Presence Of Gastritis Research Articles

Benign gastric polyps: morphological and functional origin.

The most common types of benign gastric polyps are fundic gland polyps, hyperplastic polyps, and adenomas. The aim of this study was to determine on which morphological and functional background benign gastric polyps develop. The study includes 85 consecutive patients with gastric polyps and sex- and age-matched controls without polyps selected at random from a general population sample. The type of polyp was hyperplastic in 52 (61%), fundic gland in 18 (21%), adenoma in 10 (12%), carcinoid in 2 (2%), hamartoma in 2 (2%), and inflammatory fibroid in 1 (1%) of the cases. Routine biopsies from the gastric corpus and antrum were examined for presence of gastritis and H. pylori. Blood samples were analyzed for H. pylori antibodies, H+,K+-ATPase antibodies, gastrin, and pepsinogen I. Patients with hyperplastic polyps had increased P-gastrin concentrations and S-H+,K+-ATPase antibody titers and decreased S-pepsinogen I concentrations with a high prevalence of atrophic corpus gastritis or pangastritis. A similar pattern was observed among patients with adenomas, whereas patients with fundic gland polyps had normal serology and a lower prevalence of gastritis and H. pylori infection than controls. In conclusion, hyperplastic polyps and adenomas are generally associated with atrophic gastritis. Patients with fundic gland polyps seem to have a sounder mucosa than controls. Whereas the risk of malignant gastric neoplasia is increased in patients with hyperplastic polyps or adenomas, this does not seem to be the case in patients with fundic gland polyps.

Gastric adenomas: intestinal-type and gastric-type adenomas differ in the risk of adenocarcinoma and presence of background mucosal pathology.

Gastric adenomas are neoplastic growths characterized by localized, polypoid proliferations of dysplastic epithelium. They frequently arise in stomachs with a background of mucosal atrophy and intestinal metaplasia, and a higher risk of adenocarcinoma elsewhere in the stomach has been reported in patients with gastric adenomas. Additionally, some gastric adenomas themselves demonstrate neoplastic progression to infiltrating adenocarcinoma. However, previous studies have not comprehensively evaluated the background gastric mucosa and risk of adenocarcinoma, particularly in relation to the histologic classification of adenomas as either intestinal-type or gastric-type. We studied 61 gastric adenomas from 51 patients between 1985 and 2001. The adenomas were classified as intestinal-type (containing at least focal goblet cells and/or Paneth cells), gastric-type (lined entirely by gastric mucin cells on PAS/alcian blue stain), or indeterminate. We evaluated the histologic features of both the adenomas (location, multiplicity, degree of dysplasia, presence of adenocarcinoma within the polyp) and the surrounding gastric mucosa (presence of gastritis, intestinal metaplasia, and adenocarcinoma). Gastric adenomas were distributed equally throughout the stomach, were most frequently solitary (82%), and contained adenocarcinoma in nine cases (14.8%). There were 34 intestinal-type adenomas (56%) in 31 patients, 25 gastric-type adenomas (41%) in 18 patients (including 10 patients with familial adenomatous polyposis), and 2 of indeterminate type (3%). Intestinal-type adenomas were significantly more likely than gastric-type adenomas to show high-grade dysplasia (p <0.0001), adenocarcinoma within the polyp (p = 0.016), intestinal metaplasia in the surrounding stomach (p <0.000001), and gastritis (p = 0.002). Patients with intestinal-type adenomas were also more likely to have separate adenocarcinomas (five cases vs 0 cases), although this did not reach statistical significance. Gastric adenomas are rarely truly "sporadic" lesions. In any individual patient complete removal of the adenoma should be performed, and thorough biopsy of the surrounding gastric mucosa is essential to understand the clinicopathologic context of the adenoma.

