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PubMed2001

Influence of gender difference and gastritis on gastric ulcer formation in rats.

BACKGROUND: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. METHODS: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E(2) (PGE(2)) level were also determined. RESULTS: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE(2) level was higher in female rats with acute gastritis. Both mucus and PGE(2) were increased during ulcer healing in both genders. CONCLUSIONS: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE(2) not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach.

Animals↗
PubMed1999

The role of endoscopic findings for the diagnosis of Helicobacter pylori infection: evaluation in a country with high prevalence of atrophic gastritis.

BACKGROUND: This study examines endoscopic findings in the diagnosis of Helicobacter pylori (H. pylori) in the Japanese population. MATERIALS AND METHODS: The endoscopic findings (including gastric fold findings and degree of atrophy by the Kimura-Takemoto classification system), histologic severity of inflammation, and glandular atrophy were assessed according to the Sydney system in 642 patients (419 men; 223 women; mean age 43.5 years, range 13-86). H. pylori infection was evaluated by Giemsa staining and serum IgG antibodies. RESULTS: 391 of 642 patients (60.9%) were diagnosed as having endoscopic gastritis. Of the 391 patients with endoscopic gastritis, 318 (82.6%) had histologic gastritis and 310 (79.3%) had H. pylori infection. Of the 251 patients with endoscopically normal stomachs, 43 (17.1%) had histologic gastritis and 32 (12.7%) had H. pylori infection. Atrophic gastritis was the most prevalent finding (56.3%) among those with endoscopic gastritis. The prevalence of H. pylori infection in patients with atrophic gastritis (92.7%) and rugal hyperplastic gastritis (92.3%) was significantly higher than in those with other types of gastritis or with a normal stomach (12. 7%). A markedly high prevalence of H. pylori infection was found in subjects with tortuosity, hyperrugosity, and/or hyporugosity of the gastric folds. CONCLUSIONS: The accurate endoscopic assessment of gastritis according to the Sydney system along with gastric fold findings and the endoscopically identified extent of gastric atrophy are valuable indicators for determining H. pylori infection and histologic gastritis in the Japanese population.

Adolescent↗
PubMed1999

Murine splenocytes induce severe gastritis and delayed-type hypersensitivity and suppress bacterial colonization in Helicobacter pylori-infected SCID mice.

The goal of this study was to evaluate the role of host immunity in gastritis and epithelial damage due to Helicobacter pylori. Splenocytes from H. pylori-infected and uninfected C57BL/6 mice were adoptively transferred to H. pylori-infected and uninfected severe combined immunodeficient (SCID) mice. Transfer was verified by flow cytometry, and all mice were evaluated for the presence of delayed-type hypersensitivity (DTH) by footpad inoculation with sterile H. pylori sonicate and for humoral immunity by enzyme-linked immunosorbent assay. The severity of gastritis and gastric epithelial damage was quantified histologically, epithelial proliferation was determined by proliferating cell nuclear antigen staining, and colonization was quantified by culture. C57BL/6 mice, but not nonrecipient SCID mice, developed moderate gastritis in response to H. pylori. In contrast, recipient SCID mice developed severe gastritis involving 50 to 100% of the gastric mucosa and strong DTH responses not present in C57BL/6 mice. DTH, but not serum anti-H. pylori immunoglobulin G, correlated with adoptive transfer, gastritis, and bacterial clearance. Severe gastritis, but not bacterial colonization, was associated with epithelial metaplasia, erosions, and an elevated labeling index. This study demonstrates that (i) adaptive immunity is essential for development of gastritis due to H. pylori in mice, (ii) T-cell-enriched lymphocytes in SCID mice induce DTH and gastritis, which is more severe than donor gastritis, and (iii) the host inflammatory response, not direct bacterial contact, causes epithelial damage. The greater severity of gastritis in recipient SCID mice than in donor C57BL/6 mice suggests that gastritis is due to specific T-cell subsets and/or the absence of regulatory cell subsets in the transferred splenocytes.

Adoptive Transfer↗
PubMed1998

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.

