pylori-positive patients.

Adolescent↗
PubMed1988

Campylobacter pylori--associated gastritis and peptic ulcer disease in children.

Specimens obtained at gastric biopsies performed for suspected acid peptic disease in patients 5 through 17 years of age were retrospectively reviewed for the presence of Campylobacter pylori (CP), a gram-negative bacillus associated with chronic gastritis and peptic ulcer disease in adults. Of 98 patients who underwent antral biopsy (the most reliably colonized site in the stomach), 40 had chronic gastritis histologically. Of those 40 patients, 22 (55%) had CP present on the gastric surface. None of the 58 patients without gastritis present in biopsy specimens had CP. The gastritis in children with CP was more severe than in those without the organism: 86% of those with moderate gastritis and 92% of those with severe gastritis had CP. Eight patients with duodenal ulcers and one patient with a gastric ulcer had CP on biopsy. Among those patients without CP, only one had a duodenal ulcer and eight had gastric ulcers. An additional nine patients found to have CP on gastric fundic biopsy were identified, for a total of 31 patients with CP identified by either antral (22) or fundic (nine) biopsy. Initial resolution of symptoms with standard acid-antagonist therapy was noted in the 25 of 31 CP(+) patients so treated, but a high relapse rate was noted within one to two years in the patients who also had gastritis and duodenal ulcer. These findings support a strong association between CP colonization of the stomach and the presence of chronic gastritis and duodenal ulcer disease in children.

Adolescent↗
PubMed1998

The role of the HLA-DQA1 gene in resistance to atrophic gastritis and gastric adenocarcinoma induced by Helicobacter pylori infection.

BACKGROUND: It has been suggested that immunogenetic factors for susceptibility or resistance to disease caused by Helicobacter pylori exist in the host. To examine host genetic factors that increase the risk of gastric adenocarcinoma among H. pylori-infected persons, the HLA-DQA1 locus was examined in patients with gastric adenocarcinoma. METHODS: Eighty-two gastric adenocarcinoma patients and 167 unrelated controls were examined for H. pylori infection and HLA-DQA1 genotyping. In addition, serum pepsinogen A (PGA) and pepsinogen C (PGC) values and the PGA/PGC ratio, which have been characterized as markers of gastric mucosal atrophy, also were analyzed. RESULTS: Of the 167 controls, 121 were H. pylori positive (+) and 46 were H. pylori negative (-). All H. pylori (-) individuals had normal endoscopic and histologic findings. Among the 121 H. pylori (+) controls, 36 had superficial gastritis and 85 had atrophic gastritis. The allele frequency of DQA1*0102 was significantly lower in the H. pylori (+) atrophic gastritis group than in the H. pylori (+) superficial gastritis and H. pylori (-) normal control groups. In addition, the allele frequency of DQA1*0102 also was significantly lower in the H. pylori (+) intestinal type gastric adenocarcinoma group than in the H. pylori (-) normal control, H. pylori (+) superficial gastritis, and H. pylori (-) diffuse type gastric adenocarcinoma groups. Serum PGA and PGC values and the PGA/PGC ratio did not differ significantly among HLA-DQA1 genotypes; however, the PGA/PGC ratio was significantly lower in the H. pylori (+) atrophic gastritis and H. pylori (+) intestinal type gastric adenocarcinoma groups than in the H. pylori (-) normal control and H. pylori (+) superficial gastritis groups. CONCLUSIONS: The DQA1*0102 allele may contribute to resistance against H. pylori-associated gastric atrophy and its association with intestinal type gastric adenocarcinoma, whereas the absence of DQA1*0102 may be a host genetic risk factor for H. pylori-associated atrophic gastritis and intestinal type gastric adenocarcinoma.

Adenocarcinoma↗
PubMed1996

Protective factor against progression from atrophic gastritis to gastric cancer--data from a cohort study in Japan.

To investigate the association between atrophic gastritis and gastric cancer and to identify the risk and protective factors for the progression of atrophic gastritis to cancer, we conducted a prospective study on 5,373 subjects with neither cancer nor resected stomach who underwent gastroscopic examination and completed a life-style questionnaire. After an average of 6 years of follow-up, 69 gastric-cancer cases were identified, 65 from the subjects without atrophic gastritis and 4 from the subjects without atrophic gastritis. The presence of atrophic gastritis increased the risk of gastric cancer 2.19-fold, the risk trend increasing with the degree and the extension of atrophy [relative risk (RR) 1.60 for mild atrophy and 2.85 for moderate and severe atrophy]. Among the subjects with atrophic gastritis, family history of gastric cancer (RR 2.27) and a preference for spicy food (RR 1.84) increased the risk and self-administered meal controls, such as portion reduction (RR 0.44) reduction of salty food (RR 0.56) and the change to the consumption of easily digested food (RR 0.57) decreased the risk of gastric cancer. The results of this study suggest that atrophic gastritis increases the risk of gastric cancer but that dietary modification prevents the progression from atrophic gastritis to gastric cancer, regardless of pre-cancerous lesions.