Helicobacter pylori infection in diabetic patients: prevalence and endoscopic findings

Background: In patients with diabetes mellitus, chronic infections are frequent and severe, due to the impairment of their immune status. However, data on the prevalence of Helicobacter pylori ( H. pylori) infection in diabetics are scanty and contradictory. The aim of our study was to assess the prevalence of H. pylori infection in diabetic patients and to evaluate the association between endoscopic features and H. pylori colonization of the gastric mucosa in diabetes mellitus. Methods: A cross-sectional study of 172 dyspeptic patients (67 diabetics and 105 nondiabetic subjects) was designed. In all cases, an upper gastrointestinal endoscopy was performed, gastroduodenal lesions were noted, and the presence of gastritis and H. pylori was assessed by histopathological examination. Differences between diabetic patients and nondiabetic subjects were evaluated. Results: The difference of H. pylori prevalence between diabetics (37.3%) and nondiabetics (35.2%) was not significant ( P=0.78). Nor did the prevalence of gastritis and peptic ulcer differ significantly between the two groups (59.7% vs. 49.5%, P=0.19; and 32.8% vs. 40.9%, P=0.08, respectively). Studying only H. pylori-positive patients, we found no difference between diabetics and nondiabetics with regard to the prevalence of either gastritis (80% vs. 72.9%, P=0.71) or peptic ulcer (91.8% vs. 76%, P=0.09). Conclusions: Our data do not support an association between H. pylori infection and diabetes mellitus. This is confirmed by the lack of difference between diabetics and nondiabetics with regard to the prevalence of both H. pylori infection and H. pylori-related gastroduodenal disorders.

Determination of Helicobacter pylori cagA, vacA genotypes with real-time PCR melting curve analysis

Objectives: genotypes of Helicobacter pylori are the focus of interest because they play a prominent role in mucosal injury. The purpose of this study was to determine cagA and vacA genotypes of H. pylori using real-time polymerase chain reaction (PCR) method with a double strain DNA binding SYBR Green I.dye, and to compare this with those of two immunohistochemical methods. Methods: forty-three paraffin-embedded biopsy tissue samples were examined by histology, epidermal growth factor receptor (EGFR), proliferating cell nuclear antigen (PCNA) immunohistochemistry and melting curve analysis of real-time PCR. Results: the presence of cagA gene was associated with a significantly higher frequency of gastritis ( P=0.003) than that of vacA gene with intestinal metaplasia ( P=0.045). Significant difference was found between the presence of cagA gene and EGFR expression in intestinal metaplasia cases in comparison with cagA negative samples ( P=0.0418). Statistically significant difference was detected between increased cell proliferation and the presence of gastritis. Conclusions: this method seems to be suitable for H. pylori genotype determination. Sensitivity, speed and simplicity are key areas in the development of PCR assays for H. pylori. Results supported the notion that infection with cagA positive H. pylori strain causes more augmentated cell proliferation in the stomach mucosa.

Non-Helicobacter pylori and non-NSAID peptic ulcer disease in the Japanese population

Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs) are recognized as the major causes of peptic ulcer disease. The status of H. pylori infection in the background population may influence the incidence of H. pylori-negative peptic ulcer disease. To examine the incidence of H. pylori-negative peptic ulcer disease without intake of NSAIDs in Japan. A total of 398 patients who had no eradication therapy for H. pylori prior to this study, including 246 patients with gastric ulcer (GU) and 152 patients with duodenal ulcer (DU), were enrolled. H. pylori status was assessed by rapid urease tests, histological examinations (haematoxylin & eosin stain, Giemsa stain and/or immunostaining) and serum IgG antibody. Two biopsy specimens were taken from the antrum within 3 cm of the pyloric and two from the middle corpus of the stomach, along the greater curvature. Patients were asked a series of questions regarding risk factors, including the use of NSAIDs. The presence of gastritis, gastric atrophy and intestinal metaplasia was examined according to the updated Sydney system. Of the 246 patients with GU, 12 patients (4.9%) were considered to be H. pylori-negative. Of the 152 patients with DU, two patients (1.3%) were considered to be H. pylori-negative. Hence, a total of 14 patients were found to be H. pylori-negative. Nine of them were taking NSAIDs. Consequently, the frequency of H. pylori-negative ulcer without intake of NSAIDs was 1.3%. There was no significant difference in the frequencies of H. pylori-negative patients between the GU and DU groups. The incidence of H. pylori-negative peptic ulcer disease without intake of NSAIDs was very low in the Japanese population.

