Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy

BACKGROUND: Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection. AIMS: To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients. PATIENTS/METHODS: A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence. RESULTS: Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection. CONCLUSIONS: Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.     

Relations between circulating gastrin and endocrine cell proliferation in the atrophic gastric fundic mucosa

It has been suggested that gastrin may be a causative factor in the proliferation of gastric fundic mucosal endocrine cells, as seen in the Zollinger-Ellison syndrome and in atrophic gastritis with hypergastrinemia of antral origin. In the present study, morphometrically determined densities of endocrine cells in fundic mucosal biopsy specimens were related to basal levels of serum gastrin in 10 normal controls and 60 patients with achlorhydric fundic atrophic gastritis, of which 45 had pernicious anemia (5 with fundic mucosal carcinoid) and 15 had atrophic gastritis without pernicious anemia. The densities of fundic mucosal endocrine cells were positively related to the levels of serum gastrin (atrophic gastritis, rs = 0.65; atrophic gastritis and normal controls, rs = 0.72). The highest levels of serum gastrin were found in patients with carcinoid tumors (mean, 1659.3 pmol/l), followed by those in patients with focal hyperplasias (cluster formation) of endocrine cells (mean, 503.2 pmol/l) and those in patients without focal hyperplasias (mean, 304.4 pmol/l) (p = 0.03 and p = 0.04, respectively).     

Biomarkers in Various Types of Atrophic Gastritis and Their Diagnostic Usefulness

Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (¹³C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.     

A close relationship between Helicobacter pylori infection and gastric xanthoma.

BACKGROUND: Although the pathogenesis of gastric xanthoma (GX) remains unclear, an association of GX with atrophic gastritis has been reported. Helicobacter pylori is closely related to atrophic gastritis. The aim of this study was to investigate the relationship among GX, H. pylori, and atrophic gastritis. METHODS: Sixty-seven patients with GX were assessed for H. pylori infection by serum anti-H. pylori IgG antibody, in addition to the rapid urease test, culture, and histologic examination using biopsy specimens of the antrum and corpus. The findings were compared with 67 age- and sex-matched control subjects without GX. The distribution of atrophic gastritis was assessed endoscopically. The severity of atrophic gastritis was determined endoscopically and histologically. Serum pepsinogen (PG) levels were also measured. Immunohistochemical staining of GX samples for H. pylori antigen was performed. H. pylori clinical isolates from patients with GX and controls were assessed for cagA by means of polymerase chain reaction. RESULTS: The prevalence of H. pylori was significantly higher in patients with GX than in controls (94% and 72%, respectively). A significantly more extensive atrophic gastritis was present in patients with GX, as determined endoscopically and histologically, than in controls. Serum PG-I levels and the PG-I/PG-II ratio were significantly lower in the GX group than in the control group. H. pylori antigens were frequently identified in the cytoplasm of xanthoma cells in H. pylori-positive specimens of GX (54 of 63 specimens, 86%), whereas no immunoreactivity for H. pylori antigens was detected in H. pylori-negative specimens of GX. There was no significant difference in the positive rate of cagA between the two groups. CONCLUSIONS: Our results identified a close relationship among H. pylori infection, GX, and atrophic gastritis. A proportion of GXs may be provoked by H. pylori infection.     

Atrophic Gastritis Serum Levels of Amidated Gastrin-17 and Pepsinogen I in Atrophic Gastritis: An Observational Case-Control Study

Background: Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed nonendoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing. Methods: The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method. Results: A low S-PGI (<25 μg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori -associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori -related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; CI 95%: 81%-97%) had a low SPGI and/or a low S-G-17prand with positive H. pylori serology. Such low values were found in 3 of the 44 control patients (7%; CI 95%: 0%-14%). Conclusions: Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori .     

