The relationship of gastrin, pepsinogen, and Helicobacter pylori in erosive reflux esophagitis]

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection is known as a major cause of atrophic gastritis and is associated with serum gastrin, pepsinogen, and gastric acid secretion. There is still a controversial association between gastroesophageal reflux disease and H. pylori infection. This study was designed to investigate the relationship among serum gastrin, pepsinogen, and H. pylori infection in the erosive reflux esophagitis (ERD) patients. METHODS: Patients who were diagnosed as ERD by one gastroenterologist at the Kangnam St. Mary's hospital were prospectively enrolled. The persons without ERD in the control group were matched for age and sex. We examined the gastrin, pepsinogen I (PG I), PG II, PG I/II ratio, and H. pylori infection. RESULTS: Forty five patients were enrolled in ERD group and 66 persons in control group. The H. pylori infection rate in ERD group was lower than that in the control group (11.1% vs. 43.9%, p<0.001). PG I/II ratio in ERD group was higher than that in the control group (7.0+/-3.1 vs. 5.3+/-2.6, p=0.003). The PG II (p=0.016) and gastrin (p=0.029) in ERD group were lower than those in the control group. BMI in ERD group was higher than that in the control group (24.5 vs. 23.1 kg/m2, p=0.013). CONCLUSIONS: The H. pylori infection rate in ERD group was lower and PG I/II ratio was higher than that in the control group. Reflux esophagitis is thought to be reversely associated with the atrophy of gastric mucosa.     

Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population.

A seroepidemiologic study of the prevalence of Helicobacter pylori infection in Japan was performed, and the relationship between serum pepsinogen I and II levels (markers of gastritis and gastric atrophy) and H. pylori infection was investigated. Four hundred and eighteen asymptomatic children and adults were studied. The prevalence of anti-H. pylori immunoglobulin G antibody increased with age. For persons born after 1950, the frequency of H. pylori infection increased at approximately 1% per year; for those born before 1950 the prevalence was high (70%-80%) and relatively constant. Serum pepsinogen I and II levels were significantly higher in H. pylori-infected volunteers than in H. pylori-uninfected volunteers [51.6 +/- 3 vs. 42.9 +/- 2 ng/mL (P less than 0.05) for pepsinogen I; 16.0 +/- 1 vs. 7.5 +/- 0.8 ng/mL (P less than 0.001) for pepsinogen II]. The ratio of pepsinogen I to pepsinogen II was significantly lower in H. pylori-infected volunteers (3.5 +/- 0.2) than in uninfected volunteers (6.3 +/- 0.3; P less than 0.001). The apparent decrease in prevalence of H. pylori accompanying the Westernization of Japan may eventually be accompanied by a reduction in the frequency of atrophic gastritis, the precursor lesion of the epidemic form of gastric carcinoma, and ultimately result in a decrease in the incidence of gastric carcinoma in Japan.     

Interleukin 1beta polymorphisms increase risk of hypochlorhydria and atrophic gastritis and reduce risk of duodenal ulcer recurrence in Japan

BACKGROUND & AIMS: Interleukin-1 beta (IL-1beta) polymorphisms are associated with increased risk of gastric cancer in whites. This study aimed to examine effects of these polymorphisms on gastric acid secretion, atrophic gastritis, and risk of peptic ulcer in Japan. METHODS: We determined IL-1B-511/-31 and IL-1RN genotypes and measured gastric juice pH, serum pepsinogen (PG) I and II levels, and gastritis and atrophy scores in Helicobacter pylori-positive patients with gastritis only, gastric ulcers, or duodenal ulcers (DUs), and H. pylori-negative controls. RESULTS: In the H. pylori-positive group, subjects with the proinflammatory IL-1B-511 T/T genotype had the highest atrophy and gastritis scores, the highest median gastric juice pH, and the lowest median serum PG I/PG II ratios. Although gastric juice pH significantly increased and serum PG I and PG I/PG II ratios significantly decreased in the IL-1B-511 T/T genotype group with age, no such age-dependent changes were observed in the C/C genotype group. Changes in the C/T genotype group were intermediate. In the H. pylori-negative group, the IL-1 loci had no effect on any of the physiologic or morphologic parameters. Carriage of IL-1RN allele 2 significantly protected against DU disease while the IL-1B-511 T/T genotype significantly protected against DU recurrence in patients older than 60 years. CONCLUSIONS: Proinflammatory IL-1beta polymorphisms are associated with hypochlorhydria and atrophic gastritis in Japan. The effects are dependent on H. pylori infection and become more significant with advancing age. This may explain the high incidence of gastric cancer in Japan and also the age-dependent decrease in DU recurrence in infected subjects.     

Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa

BACKGROUND: Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU). AIMS: We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions. PATIENTS: A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study. METHODS: Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa (Heliobacter pylori infection was determined only by histology). RESULTS: The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex (p = 0.046), Heliobacter pylori-positive chronic gastritis (p = 0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease (p < 0.001), duodenal ulcer (p < 0.001), and duodenal bulb deformity and scarring in endoscopy (p < 0.001), but not with age (p = 0.7) nor use of nonsteroidal anti-inflammatory drugs (p = 0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1-2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4-36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3-0.8). CONCLUSIONS: In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.     

Serum pepsinogen levels and their influencing factors： A population-based study in 6990 Chinese from North China

AIM: To explore the essential characteristics of serum pepsinogen (PG) levels in Chinese people, by analyzing the population-based data on the serum levels of PG I and II and the PG I/II ratio, and their influencing factors in Chinese from North China. METHODS: A total of 6990 subjects, who underwent a gastric cancer screening in North China from 1997 to 2002, were collected in this study. Serum pepsinogen levels were measured by enzyme-linked immunosorbent assay (ELISA). H pylori status was determined by histological examination and H pylori-IgG ELISA. The cut-off point was calculated by using receiving operator characteristics (ROC) curves. Factors linked to serum PG I/II ratio were identified using a multivariate logistic regression. RESULTS: The serum PG I and PG II levels were significantly higher in males than in females (95.2 microg/L vs 79.7 microg/L, P < 0.01; 12.1 microg/L vs 9.4 microg/L, P < 0.01), PG I/II ratio was significantly lower in males than in females (7.9 vs 8.3, P < 0.01). The PG I/II ratio decreased significantly in the aged groups following the progression of gastric mucosa from normal to non-atrophic and atrophic lesions (10.4, 8.8, and 6.6, respectively). The serum PG I and II levels were significantly higher in patients with H pylori infection than in those without H pylori infection (88.7 microg/L vs 81.4 microg/L, P < 0.01; 11.4 microg/L vs 8.4 microg/L, P < 0.01), while the PG I/II ratio was significantly lower in patients with H pylori infection than in those without H pylori infection (7.7 vs 9.6, P < 0.01). For patients with atrophic lesions, the area under the PG I/II ROC curve was 0.622. The best cut-off point for PG I/II was 6.9, with a sensitivity of 53.2%, and a specificity of 67.5%. Factors linked to PG I/II were sensitive to identified PG using a multinomial logistic regression relying on the following inputs: males (OR: 1.151, 95% CI: 1.042-1.272, P = 0.006), age > or = 61 years (OR: 1.358, 95% CI: 1.188-1.553, P = 0.000), atrophic lesion (OR: 2.075, 95% CI: 1.870-2.302, P = 0.000), and H pylori infection (OR: 1.546, 95% CI: 1.368-1.748, P = 0.000). CONCLUSION: The essential characteristics of serum PG levels in Chinese are significantly skewed from the normal distribution, and influenced by age, sex, gastric mucosa lesions and H pylori infection. PG I/II ratio is more suitable for identifying subgroups with different influence factors compared with PG I or PG II alone.     

Long-term strict monitoring of plasma ghrelin and other serological markers of gastric diseases after Helicobacter pylori eradication

We report on a case of chronic atrophic gastritis in which the serological markers of gastric diseases were strictly monitored for 2 years after successful Helicobacter pylori (H. pylori) eradication. A 31-year-old man with upper abdominal pain was diagnosed as having H. pylori infection. Laboratory examination revealed low serum levels of pepsinogen (PG) I, low PG I/II ratio, and low plasma levels of ghrelin. Upper gastrointestinal endoscopy revealed severe corpus-dominant atrophic gastritis. H. pylori eradication therapy was performed. Successful eradication was confirmed three months later by the 13C urea breath test. Decreased serum PG II levels and an increased serum PG I/II ratio were detected a week after completion of the eradication therapy. The serum anti-H. pylori IgG titer decreased to less than 75% of the baseline level by 24 weeks after completion of the eradication therapy. On the other hand, the plasma levels of total and active ghrelin showed no marked changes after successful eradication therapy. This is the first report of long-term follow-up of changes of the plasma ghrelin levels after H. pylori eradication therapy, the observations suggesting that reduction of plasma ghrelin levels cannot be achieved merely by H. pylori eradication, without resolution of the gastric atrophy.     

Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis

OBJECTIVE: Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan. METHODS: A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio. RESULTS: H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it. CONCLUSIONS: These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.     

Helicobacter pylori eradication in the healing of atrophic gastritis: a one-year prospective study

OBJECTIVE: Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. MATERIAL AND METHODS: Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58+/-12.6 years (mean+/-SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. RESULTS: Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). CONCLUSIONS: Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.     

Size of the peptic ulcer in Helicobacter pylori-positive patients: association with the clinical and histological characteristics

OBJECTIVE: Based on a large trial of Helicobacter pylori-positive peptic ulcer patients, we studied whether the size of the ulcer, along with other clinical and histological characteristics, has any effect on healing. We also studied the clinical and endoscopic characteristics associated with size of the peptic ulcer. MATERIAL AND METHODS: A total of 333 consecutive patients with H. pylori infection and peptic ulcer were enrolled (mean age 54.8+/-12.7 years). Location of the ulcer was recorded by gastroscopy and the presence of H. pylori was assured by rapid urease test, histology and by serum H. pylori IgG and IgA antibody measurement. The diameter of the ulcer was measured by placing the opened biopsy forceps (7 mm) beside it. Biopsy specimens were examined in accordance with the Sydney system. RESULTS: Mean size of the peptic ulcer was 13.2+/-8.3 in corpus, 11.3+/-5.3 in antrum, 13.8+/-7.8 in angulus, 9.5+/-5.3 in prepylorus and 9.2+/-4.7 mm in duodenum (duodenal versus gastric type; p<0.05). Average size of the ulcers was 9.4+/-5.3 mm in patients with Forrest III type and 11.5+/-6.8 in other types (p<0.05). Patients who were >or=50 years of age, currently smoking, or who had corpus-predominant chronic gastritis or atrophic gastritis, had larger ulcers than others. Size of index ulcers, successful eradication of H. pylori and the presence of atrophic gastritis were independent factors for healing. The odds ratio was 11.5 (95% CI 3.3-40.5; p<0.01) for eradication of H. pylori, 3.5 (95% CI 1.1-11.2; p<0.05) for size of the index ulcer (10 mm) and 3.4 (95% CI 1.2-9.8; p<0.05) for atrophic gastritis versus no atrophy. CONCLUSIONS: Size of the peptic ulcer, successful H. pylori eradication and atrophic gastritis were independent factors for the healing of peptic ulcers. A number of clinical and endoscopic variables (age, current smoking, corpus-predominant gastritis, Forrest classification) were associated with size of the peptic ulcer in H. pylori-positive patients.     

Histological changes of gastric atrophy and intestinal metaplasia after Helicobacter pylori eradication]

BACKGROUND/AIMS: Long-term Helicobater pylori infection results in atrophic gastritis and intestinal metaplasia, and increases the risk of gastric cancer. However, it is still controversial that eradication of H. pylori improves atrophy or metaplasia. Therefore, we investigated histological changes after the H. pylori eradication in patients with atrophy or metaplasia. METHODS: One hundred seven patients who received successful eradication of H. pylori infection in Hanyang University, Guri Hospital from March 2001 to April 2006, were enrolled. Antral biopsy was taken before the eradication to confirm the H. pylori infection and grade of atrophy or metaplasia by updated Sydney System. After a certain period of time, antral biopsy was repeatedly taken to confirm the eradication and investigate histological changes of atrophy or metaplasia. RESULTS: Mean age of the patients was 55.3+/-11.3, and average follow-up period was 28.7+/-13.9 months. Endoscopic diagnosis included gastric ulcer, duodenal ulcer, non-ulcer antral gastritis. Atrophy was observed in 41 of 91 and their average score was 0.73+/-0.92. After the eradication of H. pylori, atrophy was improved (0.38+/-0.70, p=0.025). However, metaplasia which was observed in 49 of 107, did not significantly improve during the follow-up period. Newly developed atrophy (7 of 38) or metaplasia (18 of 49) was observed in patients who without atrophy or metaplasia initially. Their average scores were slightly lower than those of cases with pre-existing atrophy or metaplasia without statistical significance. CONCLUSIONS: After the eradication of H. pylori infection, atrophic gastritis may be improved, but change of intestinal metaplasia is milder and may take longer duration for improvement.     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