Effect of cagA status on the sensitivity of enzyme immunoassay in diagnosing Helicobacter pylori-infected children.

The aims of our study were twofold. First, we sought to evaluate in symptomatic children the influence of the Helicobacter pylori genotype on gastritis, abdominal pain, and circulating anti-H. pylori IgG antibodies (anti-H. pylori IgG) or pepsinogen A (PGA) and C (PGC). Additionally, we sought to assess anti-H. pylori IgG, PGA, and PGC patterns in a large cohort (N = 921) of asymptomatic children. In 183 symptomatic children, H. pylori infection and the presence of gastritis were evaluated by histology. In a subgroup of 20 H. pylori-positive children, the H. pylori genotype was evaluated also by polymerase chain reaction. Nine hundred and twenty-one asymptomatic children, aged 11 to 14 years, were studied by anti-H. pylori IgG, PGA, and PGC serum determination. The infection was found in 33 of 183 symptomatic children; among the 20 H. pylori-positive children for which the H. pylori genotype was available, cagA was present or absent in equal percentages. H. pylori infection was associated with more severe gastritis and higher serum levels of anti-H. pylori IgG and PGC but not with abdominal pain. In infected children, higher levels of anti-H. pylori IgG and the presence of abdominal pain were associated with infections caused by cagA-positive strains. In the cohort of 921 asymptomatic children, raised levels of anti-H. pylori IgG, PGA, and PGC were found in approximately 5% of the cases. Infection with cagA-positive H. pylori strains can be associated with increased frequency of reported abdominal pain and higher circulating levels of anti-H. pylori IgG. The serological assessment of H. pylori IgG using H. pylori antigens containing significant amounts of cagA protein may, therefore, underestimate the true prevalence of infection.

Characteristics of intestinal metaplasia in the gastric cardia

OBJECTIVE: Intestinal metaplasia of the gastroesophageal junction is frequently grouped together with Barrett’s esophagus. The area of the gastroesophageal junction is comprised of the distal esophagus and the gastric cardia. The aim of the present study was to assess whether intestinal metaplasia in the distal esophagus and gastric cardia represent two different entities with a different set of risk factors. METHODS: Patients presenting for elective upper endoscopy were enrolled into a prospective study. The presence of gastritis and intestinal metaplasia was evaluated in gastric biopsies taken from the antrum, corpus, and cardia. Barrett’s esophagus was defined by the presence of any length of columnar mucosa above the gastroesophageal junction. RESULTS: Of 302 patients, 50 patients had intestinal metaplasia of the gastric cardia, 73 Barrett’s esophagus, and 116 erosive esophagitis. Men were more prone than women to develop Barrett’s esophagus or erosive esophagitis. Both conditions were also more common among whites than nonwhites. Smoking was particularly common among patients with Barrett’s esophagus. Patients with cardiac intestinal metaplasia did not share these demographic characteristics. The prevalence of daily reflux symptoms, erosive esophagitis, and Barrett’s esophagus was similar among patients both with and without cardiac intestinal metaplasia. However, atrophy and intestinal metaplasia of the gastric antrum and corpus were found more frequently among patients with than without cardiac intestinal metaplasia. CONCLUSIONS: Intestinal metaplasia of the gastric cardia is different from Barrett’s esophagus. Although cardiac intestinal metaplasia is closely associated with signs of gastritis in other parts of the stomach, gastroesophageal reflux disease does not seem to be a risk factor. A diagnosis of Barrett’s esophagus should not be made based on the presence of intestinal metaplasia within the cardiac portion of the gastroesophageal junction.