Positive serum antibody and negative tissue staining for Helicobacter pylori in subjects with atrophic body gastritis

Helicobacter pylori is rarely found in gastric biopsy specimens from individuals with atrophic gastritis of the body mucosa. To determine if subjects with atrophic body gastritis have evidence of previous infection with H. pylori, immunoglobulin G antibody to H. pylori was measured by enzyme-linked immunosorbent assay in sera of 399 Finnish subjects. In 124 subjects, multiple biopsy specimens from body and antrum had been evaluated for the presence of H. pylori by Giemsa staining. Antibody correlated well with H. pylori staining except in the subgroup with atrophic body gastritis, in whom the prevalence of seropositivity (86%) was significantly greater than the prevalence of positive staining (33%) (P less than 0.001). Twenty-five subjects had positive antibody and negative staining. This group had a significantly higher prevalence of atrophic body gastritis (80%), lower maximal acid output, lower serum pepsinogen I levels, and higher serum gastrin concentrations than did seropositive subjects with H. pylori. These data suggest that most patients with atrophic body gastritis, despite having a low incidence of current overt infection, have been infected with H. pylori at some point in their lives.     

Seroepidemiology of gastritis in Japanese and Dutch working populations: evidence for the development of atrophic gastritis that is not related to Helicobacter pylori.

Serological markers of gastritis, like pepsinogen A, pepsinogen C, gastrin, and Helicobacter pylori antibodies, can be used to explore the state of the gastric mucosa in populations with contrasting cancer risks. A decreasing pepsinogen A:C ratio and an increasing serum gastrin are known to reflect an increasing severity of atrophic corpus gastritis, which is a precursor of gastric cancer. In 723 subjects (without gastroduodenal surgery) from Japanese (n = 225) and Dutch (n = 498) working populations, which had a similar composition of age (mean 48 years), sex (male to female ratio 6:1), and type of occupation, fasting serum samples were analysed for IgG antibodies to H pylori, pepsinogen A, pepsinogen C, and gastrin in the same laboratory. H pylori infection was significantly more prevalent in the Japanese than in the Dutch (74.7% and 31.3%); as was a very low pepsinogen A, indicative of severe mucosal atrophy (4.4% and 1.6%). Among subjects with and without severe mucosal atrophy the H pylori seropositivity rate was similar. Between the Japanese and the Dutch there were significant differences in mean gastrin (31.8 and 13.4 pmol/l) and pepsinogen A:C ratio (1.7 and 2.9). These intercountry differences were as great for H pylori negative subjects (gastrin: 23.7 and 10.3 pmol/l, pepsinogen A:C ratio: 2.4 and 3.2) as for H pylori positive subjects (gastrin: 34.6 and 20.1 pmol/l, pepsinogen A:C ratio: 1.5 and 2.5). The intercountry difference in gastrin nearly disappeared after stratification into categories of pepsinogen A:C ratio. In conclusion, the intercountry differences in pepsinogen A:C ratio and gastrin reflect a higher prevalence of mild and severe mucosal atrophy of the corpus in the Japanese than in the Dutch, both among H pylori positive and negative subjects. Thus, these findings suggest that in the Japanese the development of atrophic gastritis is in part unrelated to H pylori.     

Expression of bcl-2 in Autoimmune and Helicobacter pylori-Associated Atrophic Gastritis

Chronic atrophic gastritis can be induced eitherby H. pylori or by an autoimmune process. The proteinproduct of bcl-2, which is a protooncogene, blocksapoptosis. Aberrant bcl-2 expression has been found in 68% of atrophic gastritis patients. The aimof this study was to compare bcl-2 expression in 20autoimmune atrophic gastritis patients to that in 20 H.pylori-associated atrophic gastritis patients. Twenty patients with H. pylori antral gastritisbut without atrophy served as controls. The bcl-2expression was assessed by immunohistochemical stainingof gastric biopsies, using mouse anti-human bcl-2 monoclonal antibodies. Autoimmune atrophicgastritis patients were younger, mainly females, with asignificantly higher serum gastrin level than the H.pylori-associated atrophic gastritis group (P < 0.001). The bcl-2 was expressed in 10/20 (50%)of autoimmune atrophic gastritis patients, in 9/20 (45%)of H. pylori-associated atrophic gastritis patients (P= 0.73), and in 2/20 (10%) of controls. There was no correlation between bcl-2expression and the presence of intestinal metaplasia (P= 0.35). Our findings confirm that H. pylori-associatedatrophic gastritis and autoimmune atrophic gastritis are two different conditions, but with equalexpression of bcl-2. Excessive expression of bcl-2 isfound only in atrophic gastritis, but not in H. pyloriantral gastritis without atrophy.     