Adult↗
PubMed1994

Chronic nonatropic ('superficial') gastritis increases the risk of gastric carcinoma. A case-control study.

Atrophic gastritis is a well-known risk condition for gastric carcinoma (GCA). Less is known about the risk of GCA in subjects with nonatrophic ('superficial') gastritis. To investigate this, we estimated the risk of GCA in patients with nonatrophic gastritis as compared with that in subjects with normal, nongastritic mucosa. Two hundred and forty-three consecutive GCA patients and 1408 non-GCA outpatients (controls), for whom histologic data (endoscopic biopsy) of gastric mucosa was available, were included in the study. To estimate the relative risk (RR) of GCA, the odds ratio of gastritis was calculated in patients and controls by adjusting for age and sex. The RR (95% confidence interval) of GCA in patients with nonatrophic antral gastritis and with nonatrophic pangastritis was 1.8 (1.2-2.7) and 2.5 (1.4-4.3), respectively. Correspondingly, the risks of GCA were 9.1 (5.4-15.5) in patients with atrophic antral gastritis or pangastritis (atrophy of any degree) and 4.4 (1.9-10) in those with severe atrophic corpus gastritis (severe corpus limited atrophy of 'A type'). In nonatrophic gastritis the risk of diffuse-type GCA was emphasized, whereas the risk of intestinal-type GCA was emphasized in patients with atrophic gastritis. These results indicate that an increased risk of GCA is not confined to subjects with atrophic gastritis but is also slightly but significantly increased in patients with chronic nonatrophic gastritis.

Adult↗
PubMed2001

The role of T cell subsets and cytokines in the pathogenesis of Helicobacter pylori gastritis in mice.

Gastritis due to Helicobacter pylori in mice and humans is considered a Th1-mediated disease, but the specific cell subsets and cytokines involved are still not well understood. The goal of this study was to investigate the immunopathogenesis of H. pylori-induced gastritis and delayed-type hypersensitivity (DTH) in mice. C57BL/6-Prkdc(scid) mice were infected with H. pylori and reconstituted with CD4+, CD4-depleted, CD4+CD45RB(high), or CD4+CD45RB(low) splenocytes from wild-type C57BL/6 mice or with splenocytes from C57BL/6(IFN-gamma-/-) or C57BL/6(IL-10-/-) mice. Four or eight weeks after transfer, DTH to H. pylori Ags was determined by footpad injection; gastritis and bacterial colonization were quantified; and IFN-gamma secretion by splenocytes in response to H. pylori Ag was determined. Gastritis and DTH were present in recipients of unfractionated splenocytes, CD4+ splenocytes, and CD4+CD45RB(high) splenocytes, but absent in the other groups. IFN-gamma secretion in response to H. pylori Ags was correlated with gastritis, although splenocytes from all groups of mice secreted some IFN-gamma. Gastritis was most severe in recipients of splenocytes from IL-10-deficient mice, and least severe in those given IFN-gamma-deficient splenocytes. Bacterial colonization in all groups was inversely correlated with gastritis. These data indicate that 1) CD4+ T cells are both necessary and sufficient for gastritis and DTH due to H. pylori in mice; 2) high expression of CD45RB is a marker for gastritis-inducing CD4+ cells; and 3) IFN-gamma contributes to gastritis and IL-10 suppresses it, but IFN-gamma secretion alone is not sufficient to induce gastritis. The results support the assertion that H. pylori is mediated by a Th1-biased cellular immune response.

Adoptive Transfer↗
PubMed2000

The role of Helicobacter pylori and gastritis in children with recurrent abdominal pain.