Characteristics of intestinal metaplasia in the gastric cardia.

Intestinal metaplasia of the gastroesophageal junction is frequently grouped together with Barrett's esophagus. The area of the gastroesophageal junction is comprised of the distal esophagus and the gastric cardia. The aim of the present study was to assess whether intestinal metaplasia in the distal esophagus and gastric cardia represent two different entities with a different set of risk factors. Patients presenting for elective upper endoscopy were enrolled into a prospective study. The presence of gastritis and intestinal metaplasia was evaluated in gastric biopsies taken from the antrum, corpus, and cardia. Barrett's esophagus was defined by the presence of any length of columnar mucosa above the gastroesophageal junction. Of 302 patients, 50 patients had intestinal metaplasia of the gastric cardia, 73 Barrett's esophagus, and 116 erosive esophagitis. Men were more prone than women to develop Barrett's esophagus or erosive esophagitis. Both conditions were also more common among whites than nonwhites. Smoking was particularly common among patients with Barrett's esophagus. Patients with cardiac intestinal metaplasia did not share these demographic characteristics. The prevalence of daily reflux symptoms, erosive esophagitis, and Barrett's esophagus was similar among patients both with and without cardiac intestinal metaplasia. However, atrophy and intestinal metaplasia of the gastric antrum and corpus were found more frequently among patients with than without cardiac intestinal metaplasia. Intestinal metaplasia of the gastric cardia is different from Barrett's esophagus. Although cardiac intestinal metaplasia is closely associated with signs of gastritis in other parts of the stomach, gastroesophageal reflux disease does not seem to be a risk factor. A diagnosis of Barrett's esophagus should not be made based on the presence of intestinal metaplasia within the cardiac portion of the gastroesophageal junction.

Prevalence and etiology of gastroduodenal ulcer in HIV-positive patients: a comparative study of 497 symptomatic subjects evaluated by endoscopy

Objective : In 497 HIV-positive (+) patients with upper digestive tract symptoms, 23 (5%) had gastroduodenal ulcers (GDU) at upper endoscopy. Methods : To establish the causes of GDU in this setting, 16 of these patients who had had comprehensive histological evaluation (group I) were compared with 20 HIV+ subjects with upper gastrointestinal symptoms but without ulcer (group II), and with 16 seronegative patients with GDU (group III). Eighty-one percent of group I subjects and 90% of group II patients had C3 AIDS. The presence of gastritis and Helicobacter pylori , fungi, mycobacteria, viruses (especially cytomegalovirus [CMV] and herpes simplex [HSV]), and parasites was determined in all three groups by histopathological and microbiological studies. Results : The prevalence of chronic active gastritis was 13/16 (81%) in group I, 12/20 (60%) in group II, and 15/16 (94%) in group III. It was associated with H. pylori in group III, and with opportunistic pathogens in groups I and II and with none in group III. H. pylori was detected in 5/16 patients (31%) in group I, in 12/20 (60%) in group II, and 11/16 (69%) in group III. Cytomegalovirus was histologically diagnosed in 8/16 patients (50%) in group I and in 1/20 (5%) in group II. This virus was the only factor shown to be significantly associated with GDU in these cases ( p = 0.0046). Cryptosporidium was found in 2/16 (12.5%) patients in group I, in 1/20 (5%) in group II, and in none in group III. Differences between groups I and II were not statistically significant. No other organisms were observed in the three groups. Conclusions : Gastroduodenal ulcers were infrequent in HIV+ subjects with upper digestive tract symptoms and CMV was the only organism significantly associated with GDU in HIV+ patients. Among HIV+ patients, H. pylori was an uncommon cause of ulcer. Among HIV+ subjects with ulcer, chronic active gastritis was more common than H. pylori and it was associated with other pathogens. Finally, HIV+ patients with GDU should have endoscopic biopsies to detect opportunistic infections, especially CMV, because H. pylori infection is uncommon.