Adult↗
PubMed1988

Lymphocytic gastritis--relationship to Campylobacter pylori infection.

The existence of a distinctive form of chronic gastritis characterized by marked infiltration of the surface and pitlining epithelium by mature T lymphocytes has been confirmed. Seventeen cases were identified amongst 382 patients with active chronic gastritis (4.5 per cent). The cases with lymphocytic gastritis had significantly higher counts of intraepithelial lymphocytes than sex and age-matched controls drawn from a series of patients with the usual form of active Type B chronic gastritis. Furthermore, the lymphocytic gastritis group exhibited unusual endoscopic findings, namely erosions and 'raised lesions', in the body of the stomach. Such appearances have been previously described as 'varioliform' gastritis. Only seven of the patients (41 per cent) had C. pylori-positive biopsies, compared with over 90 per cent in the generality of active chronic gastritis, but all but two of the eleven cases tested had serological evidence of C. pylori infection. While the pathogenesis of this condition is unclear, the histological resemblance to coeliac disease suggests that lymphocytic gastritis might also represent an abnormal response to a local antigen to which the patient has become sensitized. It is possible that this antigen is C. pylori.

Adult↗
PubMed2006

[Gastritis from a histological point of view].

Since the rediscovery of spiral-shaped gastric bacteria in 1983 by Warren and Marshal numerous detailed facts have enlarged our knowledge base for a better understanding of gastritis. The WHO classified Helicobacter as a class 1 carcinogen. Helicobacter plays a role in many diseases of the upper GI tract (gastric and duodenal ulcer, MALT lymphoma, and gastric cancer). Knowledge of the interaction between bacterium and host led to an improvement of the diagnosis of gastritis. Unfortunately endoscopy, histology, and patient's symptoms do not correlate with each other. Therefore, gastritis is a purely histological diagnosis. A histological diagnosis always needs to be accompanied by an etiological cause of the inflammation. Only when this information is given a clinical consequence can be drawn from a histological diagnosis. In Germany the so-called ABCD scheme of gastritis is widely used (A: autoimmune gastritis, B: bacterial gastritis, C: chemical reactive gastritis, D: other forms of gastritis). At least two antrum and two corpus biopsies (matrix diagnostics) are necessary to reach representative tissue with an acceptable probability. If less than these four (minimal standard) biopsies are taken, the histological diagnosis will remain uncertain.

Bacterial Infections↗
PubMed1997

Differing degree and distribution of gastritis in Helicobacter pylori-associated diseases.

Infection with Helicobacter pylori (H. pylori) causes gastritis, and may be associated with gastric and duodenal ulcers and also with such malignant diseases as MALT lymphoma and gastric carcinoma. In order to determine whether there are differences in the degree and distribution of gastritis, each patient with H. pylori gastritis only (n = 50) was matched for sex and age with four patients, one each with H. pylori-associated duodenal ulcer, gastric ulcer, gastric carcinoma or MALT lymphoma. From each patient, two biopsies were taken from the antrum and two from the corpus for histopathological examination of H. pylori gastritis. The median summed gastritis score decreases in the following order: antrum: gastric ulcer > duodenal ulcer > gastritis alone > carcinoma > MALT lymphoma, and corpus: gastric ulcer > carcinoma > MALT lymphoma > gastritis alone and duodenal ulcer. We conclude that the degree and distribution of H. pylori gastritis differs significantly among H. pylori-associated diseases. These differences may explain some of the underlying pathomechanisms associated with H. pylori infection.

Adult↗
PubMed2004

The prevalence of Helicobacter pylori in Japanese children with gastritis or peptic ulcer disease.

