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PubMed2001

[Focal atrophy with stellate scars in children with chronic gastritis associated to Helicobacter pylori. Is this early atrophic gastritis?].

BACKGROUND: Atrophic gastritis has not been described in children in the setting of Helicobacter Pylori infection. METHODS: Gastric biopsies of six children (7 to 11 years old) with history of HpCG and recent therapeutic eradication of H. Pylori, were reviewed. In the 6 H. Pylori was documented with histology, culture, direct visualization and/or serology before treatment. Cases were compared with five biopsies of age-matched patients showing none of the above-mentioned clinical data. All the biopsies were formalin-fixed, paraffin embedded and stained with hematoxilin-eosin, Masson trichrome and reticulin stain. RESULTS: The biopsies of the six treated patients showed variable-in-size stellate-shaped spots of glandular loss replaced by dense connective tissue with few inflammatory cells. The fibrous tissue showed a central area of scarring and radially oriented spikes extending to adjacent interglandular tissue, more evident with the Masson trichrome stain. Density of inflammatory cells in the lamina propria was variable. H. Pylori organisms were consistently absent. On the reticulin stain the atrophic areas showed coarser and compacted reticulin. Stellate scars were not present in the five controls. CONCLUSIONS: Small foci with fibrous scars may be found in children with long standing HpCG, perhaps as an early sequel of it. We hypothesize that if the chronic gastritis-gastric atrophy process is a continuum, these stellate scars may be representing the very beginning of the multifocal atrophic gastritis usually seen in adult patients.

Atrophy↗
PubMed2002

Role of anti-parietal cell antibody in Helicobacter pylori-associated atrophic gastritis: evaluation in a country of high prevalence of atrophic gastritis.

BACKGROUND: Helicobacter pylori plays an important part in the progression of atrophic gastritis; however, markers for predicting the progression of atrophic gastritis remain unidentified. We investigated the relation between the degree of atrophic gastritis and the amount of anti-parietal cell antibodies (APCAs) present. METHODS: In 219 Japanese patients, APCA was investigated by enzyme-linked immunosorbent assay (ELISA) and by Western blotting. The grade of corpus atrophy was estimated by histology and serum pepsinogen levels. Serum levels of pepsinogen were evaluated by radioimmunoassay. RESULTS: Helicobacter pylori infection did not affect the APCA levels determined by ELISA. Long-term administration of proton-pump inhibitors and H. pylori eradication did not influence the levels of APCAs. However, in H. pylori-positive patients, the levels of APCA determined by ELISA were statistically higher in patients with severe atrophy than in those with mild atrophy as determined histologically (0.67+/-0.48 versus 0.45+/-0.40; A492, mean+/-s, P=0.01) and serologically by pepsinogen levels (0.66+/-0.51 versus 0.44+/-0.40. P=0.002). The levels of pepsinogen I/II ratio were correlated with APCA levels only in the H. pylori-positive group. Western blotting showed that major antigen was identical with the beta-subunit of H+,K+-ATPase. CONCLUSION: APCA plays an important part in the progression of corpus atrophy after H. pylori infection.

Adolescent↗
PubMed1997

Histological classification of gastritis and Helicobacter pylori infection: an agreement at last? The International Workshop on the Histopathology of Gastritis.

An international workshop has assessed and revised the Sydney System for the reporting of gastritis. Much of the original approach was retained including division into acute, chronic and special forms, and grading of chronic inflammation, polymorph activity, atrophy, intestinal metaplasia and H. pylori density into mild, moderate and marked categories. Visual analog scales have been introduced as a simple guide to grading. The four biopsy sites have been changed to optimize detection of H. pylori, and supplemented by a fifth biopsy from the incisura angularis, the site which is most likely to yield premalignant changes. Chronic gastritis is classified into non-atrophic and atrophic forms with the latter divided into autoimmune (diffuse corpus atrophy) and multifocal. Histological reporting of gastritis should take into account the topographical pattern (antral or corpus predominant), and the final diagnostic term should ideally combine morphology and etiology to maximize the clinical value of gastric biopsy diagnosis.

Gastritis↗
PubMed2000

Induction of follicular gastritis following postthymectomy autoimmune gastritis in Helicobacter pylori-infected BALB/c mice.