BACKGROUND: Recurrent abdominal pain is a common pediatric diagnostic problem. Endoscopy is sometimes performed as part of the evaluation. Although gastritis and/or Helicobacter pylori infection is often present, it is not known if they contribute to the symptomatology. OBJECTIVES: To evaluate the role of either gastritis or H. pylori infection in the symptomatology of children with RAP. PATIENTS AND METHODS: We retrospectively studied two groups of patients, 70 children in each, who had undergone endoscopy. One group was evaluated endoscopically for RAP and the other was a heterogeneous group that underwent endoscopy for indications other than RAP. Biopsies were taken during endoscopy and Giemsa staining was performed for the presence of H. pylori. Triple therapy was given as indicated, and the children were followed for an average of 6 months. RESULTS: Microscopic gastritis was diagnosed in 39 patients (55.7%) of the RAP group and in 31 of the heterogeneous group (44.2%) (NS), and H. pylori was found in 32 patients of the RAP group and in 16 of the heterogeneous group (45.7% vs. 22.8%, P < 0.01). All children with H. pylori, except one in the heterogeneous group, had accompanying gastritis. On the other hand, gastritis without H. pylori infection was seen in 7 children in the RAP group and in 15 of the other. Endoscopy revealed macroscopic abnormalities in 52 of the 70 children with microscopic gastritis. There was a clinical improvement after triple therapy in 28 of 33 children with H. pylori-associated gastritis (84.85%), in 4 of 8 children with gastritis unassociated with H. pylori (50%), and in 8 of 15 without gastritis or H. pylori (53.3%) (P < 0.01 between the H. pylori-associated gastritis and each of the other groups). CONCLUSIONS: H. pylori infection and gastritis may be associated with RAP in a selected subgroup of children. We recommend a complete work-up, including endoscopy and invasive or non-invasive diagnostic modalities for H. pylori, and treatment of the infection.

Abdominal Pain↗
PubMed2002

Helicobacter pylori gastritis in children: endoscopical and histological aspects.

UNLABELLED: Helicobacter pylori (Hp) infection is involved in both digestive and extradigestive diseases. Endoscopically, antral location of gastritis, as well as antral nodularity, a consequence of the development of lymphoid follicles in the mucosa of this area, are considered by some authors specific for gastritis in children. Histologically, lymphoid follicles, noticed usually in children, are considered pathognomonic. AIMS: To establish prevalence of gastritis in children and the correlation between of endoscopical and histological findings. PATIENTS AND METHODS: The study group included 267 children in whom upper digestive endoscopy was performed for digestive symptoms. The diagnosis of Hp infection was based on the concordance between the positive urease test and the histological examination (documenting the presence of Hp in the gastric mucosa). RESULTS: Endoscopical aspect of antral nodular gastritis was mainly found in children infected with Hp. Follicular gastritis, considered the histological marker of nodular gastritis, was also revealed in congestive gastritis. Patients infected with Hp most often displayed chronic gastritis and noninfected patients acute gastritis. Hp was not found in gastric mucosa without histological changes. CONCLUSIONS: Nodular pattern of antral mucosa might be considered specific for Hp infection in childhood. In patients infected with Hp chronic gastritis was mainly found while in noninfected children acute gastritis was usually revealed. Hp was not found in gastric mucosa without histological changes.

Acute Disease↗
PubMedDate not supplied

Helicobacter pylori, chronic gastritis and peptic ulcer.

H. pylori infection is strongly associated with chronic gastritis and is probably the main course of chronic inflammation in the gastric mucosa. Acquisition of the infection will lead to gastritis and the eradication of the bacterium results in healing and final cure of the gastritis. Chronic gastritis and H. pylori infection may occur in antrum and/or corpus, and will gradually result in atrophy of the underlying mucosa in a great number of affected persons. Correspondingly, impairments in several important functions of the gastric mucosa are consequences of the atrophy and inflammation. Hp infection and gastritis associate with important gastroduodenal diseases, such as peptic ulcer diseases and gastric cancer. There are reasons to suggest that the infection and subsequent gastritis precede these diseases, and that they are important risk factors for both disorders. In fact, peptic ulcer can be seen a late frequent complication of an H. pylori infection. In addition, the type and grade of gastritis can be used in prediction of the ulcer risk if adequate biopsy specimens are available for microscopy from both antrum and corpus mucosa (Table II). An association between chronic gastritis and Helicobacter pylori (Hp) infection is strong. Clearly more than 80% of cases with chronic gastritis are related to coexistent Hp infection. Furthermore, both Hp and gastritis are extremely common in patients with peptic ulcer supporting the view that they are causally related to the ulcer disease. Correspondingly, similar suggestions may also be presented about the links between Hp and gastritis in the pathogenesis of gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1991

Helicobacter pylori and gastritis in children with abdominal complaints.