Gastric endocrine cell hyperplasia and carcinoid tumors in pernicious anemia

Endoscopic screening in 123 patients with pernicious anemia (PA) yielded 4 patients with solitary and 1 patient with multiple gastric carcinoid tumors. Quantitative histologic studies of multiple standardized biopsy specimens showed a significantly increased number of fundic mucosal argyrophil endocrine cells in 40 patients with PA when compared with 15 patients with simple fundic atrophic gastritis (p = 0.002) or 8 normal controls (p = 0.0001). Patients with simple atrophic gastritis had increased numbers of fundic mucosal argyrophil cells as compared with normal controls (p = 0.02). A significant difference was also noticed in the number of antral mucosal argyrophil cells between patients with PA and normal controls (p = 0.01), but not between patients with PA and patients with simple atrophic gastritis. It is concluded that, in addition to having hyperplasia of gastric mucosal argyrophil endocrine cells, patients with PA run an increased risk of developing gastric argyrophil cell carcinoid tumors, which should be regarded as potentially malignant.     

Barrett's esophagus is characterized by the absence of Helicobacter pylori infection and high levels of serum pepsinogen I concentration in Japan

Background and Aim:  It has been reported that patients with Barrett's esophagus (BE) may have gastric acid hypersecretion. Serological markers such as serum pepsinogen or gastrin have been used to estimate the gastric secretory function. The aim of this study was to compare the serum pepsinogen and gastrin concentrations in view of Helicobacter pylori infection status between BE patients and the controls.
Methods:  Thirty-six patients with long-segment BE were enrolled in this study. Three age- and sex-matched controls were assigned to each patient. Serum pepsinogen and gastrin concentrations were measured by radioimmunoassay and H. pylori infection was determined by histology and serum IgG antibodies.
Results:  Helicobacter pylori infection was present in 4 of 36 patients (11%) with BE and in 80 of 108 controls (74%), being less prevalent in BE patients than in the controls ( P  < 0.0001). When examined in the H. pylori -negative subjects, both the serum pepsinogen I and pepsinogen II concentrations in BE patients were significantly higher than those in the controls (mean pepsinogen I:BE 51.0 ± 14.0 ng/mL vs control 38.9 ± 13.5 ng/mL, P  = 0.0012; mean pepsinogen II:BE 10.8 ± 4.0 ng/mL vs control 7.9 ± 2.0 ng/mL, P  = 0.0097). There was no significant difference in the serum gastrin levels between BE patients and the controls irrespective of the H. pylori infection status.
Conclusions:  Most of the Japanese BE patients are characterized by the absence of H. pylori infection and high levels of serum pepsinogen. Determination of the serum pepsinogen level in combination with the H. pylori infection status could be a useful serological marker for BE screening.     

Dyslipidemia and H pylori in gastric xanthomatosis

AIM: To investigate the relationship among gastric xanthomatosis (GX), H pylori, dyslipidemia, and gastritis in Korea, a well-known H pylori endemic area. METHODS: A total of 771 patients who had undergone gastroduodenoscopy by one endoscopist were included in this study. Among them, 54 patients with GX were assessed for H pylori infection and their endoscopic characteristics and serum lipid profiles. The findings were compared with 54 age-and sex-matched control subjects without GX. RESULTS: The prevalence of GX was 7% (54/771) with no sex difference. GX was mainly single (64.8%) and located in the antrum (53.7%). The mean diameter was 7 ± 3 mm. Mean body mass index (BMI) of patients with GX was 23.1 ± 2.8 and no one was above 30. Compared with the controls, lipid profiles of GX group showed significantly lower HDL-cholesterol (48.8 ± 12.3 vs 62.9 ± 40.5, P = 0.028) and higher LDL-cholesterol (112.9 ± 29.9 vs 95.9 ± 22.4, P = 0.032). The level of total serum cholesterol, triglyceride and the existence of dyslipoproteinemia were not related to the presence of GX. However, GX showed a close relationship with endoscopically determined atrophic gastritis and histologic severity (24/53, 44.4% vs 8/54, 14.8%, P = 0.0082). H pylori infection and bile reflux gastritis were not significantly related with GX. CONCLUSION: The prevalence of GX is 7% and it may be an increasing entity in Korea. Moreover, dyslipidemia and atrophic gastritis are found to be related to GX, but H pylori infection is not.     