The relationship between gastric emptying determined by the breath test and H. pylori

BACKGROUND/AIMS: Helicobacter pylori infection has been implicated in atrophic gastritis and gastric ulcer disease. However, the relationship between gastric emptying and Helicobacter pylori infection is still unclear. METHODOLOGY: One hundred and two consecutive patients with functional dyspepsia were enrolled in this study (53 Helicobacter pylori positive and 49 negative). Gastric emptying was determined using both the 13C-octanoic acid breath test and the paracetamol absorption test. For grading gastric atrophy, the biopsy samples and serum pepsinogen I/II ratio were used. The relationship between gastric emptying, Helicobacter pylori infection and atrophy grade was investigated. RESULTS: There was no significant difference in all gastric emptying parameters between Helicobacter pylori positive and negative patients. However, in Helicobacter pylori positive subjects, pepsinogen I/II ratio correlated with atrophy grade, and it also correlated with all parameters of gastric emptying. Especially in the half-emptying time, an important parameter, there was significant correlation with the pepsinogen I/II ratio (R = -0.39, p < 0.01). This finding implies that gastric emptying is delayed according to the degree of gastric atrophy. CONCLUSIONS: Gastric emptying was not delayed simply according to advanced age, but according to the advance in gastric atrophy.     

Plasma ghrelin concentration correlates with the levels of serum pepsinogen I and pepsinogen I/II ratio--a possible novel and non-invasive marker for gastric atrophy

BACKGROUND/AIMS: Ghrelin, a novel growth-hormone-releasing peptide, has been reported to be localized mainly in the A-like cells in the gastric fundic mucosa. With the extension of gastric inflammation caused by H. pylori infection, gastric mucosal atrophy extends from the antrum to the corpus, which is the predominant site of localization of the ghrelin-producing A-like cells. The present study was designed to investigate the correlation between the plasma ghrelin levels and the extent of gastric mucosal atrophy in patients with chronic gastritis caused by H. pylori infection. METHODOLOGY: Sixty-nine patients with dyspeptic symptoms were enrolled for the study. Of these, 41 patients were confirmed to become negative for H. pylori after therapy to eradicate the infection. The other 28 patients were diagnosed as positive for H. pylori infection. Blood samples were collected from all the patients after 12 hours of fasting, before upper gastrointestinal endoscopy was performed. The plasma levels of total and active ghrelin, as well as the serum levels of pepsinogen I (PGI) and pepsinogen II (PGII) were measured by radioimmunoassay. Based on endoscopic assessment, the atrophic changes in the gastric mucosa were classified as open-type atrophy or closed-type atrophy. RESULTS: There were no significant differences in the plasma total and active ghrelin levels between H. pylori-positive and H. pylori-eradicated (negative) patients. The serum levels of PGI correlated well with the plasma levels of total ghrelin (p<0.01, r=0.38) and active ghrelin (p<0.05, r=0.29). The ratio of serum PGI to PGII level (PG I/II ratio) also correlated well with the plasma level of total ghrelin (p<0.05. r=0.31) and active ghrelin (p<0.05, r=0.27). The plasma levels of total as well as active ghrelin were significantly decreased in patients with low PG levels as compared with those in patients with high PG levels (PGI > 70 ng/mL or PGI/II >3.0). The plasma levels of total as well as active ghrelin were also significantly decreased in patients with endoscopically diagnosed open-type atrophy as compared with those in patients with endoscopically diagnosed closed-type atrophy (p < 0.01), especially in the H. pylori-eradicated cohorts. CONCLUSIONS: The plasma levels of ghrelin, which correlated well with the serum levels of PGI as well as the PGI/II ratio, decreased with increasing extent of gastric mucosal atrophy, suggesting that it could be a potentially useful non-invasive marker for chronic atrophic gastritis.     

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.     