Gastroscopy with biopsies was performed in 178 children with upper abdominal pain. Of them 109 (61%) had gastritis and 104 (58%) Helicobacter pylori (HP) in antrum and/or corpus. Gastritis consisted in most cases (87% of antral and 86% of corpus gastritis) of mild superficial round cell infiltration. Mucosal atrophy was not found. Accumulation of granulocytes was present in 43 patients and lymphonoduli were found in 33 patients, usually in connection with gastritis. Gastritis affected only the antrum in 18%, only the corpus in 5% and both antrum and corpus in 62% of the cases of gastritis. There was a good correlation between morphology and bacteriology in the antrum and a satisfactory one in the corpus. However, in some cases gastritis was present without bacteria and in some cases a normal mucosa was associated with bacteria. Gastritis and HP prevalences showed a general increasing trend with age, but significances were with one exception lacking. It is tentatively concluded that gastritis begins in childhood as a slight and chronic superficial infiltration affecting usually antrum and corpus simultaneously. In the majority of cases gastritis is associated with HP infection, which seems to start the process. It is possible that the HP-related gastritis is a common cause of abdominal complaints in children; however, convincing evidence is lacking.

Abdominal Pain↗
PubMed1991

Gastric chief cell mass in chronic gastritis. Count and relationships to parietal cell mass and functional indices.

The chief cell mass, expressed as the Zymogenous Index (number of cells per mm2 multiplied by the thickness of the glandular layer) was calculated in 42 subjects with chronic gastritis, and in 40 subjects with normal gastric mucosa, and was compared with the serum concentration of Pepsinogen I (PG I), with the parietal cell mass (expressed as Parietal Index: number of cells per mm2 multiplied by the thickness of the glandular layer), and with the acid output. The results showed that there are no significant variations in the chief cells in comparison with healthy controls in the case of superficial gastritis and follicular gastritis. Conversely, in the case of pre-atrophic and atrophic gastritis there is a significant reduction in the chief cell mass. The serum PG I increases significantly in the case of superficial gastritis as compared with healthy controls, while it is equivalent in the case of follicular gastritis, decreases non-significantly in pre-atrophic gastritis and is significantly reduced in the case of atrophic gastritis. The parietal cell mass shows a behavior equivalent to that of the chief cell mass, and the acid output decreases significantly in the case of pre-atrophic and atrophic gastritis, with no significant variations in the case of superficial and follicular gastritis. On comparing the behavior of the chief cell mass with that of the parietal cell mass, it was noticed that in the most severe stages of chronic gastritis there is a more pronounced reduction of the former than of the latter.

Adult↗
PubMedDate not supplied

Risk of gastroduodenal ulcer in gastritis.

The present evidence suggests that chronic gastritis is strongly associated with peptic ulcer disease. Gastritis, particularly in antrum, is nearly invariably present in patients with peptic ulcer. Gastritis is a progressive disease which begins as a superficial inflammation and progresses to atrophic gastritis. Gastritis can be considered to lower resistance of the gastric mucous membrane but it may also affect secretion of acid and pepsins from oxyntic mucosa. The presence or absence of gastritis, and its involvement in antral and/or body mucosa, can be considered to reflect the risk and probability of a person to contract peptic ulcer. Estimations of the risks of coexistent peptic ulcer in different types and grades of gastritis suggest that the relative risk (RR) of coexistent peptic ulcer disease is markedly increased in the presence of gastritis in general (RR = 7-10), as compared to patients who have a normal, non-gastritic stomach (RR = 1). This risk is particularly high in patients with gastritis of B type (atrophic gastritis is in antrum but body mucosa is non-atrophic) in whom the coexistent peptic ulcer is 20-30 times more common (RR = 20-30) than in patients who have normal stomach. On the other hand, the risk of peptic ulcer disease is low in patients who show marked atrophic alterations in the gastric body mucosa (A or AB types of gastritis), the risk being in these patients even lower (RR below 1) than that in patients with normal, non-gastritic stomach.