BACKGROUND: Although Helicobacter pylori infection is typically acquired in childhood, the role of H. pylori infection in gastroduodenal diseases in childhood remains to be defined. The purpose of this study was to evaluate the prevalence of H. pylori infection in children with gastritis, duodenal ulcer, and gastric ulcer. METHODS: This was a retrospective analysis of 283 Japanese children (mean age, 11.5 years) with non-nodular gastritis ( n = 73), nodular gastritis ( n = 67), duodenal ulcer ( n = 100), and gastric ulcer ( n = 43). H. pylori status was based on biopsy tests. Clinical symptoms at the time of endoscopy were analyzed with regard to a possible association with the infection. RESULTS: The prevalence of H. pylori in non-nodular gastritis, nodular gastritis, duodenal ulcer, and gastric ulcer was 28.8%, 98.5%, 83.0%, and 44.2%, respectively. H. pylori was significantly linked to duodenal ulcer and gastric ulcers in the age group of 10-16 years, but not in the age group of 9 years and under. In children with H. pylori infection, nodular gastritis was observed in 26.3% of gastric ulcer patients and in 74.7% of duodenal ulcer patients ( P < 0.001). H. pylori infection was significantly associated with the prevalence of anemia ( P < 0.05). CONCLUSIONS: H. pylori is the most important causal factor for the development of duodenal ulcer in childhood. While H. pylori infection appears to be a risk factor in gastric ulcer, other causes are responsible for most cases. Nodular gastritis is the most common type of H. pylori gastritis in childhood. Chronic infection with H. pylori is associated with anemia.

Adolescent↗
PubMed1990

Lymphocytic gastritis in patients with celiac sprue or spruelike intestinal disease.

A distinctive form of gastritis, characterized by lymphocytic infiltration of pit epithelium, has recently been described in association with evidence of Campylobacter pylori infection. We have evaluated simultaneous small bowel and gastric biopsies from 22 patients with diarrhea or malabsorption, all of which showed small bowel changes characteristic of sprue or spruelike disease. In 10 of 22 patients, striking lymphocytic gastritis was identified. Cases positive for lymphocytic gastritis had a mean of 46.5 lymphocytes per 100 epithelial cells, compared with a mean of 3.5 in normal gastric controls and 5.1 in abnormal controls, including cases with Campylobacter gastritis. Concurrent small bowel biopsies had a mean of 47.2 lymphocytes per 100 epithelial cells. Cases without lymphocytic gastritis had means of 10.8 and 39.9 lymphocytes per 100 gastric and intestinal epithelial cells, respectively. Campylobacter organisms were identified in only 1 of the 10 patients with lymphocytic gastritis and in 3 of the 12 patients without lymphocytic gastritis. Intraepithelial lymphocytes in small bowel and stomach were positive for the antibody MT-1, indicating a T-cell infiltrate at both sites. These findings suggest that lymphocytic gastritis may occur as a manifestation of celiac sprue or spruelike disease and that the lymphocytic infiltration of celiac sprue may affect gastric epithelial mucous cells.

Biopsy↗
PubMed1986

Chronic antral gastritis in duodenal ulcer. Natural history and treatment with prostaglandin E1.

The natural history of chronic antral gastritis in relation to the healing of duodenal ulcer and its response to treatment, if any, are unknown. We performed a double-blind controlled trial using an oral prostaglandin E1, misoprostol, in 229 patients with active duodenal ulcer randomized to receive placebo (n = 76), misoprostol 200 micrograms (n = 77), or misoprostol 300 micrograms (n = 76), q.i.d. orally. Healing of duodenal ulcer was assessed biweekly up to 12 wk by endoscopy, during which procedures at least two antral and two fundal biopsy specimens were taken. The activity and the degree of chronic inflammation of gastritis, as assessed histologically by the infiltration of polymorphs and chronic inflammatory cells, respectively, was graded blindly by two pathologists as nil, mild, moderate, or severe. Before treatment, 99% of patients had chronic antral gastritis and 1.5% had chronic fundal gastritis. In the placebo group, healed duodenal ulcer was associated with significantly (p less than 0.01, life table analysis) higher incidence of improvement of the activity of the antral gastritis (nil or mild as endpoint) than unhealed ulcer (30% vs. 4% at week 8). Irrespective of whether duodenal ulcer was healed or unhealed, significantly (p less than 0.01) more patients on misoprostol (50% at week 8) showed improvement (nil or mild as endpoint) than the placebo group. The degree of chronic inflammation of the antral gastritis showed similar significant changes in favor of misoprostol. Smoking and alcohol intake had no significant effect on the improvement of chronic antral gastritis. In conclusion, healing of duodenal ulcer was associated with improvement of the activity of chronic antral gastritis, which, as shown for the first time, could be further enhanced by a therapeutic agent--prostaglandin E1.