Helicobacter pylori is the major causative agent of chronic antral gastritis and is thought to be involved in the pathogenesis of mucosa-associated lymphoid tissue lymphoma (MALToma) developing in the human stomach. The aim of this study was to clarify whether corporal autoimmune gastritis (AIG), which is known to decrease acidity due to destruction of parietal cells, predisposes mice to H. pylori infection, thereby leading to MALToma-like pathology. BALB/c mice in which AIG had been induced by thymectomy 3 days after birth (AIG mice) were used. The AIG mice were orally administered mouse-adapted H. pylori at the age of 6 weeks and were examined histologically and serologically after 2 to 12 months. The results were compared with those obtained from uninfected AIG mice and infected normal mice. Germinal centers were induced in the corpus in 57% of the H. pylori-infected AIG mice, which elicited anti-H. pylori antibody responses in association with upregulation of interleukin-4 (IL-4) mRNA. In these mice, parietal cells remained in the corpus mucosa. These findings were in contrast to those with the uninfected AIG mice: fundic gland atrophy due to disappearance of parietal cells associated with upregulation of gamma interferon, but not IL-4, mRNA and no germinal center formation in the corpus. These observations suggest that AIG alters the infectivity of H. pylori, leading to MALToma-like follicular gastritis, at an early stage after H. pylori infection.

Animals↗
PubMed1995

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.

Adult↗
PubMed1994

Distinct profiles of gastritis in dyspepsia subgroups. Their different clinical responses to gastritis healing after Helicobacter pylori eradication.

BACKGROUND: A contribution of Helicobacter pylori gastritis to the pathogenesis of non-ulcer dyspepsia (NUD) remains uncertain. METHODS: Administration of an appropriate clinical questionnaire followed by endoscopy allowed us to select, among 139 outpatients with dyspepsia, 87 non-ulcer dyspepsia patients with more severe and group-distinctive symptoms, 35 of whom were classified as having ulcer-like (ULD). 38 as dysmotility-like (DLD), and 14 as reflux-like dyspepsia (RLD). Biopsy specimens were evaluated for H. pylori gastritis in accordance with the Sydney system. The 70 H. pylori-positive cases were treated with omeprazole, 20 mg twice daily, and amoxycillin, 1 g three times daily for 2 weeks. RESULTS: Higher rates of H. pylori colonization were found histologically in the gastric mucosa of ULD (91%) and RLD (86%) than in that of DLD (68%) or asymptomatic (42%) patients. ULD differed from RLD patients in their higher score of antritis activity. Three and 6 months after H. pylori eradication ULD (but not DLD) showed significant regression of dypspetic symptoms scores. CONCLUSIONS: It seems likely that H. pylori gastritis, with special reference to active antritis, is among causative factors of ULD. Its role in the pathogenesis of RLD and DLD needs further investigation.

Adult↗
PubMed1999

Helicobacter heilmannii gastritis: association with acid peptic diseases and comparison with Helicobacter pylori gastritis.

We analyzed 2 antral and 1 corpus full-thickness random endoscopic gastric mucosal samples obtained from 946 patients with duodenal ulcers (6077 biopsies) and from 281 patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (1794 biopsies). We stained tissue sections with hematoxylin and eosin and Warthin-Starry silver stain and immunostained them with polyclonal antibodies against Helicobacter pylori. Hematoxylin- and eosin-stained sections from 6 patients with Helicobacter heilmannii (18 biopsies) and 23 randomly selected patients with H. pylori (68 biopsies) were evaluated and semiquantitated for the presence of acute inflammation, chronic inflammation, glandular atrophy, intestinal metaplasia, H. pylori, H. heilmannii, lymphoid follicles, or vasodilatation. Additional specimens were obtained for H. pylori culture, a CLO test, and serologic examination. H. heilmannii was detected in 6 (0.49%) of 1227 patients (14 [0.18%] of 7871 biopsies). Of these, 4 (0.42%) of 946 were patients with duodenal ulcers (9 [0.15%] of 6077 biopsies), and 2 (0.71%) of 281 were patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (5 [0.28%] of 1794 biopsies). We found H. heilmannii with hematoxylin and eosin stain, Warthin-Starry stain, and immunoperoxidase stain for H. pylori. Culture for H. pylori was negative in the four patients with duodenal ulcers. The CLO and serologic tests were positive in three of five and five of five patients, respectively. Our results indicate that H. heilmannii, like H. pylori, is associated with peptic ulcer disease (both active and inactive gastritis) and that it preferentially colonizes the gastric antrum. The severity of the H. heilmannii-associated gastritis is less intense and lymphoid aggregates are less common than in H. pylori-associated gastritis. Morphologic detection seems to be the method of choice for detecting H. heilmanni. Immunoperoxidase stain specific for H. pylori also stains H. heilmannii, indicating cross-reacting antigenic epitopes between H. heilmannii and H. pylori.