Helicobacter pylori: prevalence, transmission, and serum pepsinogen II concentrations in children of a poor periurban community in Bangladesh.

The aim of this study was to determine the age-specific prevalence of Helicobacter pylori infection in infants and children aged 1-99 months from a poor periurban community in Bangladesh. We also examined the frequency of infection among infants and their 53 immediate family members and evaluated the relationship between infection and fasting serum group II pepsinogen (pepsinogen II) concentration in 76 children. Sixty-one percent of 1-3 month-old infants tested positive for H. pylori; this rate declined steadily to 33% in children aged 10-15 months and then increased to 84% in children aged 5-8 years. The H. pylori infection rate was 2.5 times higher in children with illiterate mothers. No difference in infection rate was detected among the family contacts of infected vs. noninfected infants. H. pylori-infected children had significantly higher serum pepsinogen II concentrations than did noninfected children (P < .001). We conclude that infection with H. pylori is highly prevalent and occurs at an early age. An environmental factor or factors, rather than or in addition to intrafamilial spread of this infection, are important in poor communities of Bangladesh. The higher levels of serum pepsinogen II in H. pylori-positive children might indicate the presence of gastritis in such asymptomatic children.

Helicobacter pylori infection and upper gastrointestinal patholgy in a British immigrant Indian community.

To assess the pattern of upper gastrointestinal pathology and the prevalence of Helicobacter pylori infection in the Southall Indian community. A prospective study of endoscopic findings in 124 Indian and 107 whites from the Southall area. In a separate study blood samples were taken from 100 Indian subjects presenting to a single general practitioner in Southall. The presence of gastritis and H. pylori infection was assessed histologically in Indian and white patients undergoing endoscopy. Serum samples were analysed using a specific enzyme-linked immunosorbent assay (ELISA) for anti-H. pylori immunoglobulin G. In the endoscopic study, Indian and white patients had the same rate of H. pylori infection (52% vs. 43%, respectively) (P= NS). The pattern of upper gastrointestinal pathology was similar in whites and Indians. In the general practice based study 41 subjects were H. pylori seropositive. Seropositivity increased with age (P<0.05). There is no excess of H. pylori-related pathology in Southall immigrant Indians. The similarity of upper gastrointestinal pathology in UK Indian and white patients presenting for endoscopy suggests that the high rates of duodenal ulceration, gastritis and H. pylori infection in India are environmentally rather than racially determined.

Ornithine decarboxylase activity is a marker of premalignancy in longstanding Helicobacter pylori infection.

Longstanding Helicobacter pylori infection may increase the risk of developing gastric adenocarcinoma. The sequence of chronic active gastritis leading to gastritis with atrophy and subsequent intestinal metaplasia is thought to be a key step in gastric carcinogenesis. Ornithine decarboxylase (ODC) activity is increased in some pre-malignant gastrointestinal conditions and is essential for malignant transformation in vitro. To measure ODC activity in the antrum of H pylori infected and non-infected subjects and to relate this to histological abnormalities associated with recent and longstanding H pylori infection. Six antral mucosal biopsy specimens were obtained from 75 patients for detailed histological assessment and measurement of ODC activity. Samples were measured in duplicate and results expressed as median, interquartile range in pmol/mg protein/h. ODC activity was significantly higher in H pylori positive (164, 88-259 pmol/mg/h) than H pylori negative subjects (99.8, 55-158 pmol/mg/h, p = 0.003). However the presence of gastritis, irrespective of the severity of inflammation or activity had no influence on ODC activity. Gastritis with atrophy was associated with increased ODC activity, which was closely related to the severity of the atrophy (p = 0.01). Similarly, ODC activity was significantly increased in subjects with intestinal metaplasia (196, 83-25) compared with those without intestinal metaplasia (111.7, 65-175, p < 0.04). These results indicate that the histological changes associated with longstanding H pylori infection rather than inflammation alone are associated with increased polyamine biosynthetic activity. This may be relevant to H pylori associated gastric carcinogenesis.