Gastritis↗
PubMed1997

Role of Helicobacter pylori in the pathogenesis of atrophic gastritis.

BACKGROUND: Atrophic gastritis is defined as a loss of the glandular structures and a collapse of the reticulin skeleton of the stomach mucosa. It is often accompanied by intestinal metaplasia. Both conditions result from long-term persistent chronic active gastritis and significantly increase the risk for gastric cancer. METHODS: Review of the role of Helicobacter pylori in the pathogenesis of atrophic gastritis. Specific attention is given to the classifications and histologic features of atrophic gastritis, the frequency with which atrophic gastritis occurs in H. pylori-infected subjects, the factors that influence the process of development of atrophic gastritis in the presence of infection, and the various mechanisms by which this bacterial infection may induce atrophic gastritis. In addition, the possible role of H. pylori in the etiology of auto-immune atrophic gastritis and pernicious anemia is discussed. CONCLUSIONS: H. pylori infection eventually causes atrophic gastritis in a considerable number of infected subjects. In different populations, the prevalence of atrophic gastritis increases by 1 to 3% per annum. Factors that may increase the risk for atrophy are infection at an early age, cytotoxin production by the infecting strain, and lowering of acid output. The association between H. pylori infection and the development of atrophic gastritis significantly supports the role of this infection in gastric carcinogenesis.

Gastritis, Atrophic↗
PubMed2003

Pancreatic acinar cell metaplasia in autoimmune gastritis.

OBJECTIVE: To determine the frequency and significance of pancreatic acinar cells in the gastric oxyntic mucosa. DESIGN: One hundred gastric oxyntic mucosal biopsy specimens from patients with chronic active gastritis (n = 30), multifocal atrophic gastritis (n = 15), autoimmune gastritis (n = 18), and normal gastric oxyntic mucosa (n = 37) were evaluated for the presence of pancreatic acinar cells. Formalin-fixed, paraffin-embedded tissues were stained with hematoxylin-eosin, and those positive for pancreatic acinar cells were immunostained with antibodies against trypsin and pancreatic amylase. RESULTS: Eleven (11%) of 100 oxyntic mucosal tissue samples contained pancreatic acinar cells. These samples came from 9 of the 18 (50%) specimens of autoimmune gastritis, 1 of the 15 (6.6%) specimens of multifocal atrophic gastritis, and 1 of the 37 (2.7%) specimens of normal oxyntic mucosa. None of the samples with chronic active gastritis contained pancreatic acinar cells. CONCLUSIONS: Pancreatic acinar cells were found in the oxyntic mucosa of patients with autoimmune gastritis significantly more frequently (P <.001) than in individuals with multifocal atrophic gastritis, normal oxyntic mucosa, or chronic active gastritis. Our study supports a metaplastic origin for pancreatic acinar cells in the oxyntic mucosa. Furthermore, detection of pancreatic acinar cells in the oxyntic mucosa of patients with gastritis strongly suggests an autoimmune pathogenesis.

Autoimmune Diseases↗
PubMed1997

Helicobacter pylori gastritis--epidemiology.