Adult↗
PubMed1975

Is chronic gastritis a reversible process? Follow-up study of gastritis by step-wise biopsy.

In 36 patients step-wise biopsies of gastric mucosa were performed in 1971 and in 1974/75. A comparison of the histological changes revealed identical findings in 15, progression of superficial gastritis in 9 and regression of superficial gastritis in 7. In 5 patients regression of chronic atrophic gastritis was seen. In one patient an essentially normal mucosa was found in all biopsy specimens, in other patients parietal cells reappeared without any specific therapy.

Adult↗
PubMed2002

High incidence of B-cell monoclonality in follicular gastritis: a possible association between follicular gastritis and MALT lymphoma.

Many studies have indicated a close association between gastric mucosa-associated lymphoid tissue (MALT) lymphoma and Helicobacter pylori ( Hp) infection. Follicular gastritis (FG), a rare type of gastritis, is also closely associated with Hp infection and histologically similar to MALT lymphoma. However, there are few studies investigating the relationship between FG and MALT lymphoma. To clarify the issue, we examined the B-cell monoclonality in FG by immunoglobulin heavy chain (IgH) gene rearrangement. Seventy FG patients (all Hp-positive, 23 males and 47 females, median age 33 yr) were investigated; 70 age-and gender-matched non-FG Hp-positive controls and 24 non-FG Hp-negative controls were also examined. Two gastric biopsies, one from the antrum and one from the corpus, were obtained from each patient. DNA was extracted from formalin-fixed, paraffin-embedded biopsy specimens. IgH gene rearrangement was examined by semi-nested polymerase chain reaction (PCR). In the antral mucosa, monoclonal B-cell populations were detected in 19 (32%) of 60 FG, in 6 (10%) of 60 Hp-positive controls, and in none of 20 Hp-negative controls. In the corporal mucosa, monoclonal B-cell populations were detected in 14 (30%) of 47 FG, in 6 (11%) of 54 Hp-positive controls, and in none of 20 Hp-negative controls. The incidence of monoclonal B-cell populations in the FG patients was higher than in both Hp-positive and Hp-negative controls ( P<0.05). The monoclonal B-cell populations disappeared after successful Hp eradication in 8 of 8 FG patients examined. These data suggest that FG may be strongly associated with MALT lymphoma, and that Hp eradication therapy may be indicated in FG.

Adolescent↗
PubMed1987

Erosive gastritis and gastrointestinal bleeding in a female runner. Prevention of the bleeding and healing of the gastritis with H2-receptor antagonists.

A 33-yr-old female runner presented with upper gastrointestinal symptoms and iron deficiency anemia. She was found to have erosive gastritis that was present when she exercised and which was associated with symptoms. Gastrointestinal blood loss during exercise periods was confirmed by measuring fecal blood loss using 51Cr-labeled red cells. Symptoms, gastritis, and blood loss disappeared with cessation of running or with H2-receptor antagonist therapy.

Adult↗
PubMed2002

Helicobacter pylori eradication therapy improves atrophic gastritis and intestinal metaplasia: a 5-year prospective study of patients with atrophic gastritis.

AIM: : To investigate the effect of the eradication of Helicobacter pylori on histological gastritis. METHODS: : Twenty-six patients with moderate to severe atrophy received successful eradication therapy of H.pylori. Four patients dropped out and 22 were followed up prospectively for 5 years. The grades of gastritis were estimated from gastric biopsy specimens. The grade of intestinal metaplasia was also evaluated by dye-endoscopy using methylene blue (methylthioninium chloride). The serum levels of pepsinogen, gastrin and anti-parietal cell antibody were also determined. RESULTS: : The grades of atrophy decreased in patients with successful eradication therapy in the gastric corpus (before vs. 5 years after eradication, 2.09 +/- 0.15 vs. 0.91 +/- 0.17; P < 0.01) and in the antrum (2.14 +/- 0.17 vs. 1.36 +/- 0.17; P < 0.01). The levels of intestinal metaplasia were also decreased in the corpus (0.91 +/- 0.24 vs. 0.50 +/- 0.16; P < 0.05) and in the antrum (1.41 +/- 0.20 vs. 1.00 +/- 0.16; P < 0.05), which was also demonstrated by the methylene blue (methylthioninium chloride) staining method (33.4 +/- 8.2% vs. 23.0 +/- 6.5%; P < 0.05). The improvement of corpus atrophy correlated well with the high serum level of pepsinogen I (P = 0.005), but showed no correlation with the levels of anti-parietal cell antibody. CONCLUSIONS: : These results suggest that gastric atrophy and intestinal metaplasia are reversible events in some patients.