Role of luminal ammonia in the development of gastropathy and hypergastrinemia in the rat

Background/Aims: Chronic infection with Helicobacter pylori causes persistent elevations in gastric juice ammonia levels. Thus, we studied the effects of experimentally induced increases in gastric juice ammonia levels on gastric structure and function and gastrin homeostasis. Methods: Rats were fed either normal chow or the diet supplemented (20 g/dL) with ammonium or sodium acetate. Results: Long-term dietary ammonium loading for 2 weeks or longer resulted in a 1.5–2-fold increase in the weight and mucosal thickness of the stomach and proximal duodenum with evidence of mild gastritis and enterochromaffinlike cell hyperplasia. The ammonium-containing diet also induced a significant 2–3-fold increase in both circulating gastrin levels of fed rats and an increase in the postprandial gastrin responses over control values. Antral gastrin levels were also markedly elevated by long-term ingestion of the test diet, which was increased 3–4-fold over control values in fasted animals and less so after meal stimulation. Consistent with these findings, gastrin-specific messenger RNA was increased 2.5–3-fold in the antrum of ammonium fed rats, whereas actin-specific messenger RNA was not affected or decreased. Animals fed a diet supplemented with 20 g/dL sodium acetate sustained modest increases in mucosal thickness and serum and antral gastrin concentration, suggesting that nonspecific gastric injury and inflammation is also a factor that influences G-cell function. Conclusions: Long-term exposure of the antral mucosa to elevated levels of ammonia in the gastric juice in the presence of gastritis, conditions similar to that occurring in subjects infected with H. pylori, seem to be causative factors in the development of G-cell hyperfunction.

Distinct Features of Upper Gastrointestinal Endoscopy in the Newborn

Between January 1987 and December 1990, 293 upper GI endoscopic procedures were performed in 219 neonates &lt;1 month of age. No lesion was found in 57 cases (26%; group 1), whereas esophagitis was present in 158 cases, alone in 45 cases (20.6%; group 2) and associated with gastritis in 113 cases (51.8%; group 3). The association of esophagitis with gastritis seems to be a specific feature of neonates and not older children. The presence of gastritis with esophagitis suggests that a primary peptic mechanism is unlikely to explain all endoscopic findings, although the presence of such a mechanism secondary to esophagitis could contribute to the esophageal lesions. Acute fetal distress was more frequent in group 3 than in the other groups. Symptoms associated with endoscopic lesions in groups 2 and 3 were, respectively, malaise (38 and 42%), hematemesis (4 and 35%), frequent regurgitation (45 and 26%), and difficult feeding and/or failure to thrive (26 and 24%). In Group 3, minor symptoms often led to the diagnosis of severe mucosal lesions, and antireflux therapy elicited prompt relief of clinical symptoms. The causes of neonatal esophagogastritis remain unknown. Wide use of en‐doscopy in the presence of discrete clinical abnormalities is likely to considerably improve the clinical condition of some children in their first days of life.

Distinct Features of Upper Gastrointestinal Endoscopy in the Newborn

Between January 1987 and December 1990, 293 upper GI endoscopic procedures were performed in 219 neonates < 1 month of age. No lesion was found in 57 cases (26%; group 1), whereas esophagitis was present in 158 cases, alone in 45 cases (20.6%; group 2) and associated with gastritis in 113 cases (51.8%; group 3). The association of esophagitis with gastritis seems to be a specific feature of neonates and not older children. The presence of gastritis with esophagitis suggests that a primary peptic mechanism is unlikely to explain all endoscopic findings, although the presence of such a mechanism secondary to esophagitis could contribute to the esophageal lesions. Acute fetal distress was more frequent in group 3 than in the other groups. Symptoms associated with endoscopic lesions in groups 2 and 3 were, respectively, malaise (38 and 42%), hematemesis (4 and 35%), frequent regurgitation (45 and 26%), and difficult feeding and/or failure to thrive (26 and 24%). In Group 3, minor symptoms often led to the diagnosis of severe mucosal lesions, and antireflux therapy elicited prompt relief of clinical symptoms. The causes of neonatal esophagogastritis remain unknown. Wide use of endoscopy in the presence of discrete clinical abnormalities is likely to considerably improve the clinical condition of some children in their first days of life.