Adult↗
PubMed2003

Enterococcus gastritis.

Helicobacter pylori infection is the most common cause of gastritis with its associated sequelae. Gastritis secondary to other bacteria is rare. This report describes Enterococcus-associated gastritis in a 59-year-old diabetic man. Nine months after receiving treatment for H. pylori-associated gastritis, he underwent endoscopy to confirm H. pylori eradication and to evaluate the status of previously seen ulcers. Mucosal biopsy specimens revealed severe active but focal gastritis adjacent to gram-positive coccobacilli in short to long chains with no H. pylori. Culture grew an Enterococcus similar to E. hirae and E. durans. No treatment was given, and endoscopy done 2 months later showed complete resolution of the gastritis and absence of H. pylori or enterococci. Our patient's gastritis represents a previously undescribed manifestation of Enterococcus infection. It is possible that the presence of NSAID gastric mucosal injury and diabetes predisposed this individual to the development of transient Enterococcus gastritis.

Enterococcus↗
PubMedDate not supplied

Helicobacter pylori may cause "reflux" gastritis after gastrectomy.

Patients with "reflux" gastritis after gastrectomy suffer from a variety of symptoms, and this type of gastritis may sometimes compromise the quality of life of these patients. Since Helicobacter pylori is considered to be one of the most important pathogenetic factors in gastritis, the association between H. pylori and reflux gastritis was investigated in this study. A total of 145 patients with gastrectomy were entered into the study. Five biopsy specimens from the gastric remnant were taken at upper gastrointestinal endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. Fifty-two patients (36%) demonstrated H. pylori infection. The prevalence of H. pylori was significantly higher in patients who had a partial gastrectomy, and it was significantly lower in patients who had undergone gastrectomy more than 4 years previously. The histologic gastritis score in patients with H. pylori infection was significantly higher. Furthermore, H. pylori was eradicated in patients with some symptoms of gastritis and no bile reflux to the residual stomach at endoscopy; in these patients the symptoms were relieved and the histologic gastritis score decreased significantly. In conclusion, possible involvement of H. pylori is suspected in the pathogenesis of "nonreflux" gastritis after gastrectomy.

Aged↗
PubMed2001

Atrophic gastritis and intestinal metaplasia in Japan: results of a large multicenter study.

BACKGROUND: This study evaluated the relationship between Helicobacter pylori infection, atrophic gastritis and intestinal metaplasia in Japan. MATERIALS AND METHODS: This was a multicenter study performed in 21 centers in Japan. A total of 2455 individuals were enrolled. H. pylori status was determined by validated ELISAs. Atrophic gastritis was diagnosed by histology, endoscopy with Congo Red dye scattering or the Kimura-Takemoto endoscopic classification. RESULTS: Atrophic gastritis increased from 9.4% in those less than 20 years of age to > 70% in those aged 60 or older and was strongly associated with H. pylori infection. The overall prevalence of atrophic gastritis in H. pylori infection was 82.9% (1272/1534) compared with 9.8% (90/921) among uninfected (OR = 44.8; 95% CI = 34.7-57.8). Intestinal metaplasia was present in 43.1% (542/1258) of H. pylori positive persons compared with 6.2% (51/823) among the uninfected (OR = 11.5; 95% CI = 8.5-15.5). Atrophic gastritis in H. pylori positive Japanese was very high in the younger generation (38.5% in those aged 20 or less and 58.5% in those 21-30). CONCLUSIONS: Atrophic gastritis and intestinal metaplasia were strongly associated with H. pylori and not with aging. The fall in prevalence of H. pylori in Japan has not been associated with a corresponding fall in the prevalence of atrophic gastritis among those with H. pylori infection. The high prevalence of the precursor lesion, atrophic gastritis with intestinal metaplasia, among those with H. pylori infection suggests that the risk of development of early gastric cancer will continue to remain high in Japan.

Adult↗
PubMed2000

Clinical usefulness of microsatellite instability for the prediction of gastric adenoma or adenocarcinoma in patients with chronic gastritis.