Systemic and local immune responses against Helicobacter pylori urease in patients with chronic gastritis: distinct IgA and IgG productive sites

BACKGROUND: Helicobacter pylori urease is a major target for immune responses among various bacterial components in H pylori infected patients. AIMS: To analyse the relation between systemic and local humoral immune responses to H pylori urease and grades of chronic gastritis. PATIENTS: Seventy five patients with chronic gastritis associated with H pylori infection were classified into three groups (grade I, superficial gastritis; II, atrophic gastritis, quiescent; or III, atrophic gastritis, active). METHODS: Anti-H pylori urease specific antibodies in the serum, gastric juice, and biopsy specimens were determined by ELISA or western blotting analysis. The sites for H pylori urease and its specific antibody producing B lymphocytes were confirmed by immunohistochemical analysis. RESULTS: In the sera of patients with grade I gastritis, weak IgG but relatively strong IgG responses to H pylori urease were observed; dominant strong IgG responses were detected in grade II gastritis. In grade III gastritis, significant IgG and IgA responses were obtained. A similar pattern of IgA and IgG responses was detected in gastric juice and tissue. H pylori urease specific, antibody producing B cells were not found in the gastric mucosa of patients with grade I gastritis despite the presence of such B cells in the duodenal bulb. Specific B cells were observed in the gastric mucosa of patients with grade II and III gastritis with atrophy. CONCLUSIONS: Purified H pylori urease, together with localisation of its specific antibody producing B cells, are useful for serological testing and histopathological analysis for determining the stage of chronic gastritis and studying the pathogenesis of H pylori infection.     

Two distinct aetiologies of cardia cancer; evidence from premorbid serological markers of gastric atrophy and Helicobacter pylori status

BACKGROUND: Non-cardia gastric adenocarcinoma is positively associated with Helicobacter pylori infection and atrophic gastritis. The role of H pylori infection and atrophic gastritis in cardia cancer is unclear. AIM: To compare cardia versus non-cardia cancer with respect to the premorbid state of the stomach. METHODS: Nested case-control study. To each of 129 non-cardia and 44 cardia cancers, three controls were matched. Serum collected a median of 11.9 years before the diagnosis of cancer was tested for anti-H pylori antibodies, pepsinogen I:II and gastrin. RESULTS: Non-cardia cancer was positively associated with H pylori (OR 4.75, 95% CI 2.56 to 8.81) and gastric atrophy (pepsinogen I:II <2.5; OR 4.47, 95% CI 2.71 to 7.37). The diffuse and intestinal histological subtypes of non-cardia cancer were of similar proportions and both showed a positive association with H pylori and atrophy. Cardia cancer was negatively associated with H pylori (OR 0.27, 95% CI 0.12 to 0.59), but H pylori-positive cardia cancer showed an association with gastric atrophy (OR 3.33, 95% CI 1.06 to 10.5). The predominant histological subtype of cardia cancer was intestinal and was not associated with gastric atrophy compared with the diffuse subtype ((OR 0.72, 95% CI 0.19 to 2.79) vs (OR 3.46, 95% CI 0.32 to 37.5)). Cardia cancer in patients with atrophy had an intestinal: diffuse ratio (1:1) similar to non-cardia cancer (1.9:1), whereas cardia cancers in patients without atrophy were predominantly intestinal (7:1). CONCLUSION: These findings indicate two aetiologies of cardia cancer, one associated with H pylori atrophic gastritis, resembling non-cardia cancer, and the other associated with non-atrophic gastric mucosa, resembling oesophageal adenocarcinoma. Serological markers of gastric atrophy may provide the key to determining gastric versus oesophageal origin of cardia cancer.     