Helicobacter pylori-associated gastritis in Kuwait: endoscopy-based study in symptomatic and asymptomatic children.

Information is limited concerning the prevalence of Helicobacter pylori infection in asymptomatic children. Since January 1989, we have endoscoped 60 children for recurrent abdominal pain or for obtaining small-intestinal biopsy (their ages were a mean of 6.6 (range 9 months-13 years); there were 37 boys and 23 girls. Antral biopsies were obtained from all subjects and these were studied for the presence of gastritis and stained for H. pylori using modified Gram's stain. All biopsies were cultured for H. pylori. Children endoscoped for small-intestinal biopsy (n = 18) were used for comparison. Of the 42 children who had abdominal pain, 24 showed histological gastritis and 13 had H. pylori on microscopy (31% H. pylori-associated gastritis). In the compared group, five showed histological gastritis, and all had H. pylori on microscopy (27.7%). Culture was positive in 15; sensitivity was 85.7%. Six children, three pairs of siblings, had H. pylori gastritis supporting environmental etiology. Two had coinfection with intestinal giardiasis. Seven children were treated with daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg) for 6 weeks. In 3 (42.3%) H. pylori colonization cleared with healing of gastritis and resolution of symptoms. These results indicate that H. pylori gastritis is equally prevalent in symptomatic and asymptomatic children (31 and 27.7%, respectively; p > 0.05) in our population. It seems that the combination of oral amoxycillin and tinidazole is a poor choice in the treatment of H. pylori-associated gastritis in Kuwaiti children.

Frequency ofHelicobacter pyloriand Gastritis in Healthy Subjects without Gastrointestinal Symptoms

To investigate the frequency of Helicobacter pylori and gastritis in asymptomatic adults, 30 healthy volunteers underwent upper endoscopy. Biopsy specimens were obtained from the corporeal and antral mucosa of the stomach. The specimens were examined by light microscopy for gastritis and the occurrence of H. pylori. In 12 subjects signs of gastritis were noted at endoscopy, but only in 7 of them was this diagnosis confirmed histologically. No other abnormalities were observed by the endoscopist. Histologic examination was normal in 17 subjects, but in 13 subjects (43%) inflammation was found in the gastric specimens. Ten had inflammation both in the corpus and in the prepyloric specimens, and in six of these subjects H. pylori was discovered. H. pylori was only found in subjects with inflammation in both the corpus and the antrum. Subjects with gastritis were slightly older than subjects with normal gastric mucosa (median age, 47 versus 37 years; not significant). In the group of subjects with gastritis, persons with H. pylori were older than those without (median age, 53.5 versus 36 years; p = 0.05). The results of our study indicate that gastritis is present before colonization with H. pylori occurs. This could imply that H. pylori is not the cause of gastritis but that the presence of gastritis is a prerequisite for colonization of the bacterium in the stomach.