Adult↗
PubMed1998

Aspirin-induced gastritis, like Helicobacter pylori-induced gastritis disinhibits acid secretion in humans: relation to cytokine expression.

BACKGROUND: Helicobacter pylori infection contributes to hypergastrinemia and hypersecretion of acid by blocking inhibitory reflex pathways to gastrin and parietal cells normally activated by antral distention. Our aim was to investigate whether a similar blockade of inhibitory responses could be provoked by inducing gastritis with aspirin, thus implicating a common inflammatory component, possibly a proinflammatory cytokine(s). METHODS: We studied the effects of antral distention on stimulated acid secretion and gastrin release in H. pylori-negative volunteers, before and after 3 days of aspirin therapy (2 g daily). Immediately before the examinations, the severity of gastric mucosal injury was evaluated macroscopically and histologically, and the production of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma was determined by immunohistochemistry. RESULTS: Most subjects had severe gastric injury after aspirin therapy, resulting in a substantially increased production of IL-1beta, IL-6, and IL-8 but not of TNF-alpha and IFN-gamma in the antral mucosa. In these subjects the acid-inhibitory response was abolished or markedly reduced. Conversely, aspirin therapy failed to affect the gastrin release in all subjects studied. CONCLUSIONS: The disinhibition of acid secretion in response to antral distention is a joint feature of the gastritis induced by aspirin and H. pylori infection, possibly related to the increased production of IL-1beta, IL-6, and IL-8. The H. pylori-related hypergastrinemia apparently has a different background.

Adult↗
PubMed2003

Cancer precursor lesions in intact stomach Helicobacter pylori gastritis and in resected stomach gastritis.

Hemigastrectomy for benign disease and Helicobacter pylori infection are risk conditions for the development of gastric cancer. Aim of the study was to compare gastric histology and precursor lesions of malignancy in these two conditions. The hemigastrectomy group included 351 consecutively endoscoped subjects operated for gastroduodenal benign disease. Six to ten biopsy specimens were routinely taken from the residual gastric mucosa. The intact stomach group included 2097 consecutively endoscoped symptomatic subjects, who did not receive eradication therapy against H. pylori. The histological findings were classified as normal mucosa (NM), chronic non atrophic gastritis (CNAG), chronic atrophic gastritis (CAG), intestinal metaplasia (IM) and dysplasia (DYS). One thousand and three intact stomachs were H. pylori negative, and 1094 showed H. pylori colonization. The age over fifty was a significant risk factor for the occurrence of IM (OR 2.52, P < or = 0.001) and DYS (OR 3.46, P < or = 0.001), while Hp-positivity was a risk factor for CNAG (OR 1.81, P < or = 0.001) and CAG (OR 3.88, P < or = 0.001). Gastroresection was associated to higher risk for CNAG (OR 1.53, P < or = 0.001) and DYS (OR 4.31, P < or = 0.001) and to a lower risk of CAG (OR 0.49, P < or = 0.001). Both in males and females the risk for CNAG was significantly higher in Hp-positive (males OR 1.92, P=0.000; females OR 1.70, P=0.000) and gastrectomized subjects (males OR 2.06, P=0.000; females OR 2.43, P=0.000). Gastrectomized males, furthermore, showed an increased risk for DYS (OR 5.82, P=0.000). The aged Hp-negative and Hp-positive subjects evidenced a significant risk for IM (respectively OR's 3.42, P=0.000 and 4.85, P=0.000); the risk for DYS was significant in aged Hp-negative subjects (OR 4.09 P < or = 0.020). The Hp-positive individuals evidenced a significant risk for metaplastic mucosal changes (OR 38.17, P=0.000). Subjects aged over forty at the time of surgery and those with a longer postoperative follow up endoscopy presented an increased risk for CNAG of the residual mucosa (respectively OR's 2.75, P=0.000 and 5.25, P=0.000). CNAG and IM were the most frequently observed mucosal lesions both in subjects operated for duodenal and gastric ulcer (respectively OR's 4.02, P=0.000 and 3.00, P=0.000). Our data support that hemigastrectomy for benign disease and H. pylori infection may induce an increased incidence for histological precursor lesions for gastric malignancy and suggest that carcinogenesis in a resected stomach may be different from that in the intact stomach.

Adolescent↗
PubMed1987

Campylobacter pyloridis gastritis I: Detection of urease as a marker of bacterial colonization and gastritis.