The acquisition of Helicobacter pylori is the main cause of chronic gastritis in humans. In Europe, a small proportion (less than 1%) of gastritis cases are caused by H. Heilmannii, and somewhat more (5%) are autoimmune in origin, in which condition H. pylori may not probably play a role. Recent findings on chronic gastritis and H. pylori acquisition in developed countries can be summarized as: (1) H. pylori gastritis is acquired in childhood and adolescence (age less than 20) in more than 50% of cases; (2) the risk and rate of acquisition is highest in early childhood, after which the rate exponentially declines; (3) new infections occur in adulthood but are quite rare (annual incidence 0.4%, on average, in Finland); (4) H. pylori gastritis is a birth cohort-related phenomenon; i.e., different cohorts show a rate and prevalence of H. pylori gastritis that varies between cohorts; (5) the rate and risk of H. pylori infection is high in cohorts born in the beginning of the century, but is much lower in those born later; (6) this decline is due to a decrease in the rate and risk of H. pylori acquisition in childhood in particular. H. pylori gastritis-related complications, such as peptic ulcer diseases and gastric cancer, show epidemiological features similar to H. pylori gastritis. Both peptic ulcer and gastric cancer have declined in incidence over time. Gastric cancer is a birth-cohort phenomenon in the same way as is H. pylori gastritis, and the incidence of gastric cancer shows a positive but exponential relationship with the "birth-cohort-specific" prevalence of gastritis in the general population.

Adolescent↗
PubMed1998

Apoptosis in chronic gastritis and its correlation with antigastric autoantibodies.

In the course of time, chronic gastritis may result in gastric atrophy, as in type A gastritis, where autoimmune reactions against parietal cells result in a loss of corpus glands. Two antigastric autoantibodies have been detected in Helicobacter pylori gastritis and are described as anti-luminal and anti-canalicular autoantibodies. The aim of this study was to determine whether increased apoptosis may be responsible for the loss of gastric epithelium and whether this apoptosis is correlated with antigastric autoimmunity. Gastric biopsies from normal mucosa and Helicobacter pylori gastritis were analysed for the presence of apoptosis using the TUNEL method. Helicobacter pylori gastritis was divided into cases (1) without autoantibodies, (2) with anti-luminal, and (3) with anti-canalicular autoantibodies. Apoptotic cells of the foveolar and of the glandular epithelium in the antrum and corpus were counted. The number of apoptotic cells in the gastric mucosa was significantly increased in all cases of gastritis. The highest number of apoptotic cells was observed in the gastric glands of the corpus mucosa in Helicobacter pylori gastritis with anti-canalicular autoantibodies. Apoptosis contributes to the development of gastric atrophy and there are various types of Helicobacter pylori gastritis. The positive correlation between apoptotic cell loss in the glandular zone of the corpus mucosa and the presence of anti-canalicular autoantibodies indicates a possible link between anti-gastric autoimmunity and atrophy in this type of Helicobacter pylori gastritis--similar to that in classic type A gastritis.

Adult↗
PubMed2005

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.

Adult↗
PubMed1999

Lymphocytic gastritis: association with etiology and topology.

Lymphocytic gastritis (LG) is an uncommon chronic gastritis characterized by lymphocytosis of foveolar and surface epithelium. Lymphocytic gastritis is associated with celiac disease, Helicobacter pylori (HP) gastritis, and varioliform gastritis, but its topology and severity with respect to the associated entities have not been studied in detail. Therefore, we studied 103 patients with LG classified according to the associated entities, including the distribution and severity of LG in the 70 patients from whom biopsy specimens of both antrum and body were available. In 84 patients (82%), a distinct associated entity was identified, including 39 with celiac disease, 30 with HP infection, 4 with varioliform gastritis, 2 each with inflammatory polyp, Crohn's disease, human immunodeficiency virus infection, lymphoma, and esophageal carcinoma, and 1 with lymphocytic gastroenterocolitis. Lymphocytic gastritis was found in 33% of patients with celiac disease and 4.1% of histopathologically defined HP gastritis. The severity of intraepithelial lymphocytosis was greater in antrum than in body in 83% (20 of 24) of LG associated with celiac disease, but in only 19% (4 of 21) of LG associated with HP infection (p < 0.00002). All four patients with varioliform gastritis had more severe involvement of body. Lymphocytic colitis was common (38%, 5 of 13) in celiac disease with LG. Our results indicate that lymphocytic gastritis most commonly occurs in celiac disease and HP infection, but rarely with other entities. The topology of LG can direct the clinical evaluation for associated disease.

Adolescent↗