This is a type of gastritis once referred to as Type A gastritis. It classically involves the fundic and corpus of the stomach. It is an autoimmune disease because the body produces autoantibodies to the gastric parietal cells and/or the intrinsic factor. Patients with this disease may have varying degrees of atrophy of the stomach. Clinically, patients may have pernicious anemia with achlorhydria, vitamin B12 deficiency, and hypergastrinemia.
Epidemiology Disease Associations Pathogenesis Laboratory/Radiologic/
Other Diagnostic Testing
Gross Appearance and Clinical Variants Histopathological Features and Variants Special Stains/
Differential Diagnosis Prognosis Treatment Commonly Used Terms Internet Links
EPIDEMIOLOGY CHARACTERIZATION SYNONYMS Type A gastritis
DISEASE ASSOCIATIONS CHARACTERIZATION ANEMIA
High prevalence of atrophic body gastritis in patients with unexplained microcytic and macrocytic anemia: a prospective screening study.
Marignani M, Delle Fave G, Mecarocci S, Bordi C, Angeletti S, D'Ambra G, Aprile MR, Corleto VD, Monarca B, Annibale B.
Gastroenterology Department, Universita degli Studi di Roma La Sapienza, Italy.
Am J Gastroenterol 1999 Mar;94(3):766-72 Abstract quote
OBJECTIVE: Atrophic body gastritis (ABG) is characterized by atrophy of the gastric body mucosa, hypergastrinemia, and hypo/achlorhydria. Its association with pernicious anemia is well recognized. Gastric hypo/achlorhydria is known to affect iron absorption but ABG is rarely considered as a possible cause of iron deficiency (microcytic) anemia. The aims of this study were to validate a screening methodology for the detection of ABG in a consecutive series of patients with microcytic and macrocytic anemia and to investigate the clinical and gastric morphofunctional characteristics of the two hematological presentations of ABG.
METHODS: A two-part prospective study was carried out. Part A aimed to validate the screening methodology to detect the presence of ABG in patients with macrocytic and microcytic anemia who have no specific GI symptoms, by measuring their gastrin levels and verified by performing gastroscopy with biopsy. Part B aimed to detect the presence of ABG in a larger sample of anemic patients by our validated method and, by pooling the data of ABG patients, to determine the clinical, gastric histological, and functional characteristics pertaining to the macrocytic and microcytic presentations of ABG.
RESULTS: In part A, ABG was detected in 37.5% of patients with macrocytic and in 19.5% of those with microcytic anemia. Pooling the data of the ABG patients from part A and part B, microcytic ABG patients were on average 20 yr younger than those with macrocytic anemia. The majority of microcytic ABG patients were female, most of whom were premenopausal. H. pylori infection was widely represented in the microcytic ABG group (61.1%). They also had a lesser grade of body mucosal atrophy and lower hypergastrinemia levels, suggesting a less severe oxyntic damage of shorter duration.
CONCLUSIONS: Macrocytic anemia is not the only hematological presentation of ABG. Physicians evaluating patients with unexplained iron deficiency anemia should consider ABG as a possible cause by determining fasting gastrin levels and performing gastroscopy with biopsies of the body mucosa.
High Prevalence of Manifestations of Gastric Autoimmunity in Parietal Cell Antibody- Positive Type 1 (Insulin-Dependent) Diabetic Patients1
Christophe E. M. De Block, Ivo H. De Leeuw, Luc F. Van Gaal and the Belgian Diabetes Registry
Department of Endocrinology-Diabetology, University of Antwerp, University Hospital Antwerp (C.E.M.D.B., I.H.D.L., L.F.V.G.), B-2650 Edegem; and the Belgian Diabetes Registry, B-1090 Brussels, Belgium
Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 11 4062-4067 Abstract quote
Previous studies have shown a high prevalence of gastric parietal cell antibodies (PCA) in type 1 diabetes, which can be accompanied by (sub)clinical autoimmune gastric disease. This study aimed to determine the grade of associated autoimmunity and to assess the pattern of prevalence of PCA by gender, age, duration of disease, age at onset of diabetes, and human leukocyte antigen (HLA) type in an adult type 1 diabetic population. Furthermore, to examine the clinical significance of being PCA positive, manifestations of gastric autoimmune disease were studied in PCA-positive and PCA-negative patients.