Duodenal erosions after eradication of Helicobacter pylori infection

BACKGROUND: There is interest in the development of GERD after Helicobacter pylori eradication. In contrast, the development of duodenal erosions after therapy has received scant attention. Patients were examined after eradication of H pylori infection to determine the frequency of post-therapy duodenal erosions (primary outcome) and whether there was a relation between development of duodenal and esophageal erosions. Additionally, factors were searched for that would identify patients at increased risk for duodenal erosions. METHODS: A single-center, endoscopist-blinded, observational study was conducted of 196 patients in whom H pylori was eradicated. The presence of esophageal or duodenal erosions was evaluated 4 weeks and 6 months after eradication. Serum gastrin and pepsinogen I (PG I) and II (PG II) levels were also determined for 83 patients entering the study during its final year. RESULTS: Multiple small duodenal erosions developed in 8.6% of patients after H pylori eradication and were more common in patients with pre-eradication duodenal ulcer (27.8%) compared with those with gastric ulcer (6.7%) or atrophic gastritis (1.4%) (p < 0.05). Duodenal erosions were associated with high levels of PG I before and after eradication. The frequency of duodenal erosions decreased over time (3.1% by 6 months). CONCLUSION: Duodenal erosions occur after H pylori eradication and appear to be related to duodenal ulcer and increased PG I levels, both of which are associated with increased acid secretion. Measurement of PG I may help to identify patients who have duodenal erosions develop after H pylori therapy for studies of the pathogenesis of these lesions.     

Pernicious Anemia and Helicobacter pylori Infection in Japan: Evaluation in a Country with a High Prevalence of Infection

Objectives : To evaluate the degree of gastritis and the prevalence of Helicobacter pylori in Japanese patients with pernicious anemia (PA). Methods : Histological assessment for mucosal atrophy and inflammation was performed in gastric biopsy specimens taken from 24 Japanese patients with PA and from 24 age- and sex-matched controls. The prevalence of H. pylori was evaluated by Giemsa staining and serum IgG antibodies. Serum gastrin and pepsinogens were determined by ra-dioimmunoassay. Results : All patients with PA had severe fundic atrophic gastritis, and 17 (71%) also had antral atrophic gastritis. Thirteen (54%) of 24 age- and sex-matched controls had fundic atrophic gastritis, and 15 (62%) also had antral atrophic gastritis. Mucosal inflammation was identified in the fundus of all 24 patients and in 15 (62%) controls and in the ant rum of 22 (92%) patients and 16 (67%) controls. H. pylori was not detected by Giemsa staining or serum IgG antibodies to H. pylori in any patient with PA but was present in 16 (67%) controls. Serum gastrin levels were significantly higher, and serum pepsinogen I, II, and the I/II ratio were significantly lower in patients than in controls ( p < 0.001). Conclusions : Our results confirm that H. pylori infection is infrequent in PA and is unlikely to be a factor in producing type A gastritis in PA.     

H pylori infection among 1000 southern Iranian dyspeptic patients

INTRODUCTION H pylori is a major cause of gastritis and peptic ulcer disease (PUD), and has been implicated in the development of gastric malignancy[1-3]. The prevalence of H pylori, a worldwide infection, varies greatly among countries and among populati…     

Associations of food-cobalamin malabsorption with ethnic origin, age, Helicobacter pylori infection, and serum markers of gastritis

OBJECTIVES: Food-cobalamin malabsorption is common in patients with low cobalamin levels. However, characterization of affected subjects has been limited. The aim of this study was to analyze demographic and gastric data in a large study population. METHODS: Data were collected prospectively in 202 subjects (43 volunteers and 159 patients) who underwent the egg yolk-cobalamin absorption test (EYCAT). H. pylori status was determined in 167 of the subjects, serum gastrin and antiparietal cell antibody in 158 and pepsinogen (PG) I and PG II levels in 133. RESULTS: Latin American and black patients had lower EYCAT results than did white or Asian-American ones (p = 0.0001) and had severe food-cobalamin malabsorption (EYCAT < 1%) more often (p = 0.0001). Age correlated inversely with EYCAT results (p = 0.02). H. pylori infection was associated with food-cobalamin malabsorption (p = 0.0001), especially with severe malabsorption where 29/37 subjects (78.4%) were infected. Malabsorption was also associated with higher gastrin levels (p = 0.0001) and lower PG I levels (p = 0.01) and PG I:PG II ratios (p = 0.0001). Multivariate analysis showed that ethnic origin, gastrin levels, H. pylori infection and, to a lesser extent, age were independently associated with the EYCAT results. CONCLUSIONS: Latin American and black patients have food-cobalamin malabsorption more often than do white and Asian-American patients. This association is independent of the malabsorption's association with H. pylori infection, markers of gastritis, such as gastrin, and older age. The patterns of gastric tests suggest that malabsorption may be due to diverse mechanisms, not just atrophic gastritis. The possible role of H. pylori infection in many cases of severe food-cobalamin malabsorption also suggests avenues of treatment and prevention.