To assess a role of microsatellite instability (MSI) in the development of gastric adenocarcinoma or adenoma from chronic gastritis, we analysed mutations of five microsatellite loci in gastritis, adenoma and adenocarcinoma retrospectively. Gastric mucosa was biopsied from the same area in each patient at different periods and examined for MSI. Only one of 55 patients with chronic gastritis revealed MSI-H phenotype and the other 54 patients showed microsatellite stable (MSS) phenotypes. In six of 17 patients with gastric adenoma or well-differentiated adenocarcinoma, MSI-positive phenotypes were demonstrated. Interestingly, all of six patients showing MSI, including three high-level MSI (MSI-H) cases and three low-level (MSH-L) cases, had already revealed MSI at the stage of chronic gastritis. In two of three MSI-H cases, the identical MSI patterns had been observed at the stage of gastritis 1.5-7 years before the final diagnosis of adenocarcinoma. The adjacent gastritis mucosa within 10 mm from the carcinoma demonstrated MSI as well. MSI was not found in any of 35 patients with Helicobacter pylori infection, but found in one of 30 patients without infection. Moreover, two of three cases of gastric adenoma or well-differentiated adenocarcinoma with MSI-H at the stage of chronic gastritis showed no evidence of Helicobacter pylori infection throughout the observation periods. These results indicate that MSI in biopsy specimens at the stage of chronic gastritis may predict the risk of the progression to adenoma and well-differentiated adenocarcinoma, and that Helicobacter pylori infection itself may not induce MSI directly in the gastric mucosa.

Adenocarcinoma↗
PubMed1996

The prevalence of Helicobacter pylori infection and types of gastritis in diabetic patients. The Kraków Study.

UNLABELLED: There is no unequivocal data on the prevalence of Helicobacter pylori (Hp) and different types of gastritis in diabetic patients. The aim of this study was to define the prevalence of Hp infection, chronic active gastritis and reactive gastritis in diabetics and the effect of autonomic neuropathy (AN) as evaluated in four cardiovascular tests. Gastroscopy was performed on 139 patients with symptoms related to upper alimentary tract disorders--39 with diabetes mellitus, including 11 with insulin-dependent diabetes mellitus (IDDM) and 28 with non-insulin-dependent diabetes mellitus (NIDDM) and 100 patients without diabetes. The presence of Hp and gastritis was analysed in 3 biopsies. Hp infection was significantly less frequent (P < 0.001) in diabetics (30%, 12/39) than in non-diabetics (68%, 68/100). The prevalence of chronic active gastritis in diabetic patients was 41% (16/39), whereas among the controls it was 71% (71/100) (p < 0.01). In diabetics with AN Hp infection there was less frequent prevalence (29%, 5/17) than in diabetics without AN (35%, 5/14), (NS). Compared with non-diabetics Hp infection was less frequent in patients with diabetes and AN (p < 0.01), and in patients without AN (p < 0.05). In diabetics reactive gastritis was significantly more frequent (22%, 8/36) than in non-diabetics (3%, 3/100) (p < 0.01). Reactive gastritis is regarded as less sensitive to Hp infection. CONCLUSIONS: 1. Hp seems to play a minor role in the pathology of the upper alimentary tract in diabetes mellitus than in the general population. 2. The lower prevalence of Hp infection may result from AN and from a higher frequency of reactive gastritis.

Adolescent↗
PubMed1987

Association of Campylobacter pylori on the gastric mucosa with antral gastritis in children.

We investigated the presence of Campylobacter pylori colonization of the gastric mucosa and of histologic evidence of gastritis in a prospective study of 71 consecutive children undergoing upper gastrointestinal tract endoscopy and gastric biopsies because of gastrointestinal symptoms. Two tissue samples from the gastric antrum were obtained from 67 of the 71 children (mean age [+/- SD], 11.4 +/- 3.8 years). One sample was evaluated for evidence of gastritis and stained with silver to detect organisms morphologically resembling campylobacter. The second sample was cultured for C. pylori, and a portion was used to perform a urease-screening test for the presence of C. pylori. Antral gastritis was diagnosed histologically in 18 of 67 patients. C. pylori was identified by both culture and silver staining on the antral mucosa in 7 of 10 patients with unexplained gastritis (primary gastritis) but in none of 8 patients with gastritis associated with an identifiable underlying cause (secondary gastritis). C. pylori was not identified in any of the 49 cases with normal histologic features. The urease-screening test was positive in only three of six patients with a positive culture for C. pylori. Duodenal ulcers were diagnosed by endoscopy in five patients. Each of the five had C. pylori on the antral mucosa, but organisms were not identified on the duodenal mucosa. We conclude that the presence of C. pylori on the antral mucosa is specifically associated with primary antral gastritis and may also be associated with primary duodenal ulceration.

Adolescent↗