A method to detect the presence of Campylobacter pyloridis in dyspeptic patients is described. The test procedure involves placing a gastric pinch biopsy into a small amount of a solution containing urea and a pH indicator in the well of a microtiter tray. The method depends on the ability of C. pyloridis to hydrolyse urea and release an alkaline product (ammonia). The "microtiter biopsy urease test" is 100% specific for C. pyloridis and has a 91% sensitivity after 18 h reaction time. Seventy-five percent of positive biopsies had a reaction time of less than 1 h. The test may be used to predict the presence of antral gastritis; as well as marking the presence of the bacterium; with a positive predictive value of 96% and a negative predictive value of 73%. There was a positive correlation between the biopsy urease test results and the grades of both chronic and active antral gastritis. This test is simple and can be performed in the endoscopy clinic as the formulation of the reagent obviates the need for aseptic techniques.

Ammonia↗
PubMed1977

Gastritis varioliformis. Chronic erosive gastritis with protein-losing gastropathy.

A patient with chronic erosive gastritis and protein-losing gastropathy is reported. Presentation was with weight loss and abdominal discomfort. There were endoscopic and radiological features of erosive gastritis. Radioactive chromium studies confirmed that the low serum albumin was associated with fecal protein loss. No improvement occurred with bed rest or Caved S but coincided with DeNol therapy.

Aged↗
PubMed1978

Immunological studies in chronic atrophic gastritis and chronic (superficial) gastritis.

Detection of autoantibodies, HLA typing and immunofluorescence studies on gastric biopsies were carried out in subjects with histologically proven chronic atrophic gastritis (CAG) and chronic superficial gastritis (CG). All were seronegative for parietal cell antibody and did not have pernicious anemia. Except for positive antismooth muscle and antimitochrondrial antibodies in one patient with CAG, autoantibodies (antinuclear, smooth muscle, mitochrondrial, parietal cell) were absent in patients with CAG and CG. Immunofluorescence studies showed that Ig-G and IgA were presented in the lamina propria of all cases with CAG or CG and of subjects with normal gastric histology. Ig-M was seen less often, in about half the cases. Complement C3 was an uncommon finding, being positive in only one case with CAG and one case with CG and in none of the cases with normal gastric histology. Fibrinogen was more commonly seen in patients with CG (5/5 cases) than in those with CAG (3/11 cases). Fibrinogen was found in one case with normal gastric histology. The most consistent fluorescence was obtained with antiparietal cell antiserum. All subjects with CAG showed negative or weak staining only. In contrast, subjects with CG and normal gastric histology had strong specific fluorescence. An increased frequency of HLA-A1 plus HLA-B8 was found in subjects with CAG (20.7% in controls; 40% in CAG).

Adult↗
PubMed2002

Treatment with a proton pump inhibitor promotes corpus gastritis in patients with Helicobacter pylori-infected antrum-predominant gastritis.

BACKGROUND: Proton pump inhibitors have been reported to modify the level of Helicobacter pylori gastritis. AIM: To quantitatively investigate the effect of a proton pump inhibitor on the mucosal neutrophil reaction. METHODS: Forty-six H. pylori-infected patients (17 duodenal ulcer, 29 gastric ulcer) were enrolled. During endoscopic examination, biopsy samples were obtained from the antrum and the corpus. The tissue content of neutrophil myeloperoxidase was measured by enzyme-linked immunoabsorbent assay, and H. pylori infection was histologically assessed. A proton pump inhibitor was administered orally for 8 weeks. RESULTS: In the patients as a whole, antral myeloperoxidase decreased significantly after proton pump inhibitor treatment, but corpus myeloperoxidase remained largely unchanged. In duodenal ulcer patients, myeloperoxidase significantly decreased in the antrum, but increased in the corpus. In gastric ulcer patients, a significant reduction was observed in antral myeloperoxidase, but corpus myeloperoxidase remained unchanged. In the antral myeloperoxidase > corpus myeloperoxidase subgroup (n=24), antral myeloperoxidase significantly decreased, whereas corpus myeloperoxidase increased. No changes were observed at either site in the corpus myeloperoxidase > antral myeloperoxidase subgroup. Histology showed that the antral bacterial load of H. pylori decreased in all subgroups, but that it was mostly unchanged in the corpus. CONCLUSIONS: Proton pump inhibitor treatment stimulated the neutrophil reaction in the corpus mucosa of duodenal ulcer patients and of patients in whom antral neutrophil accumulation was more predominant than that of the corpus. This phenomenon may not be caused by increased bacterial density.

2-Pyridinylmethylsulfinylbenzimidazoles↗