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

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

Role of Helicobacter pylori and autoimmunity in serological atrophic corpus gastritis in a Dutch primary care community

BACKGROUND: Atrophic corpus gastritis predisposes to vitamin B12 deficiency and gastric cancer. Little is known about the seroprevalence of atrophic corpus gastritis in the general population of Western Europe. AIM: To investigate the seroprevalence of atrophic corpus gastritis in a West-European primary care community in relation to Helicobacter pylori infection and autoimmunity. METHODS: Nine hundred and ninety-seven consecutive persons attending one general practice were asked to participate in the study by completing a questionnaire and donating fasting blood. Gastrin, pepsinogen A and C, and antibodies to H. pylori and parietal cells were measured by well-validated immunological methods. Criteria for serological atrophic corpus gastritis were pepsinogen A < 17 microg/l, pepsinogen A/C ratio <1.6, and gastrin >100 ng/l. RESULTS: Thirty-four participants (3.4%) fulfilled the serological criteria of atrophic corpus gastritis. Twenty-one of them (62%) and 17 of 34 (50%) age-matched and sex-matched nested controls were H. pylori positive [NS; odds ratio, 1.62 (0.62-4.24)], while 15 of them (44%) and one of 34 controls had antibodies to parietal cells [P < 0.005; odds ratio, 24.0 (3.00-201)]. CONCLUSIONS: The seroprevalence of atrophic corpus gastritis in this primary care community is 3.4%. When compared with controls, the approximate relative risk of having atrophic corpus gastritis was significantly higher (P < 0.025) for antibodies to parietal cells (24.0) than to H. pylori (1.62). In view of the decreasing risk of H. pylori infection in the western world, it is likely that the impact of H. pylori on the development of atrophic corpus gastritis will further diminish.     

Serological comparison of serum pepsinogen and anti-parietal cell antibody levels between Japanese and German patients

BACKGROUND: Atrophic gastritis is more common in Japan than in Germany. The expression of anti-parietal cell antibody has been implicated in the genesis of atrophic gastritis associated with Helicobacter pylori infection. OBJECTIVE: We investigated the difference in serum levels of pepsinogens and in anti-parietal cell antibody expression between Japanese and German patients. METHODS: We recruited 102 Japanese and 46 German patients with dyspepsia. Endoscopic examination detected no localized lesions in the upper gastrointestinal tract of any patients. Anti-parietal cell antibody was investigated by enzyme-linked immunosorbent assay with the purified porcine H+,K+-ATPase fraction and immunohistochemistry. H. pylori infection was diagnosed by the presence of anti-H. pylori antibody, by using the urease test and by histological examination. Serum levels of pepsinogen I and II and of gastrin were measured by a modified radioimmunoassay. RESULTS: Seventy-one Japanese (70%) and 17 Germans (37%) were positive for H. pylori. Serum levels of anti-parietal cell antibody were not significantly different between Japanese and Germans in both H. pylori negative and positive groups. The serum pepsinogen I/II ratio and gastrin levels were altered by H. pylori infection in both populations. Moreover, anti-parietal cell antibody levels were higher in H. pylori-positive patients with low pepsinogen levels than in those with high pepsinogen levels in both populations. CONCLUSIONS: The levels of anti-parietal cell antibody do not differ statistically between Japanese and Germans. Anti-parietal cell antibody might play a role in the progression of atrophic gastritis in both Japanese and German patients.     

Gastric mucosa in female patients with fundic glandular polyps.