Antral &lt;i&gt;Helicobacter pylori-&lt;/i&gt;Like Organisms in Different States of Gastric Acid Secretion

The frequency of Helicobacter pylori (H.p.) infestation in antral mucosa and the presence of gastritis were investigated in different states of gastric acid secretion. Biopsies were stained by the Warthin-Starry technique and hematoxylin-eosin. Antral H.p. was found in similar frequencies in Zollinger-Ellison syndrome (n = 17; profound acid hypersecretion, associated with duodenal ulcer disease in most cases) and the same number of age-matched controls (35% in each group) whereas H.p. could be detected in 31 out of 33 duodenal ulcer patients (94%). The incidence of H.p. infestation in H2-blocker refractory reflux oesophagitis was low (24%). Treatment of peptic lesions with omeprazole (drug-induced hypochlorhydria) led to a reduction or disappearance of H.p. in 7 out of 10 H.p.-positive patients whereas none of 19 primarily H.p.-negative patients became infected with H.p. during prolonged omeprazole therapy. It is concluded that (1) development of duodenal ulcers (as in gastrinomas) does not necessarily require H.p., and (2) at least in some patients H.p. is reduced in antral mucosa by omeprazole.

Chronic antral gastritis, Lewis(a+) phenotype, and male sex as factors in predicting coexisting duodenal ulcer.

Chronic antral gastritis, Lewis(a+) phenotype (Le(a+)), and male sex are common in patients with peptic ulcer. To approximate the relative risks (RR) and possible interactions of these factors in predicting coexisting active duodenal (DU) or gastric ulcer (GU), a consecutive endoscopic series of 140 ulcer patients and 215 non-ulcer controls was examined. The Lea phenotype (Le(a+) versus Le(a-)) was determined immunohistochemically as binding of Le(a)+-specific monoclonal antibody to surface epithelial secretory mucosubstances in gastric biopsy specimens. The presence versus absence of the gastritis was determined histologically from antral specimens. The RRs of the factors in the prediction of ulcer were approximated as age-adjusted RRs when the risk of ulcer in the absence of the factors--that is, in the absence of gastritis, in female sex and in Le(a-) phenotype--was applied as a base line (RR = 1). A case-control design, logistic linear modelling, and the maximal likelihood method were used in estimation of the risks. The RR of coexisting distal ulcer (DU or pyloric or prepyloric GU) was increased in the presence of gastritis (RR = 10.2), in male sex (RR = 3.0), and in Le(a+) phenotype (RR = 1.8). The RR of proximal ulcer (angular or corpus GU) was increased in the presence of gastritis (RR = 35) but decreased in the presence of male sex (RR = 0.5) and Le(a+) phenotype (RR = 0.7). As predictors of both distal and proximal ulcer, gastritis, sex, and Le(a) phenotype were independent of each other; that is, their joint value in prediction of ulcer is a multiplicand of the marginal risks. Thus, a 50-fold difference in the joint RR could be approximated between the extreme risk groups for distal ulcer--that is, between Le(a+) males with gastritis and Le(-a) females with normal antrum. In a consecutive series of outpatient endoscopies, 45% of females and 8% of males could be categorized to these extreme 'low'- and 'high'-risk groups, respectively. We conclude that sex, Le(a) phenotype, and gastritis are factors that, at least in ordinary outpatient endoscopy material, divide subjects to subgroups with very different risks and probabilities for having coexisting peptic ulcer.

67 CAMPYLOBACTER PYLORT CASTRITIES IN CHILDREN – A COMMON CAUSE OF SYMTOMS?

The aim of this study was to assess the incidence of Campylobacter pylori antibody in a paediatric population and relate this to symptoms, and the presence of gastritis. Three groups were studied. Group I - 51 consecutive symptomatic patients (5-16 years) undergoing upper GI endoscopy. Group II - 51 aged-matched hospital controls with no significant GI symptoms. Group III - 150 well schoolchildren. Specific serum IgG antibodies were measured using a sensitive ELISA technique. Antral biopsies were cultured from all patients in Group I and examined histologically. 20% of patients in Group I had significant titres and in all cases ≥ 1:1,600. C.pylori was present on the gastric mucosa in all of this sub-group and in no other, and histological gastritis was present in all but 2 cases. In contrast only 4% of Group II and 5% of Group III had significant antibody titres and in all cases <1:1,600.