To evaluate the characteristics of the gastric mucosa in women with fundic glandular polyps, we examined gastric acid secretion, fasting serum levels of pepsinogen I and gastrin, and gastric histology in 11 female patients with fundic polyps, and compared the results with 30 female controls without endoscopic abnormalities and 50 female patients with gastric foveolar hyperplastic polyps. No significant difference was found in gastric and secretion and fasting serum levels of pepsinogen I and gastrin between the patients with fundic glandular polyps and the control subjects. Histological examination showed that atrophic gastritis was generally not found in the patients with fundic glandular polyps. In contrast, gastric acid secretion and fasting serum levels of pepsinogen I were significantly lower and serum gastrin levels were significantly higher in the patients with foveolar hyperplastic polyps than in the other two groups. Also, patients with foveolar hyperplastic polyps had a higher prevalence and further advanced atrophic gastritis in the fundus than did the other two groups. Our investigations demonstrated that fundic glandular polyps arise from gastric mucosa without atrophic gastritis, whereas foveolar hyperplastic polyps develop from mucosa affected by atrophic gastritis, especially type A gastritis.     

The occurrence and extent of Helicobacter pylori colonization and antral and body gastritis profiles in an Estonian population sample

A series of 143 subjects representing an Estonian urban population was examined for the occurrence and extent (absent, mild, moderate, severe) of Helicobacter pylori colonization in antral and body biopsy specimens (Giemsa staining). These data were correlated with the presence and grade of chronic gastritis (normal, mild, moderate, or severe superficial chronic gastritis; mild, moderate, or severe atrophic gastritis) in the antrum and the body. Gastritis of any grade was found in the antrum and/or the body in 140 (98%) subjects. The overall extent of H. pylori colonization in the whole series did not differ between the antrum and the body. Of 93 subjects with superficial gastritis, H. pylori was found in the antrum and/or the body in 87 (94%) cases. Of 47 subjects with atrophic gastritis in the antrum and/or the body. H. pylori was not found in 12 (25%). In subjects with gastritis the absence of H. pylori either in the antrum or in the body was relatively common (in 30 of 143 subjects). The grade of superficial gastritis showed a highly significantly positive correlation with the extent of H. pylori colonization in the antrum but not in the body. Correspondingly, the grade of atrophic gastritis in the antrum correlated negatively to the grade of colonization. The total absence of H. pylori was particularly associated with the absence of gastritis in the antrum. Conversely, severe body H. pylori colonization was found in subjects who had atrophic antral gastritis, and severe antral colonization in subjects who had at least moderate superficial antral gastritis and who showed a coexistent normal or slight superficial gastritis in the body.(ABSTRACT TRUNCATED AT 250 WORDS)     

Colonization by Helicobacter pylori and its relationship to histological changes in the gastric mucosa in portal hypertension

Abstract In order to investigate the relationship between Helicobacter pylori infection of the gastric mucosa and mucosal changes in portal hypertension, gastric fundic and antral biopsies were obtained from 66 patients with portal hypertension and 49 controls with non-ulcer dyspepsia (NUD). Gastric mucosa from portal hypertensive patients exhibited typical vascular dilatation and congestion, while mild dilatation of lamina propria blood vessels was not uncommon in NUD patients with histological evidence of gastritis. Colonization of the gastric mucosa by H. pylori infection was significantly less in portal hyptertension (51.5%) compared to controls (75.5%; P <0.01). The difference was more apparent in patients with marked vascular dilatation (18.8% colonization) compared to patients with minimal vascular dilatation (66.7%). H. pylori infection was significantly associated with active superficial gastritis ( P <0.001), and with atrophic gastritis ( P <0.001), in both study groups. H. pylori -negative superficial gastritis was significantly more common in portal hypertension (25/66 patients) than in controls (7/49; P <0.05). H. pylori infection was not more common in patients who had undergone repeated sclerotherapy. The results suggest that the gastric mucosa of portal hypertension does not provide a hospitable environment for H. pylori colonization, particularly when mucosal congestion is marked. H. pylori infection does not add significantly to the gastropathy of portal hypertension.     

Antral gastrin cells and serum gastrin in achlorhydria.

Forty-five patients with achlorhydria due to severe atrophic corpus gastritis or gastric atrophy were studied by determination of serum gastrin, histological examination of multiple biopsy from the antrum, and quantitation of gastrin cells revealed by an indirect immunofluorescence technique. In a reference group of 12 persons with normal gastric secretion and without atrophic antral gastritis the mean number of gastrin cells per field of vision was 52 +/- 6.5 (S.E.M.). In a group of achlorhydric patients having normal antral mucosa (n = 24), the serum gastrin levels was 324 +/- 56 pmol/l and the number of gastrin cells was 79.6 +/- 7.5 cells/field of vision. The corresponding values for a group of achlorhydric patients with chronic superficial antral gastritis (n = 11) were 361 +/- 186 pmol/l and 88.0 +/- 14.4 cells/field of vision. In a group of achlorhydric patients with atrophic antral gastritis (n = 10) serum gastrin was 15.0 +/- 3.3 pmol/l, and the number of gastrin cells was 6.2 +/- 3.3 cells/field of vision. Compared to the subjects in the reference group, the number of gastrin cells was significantly higher in the groups of achlorhydric patients with normal or superficially inflamed antral mucosa and significantly lower in achlorhydric patients with atrophic antral gastritis. It is concluded that serum gastrin in general is a good indicator for the presence or absence of antral atrophic gastritis in achlorhydria.     

Serum biomarker tests are useful in delineating between patients with gastric atrophy and normal, healthy stomach

AIM： TO study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa： i.e. those with Helicobacter pylori （H pylori） gastritis or atrophic gastritis, who have a high risk of gastric cancer or peptic ulcer diseases. METHODS： Among 162 Japanese outpatients, pepsinogen Ⅰ （Pg Ⅰ） and Ⅱ （Pg Ⅱ） were measured using a conventional Japanese technique, and the European GastroPanel examination （Pg Ⅰ and Pg Ⅱ, gastrin-17 and H pylori antibodies）. Gastroscopy with gastric biopsies was performed to classify the patients into those with healthy stomach mucosa, Hpylori nonatrophic gastritis or atrophic gastritis. RESULTS： Pg Ⅰ and Pg Ⅱ assays with the GastroPanel and the Japanese method showed a highly significant correlation. For methodological reasons, however, serum Pg Ⅰ, but not Pg Ⅱ, was twice as high with the GastroPanel test as with the Japanese test. The biomarker assays revealed that 5% of subjects had advanced atrophic corpus gastritis which was also verified by endoscopic biopsies. GastroPanel examination revealed an additional seven patients who had either advanced atrophic gastritis limited to the antrum or antrum-predominant H pylori gastritis. When compared to the endoscopic biopsy findings, the GastroPanel examination classified the patients into groups with ＂healthy＂ or ＂diseased＂ stomach mucosa with 94% accuracy, 95% sensitivity and 93% specificity. CONCLUSION： Serum biomarker tests can be used to differentiate between subjects with healthy and diseased gastric mucosa with high accuracy.     

Antral Gastrin Cells and Serum Gastrin in Achlorhydria

Forty-five patients with achlorhydria due to severe atrophic corpus gastritis or gastric atrophy were studied by determination of serum gastrin, histological examination of multiple biopsy specimens from the antrum, and quantitation of gastrin cells revealed by an indirect immunofluorescence technique. In a reference group of 12 persons with normal gastric secretion and without atrophic antral gastritis, the mean number of gastrin cells per field of vision was 52±6.5 (S.E.M.). In a group of achlorhydric patients having normal antral mucosa (n = 24), the serum gastrin level was 324±56 pmol/1 and the number of gastrin cells was 79.6±7.5 cells/field of vision. The corresponding values for a group of achlorhydric patients with chronic superficial antral gastritis (n = 11) were 361±186 pmol/1 and 88.0±14.4 cells/field of vision. In a group of achlorhydric patients with atrophic antral gastritis (n = 10) serum gastrin was 15.0±3.3 pmol/1, and the number of gastrin cells was 6.2±3.3 cells/field of vision. Compared to the subjects in the reference group, the number of gastrin cells was significantly higher in the groups of achlorhydric patients with normal or superficially inflamed antral mucosa and significantly lower in achlorhydric patients with atrophic antral gastritis. It is concluded that serum gastrin in general is a good indicator for the presence or absence of antral atrophic gastritis in achlorhydria.