The population studied consisted of 497 type 1 diabetics (men/women, 252/245; mean age, 40.8 ± 12.1 yr; mean duration of disease, 16.4 ± 10.4 yr; mean age at onset, 26.9 ± 13.5 yr; mean hemoglobin A1c, 8.1 ± 1.6%). Associated autoantibodies were present in 39% and PCA were present in 20.9% of the subjects, particularly in older patients. Gender, duration, and age at onset of diabetes did not influence the appearance of PCA. Antithyroid peroxidase antibodies (aTPO) were more frequent in PCA-positive patients than in those without PCA (33.6% vs. 22.4%; P = 0.025), suggesting an association between gastric and thyroid autoimmunity. We could demonstrate an association between PCA and the HLA DR5 haplotype (P = 0.001) as well, but not with HLA DR3 and/or DR4. In the PCA-positive group, iron deficiency anemia was detected in 15.4%, and pernicious anemia was found in 10.5% of subjects. These autoimmune gastric manifestations were significantly more prevalent in PCA-positive diabetics than in PCA-negative subjects, in whom the percentages were 6.9% and 0.5%, respectively (P = 0.01 and P < 0.0001). PCA were prevalent in 84.6% of patients with pernicious anemia. A gastroscopic and anatomopathoplogical examination performed in a subgroup of 30 patients with gastric symptoms revealed atrophic gastritis in 13 of 14 PCA-positive patients and in 9 of 16 PCA-negative subjects (P = 0.04). PCA were present in 59.1% of patients with atrophic gastritis.
In conclusion, a high prevalence of parietal cell antibodies and associated autoimmune gastric disease is present in PCA-positive type 1 diabetics, recommending its screening. Early detection of PCA and iron deficiency anemia, pernicious anemia, and atrophic gastritis and the subsequent care could reduce the morbidity of type 1 diabetes.
Atrophic body gastritis: distinct features associated with Helicobacter pylori infection.
Annibale B, Marignani M, Azzoni C, D'Ambra G, Caruana P, D'Adda T, Delle Fave G, Bordi C.
Gastroenterology Unit, University La Sapienza Rome, Italy.
Helicobacter 1997 Jun;2(2):57-64 Abstract quote
BACKGROUND: Usually, atrophic body gastritis has been considered an autoimmune disease characterized by the presence of parietal cell antibodies. Previous investigations into the role of Helicobacter pylori infection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively investigated population of patients with corpus-predominant atrophic gastritis.
PATIENTS AND METHODS: A consecutive series of 67 newly diagnosed cases of atrophic body gastritis was derived from a screening of 326 patients with unexplained anemia or dyspepsia. Criteria for diagnosis were fasting hypergastrinemia, pentagastrin-resistant achlorhydria, and histological confirmation of body atrophy. In all 67 patients, H. pylori infection was evaluated independently by histological assay and urease test. The gastritis status of both the fundic and antral mucosa were graded according to the Sydney system. Parietal cell and intrinsic factor antibodies also were determined.
RESULTS: Active H. pylori infection was present in 26.8% of our patients and allowed us to identify a patient's subpopulation with a significantly smaller degree of body mucosa damage as shown by functional parameters (gastrin, gastric acid secretion, pepsinogen I) and histological assessment. In this subpopulation, a higher prevalence of gastric cancer familial history was found. Presence of parietal cell antibodies showed a similar prevalence in H. pylori-positive and H. pylori-negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histological differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia.
CONCLUSION: Active H. pylori infection, a potential cause of oxyntic gland atrophy, is found in one-fourth of patients with newly diagnosed atrophic body gastritis.
Healing of Active, Non-Atrophic Autoimmune Gastritis by H. pylori Eradication.
Muller H, Rappel S, Wundisch T, Bayerdorffer E, Stolte M.
Institute for Pathology, Klinikum Bayreuth, University Hospital Carl-Gustav-Carus, Technical University of Dresden, Germany.
Digestion 2001;64(1):30-9 Abstract quote
Background and Aims: The antigastric antibodies present in Helicobacter pylori infection act as a marker for an ongoing antigastric autoimmune process in the gastric mucosa, which can already be diagnosed in the non-atrophic stage. In a retrospective, uncontrolled study, therefore, we investigated the question as to whether this type of gastritis can be healed by the eradication of H. pylori.
Patients and Methods: In 80 patients with an active, not yet atrophic autoimmune gastritis, we analysed a maximum of four investigations per patient over a period of up to 39.5 months. The following parameters were graded in the antral and corpus mucosa prior to and after H. pylori eradication treatment: grade and activity of the gastritis, H. pylori colonization, atrophy, parietal cell hypertrophy, and incidence of intestinal metaplasia. In addition, the typical parameters for this type of gastritis, such as grade of the periglandular lymphocytic infiltration, grade of glandular destruction and incidence of nodular ECL cell proliferates in the corpus mucosa were determined.
Results: In 64 patients (80%), H. pylori eradication treatment was followed by healing of the active autoimmune corpus gastritis, that is, the activity of the gastritis disappeared, and lymphocytic infiltration of the glands, glandular destruction and parietal cell hypertrophy was found to be significantly reduced.
Conclusions: Our uncontrolled, retrospective study confirms the existence of an active, not yet atrophic autoimmune gastritis as a sequela of H. pylori infection.
A study of autoimmune gastritis in the postpartum period and at a 5-year follow-up.
Burman P, Kampe O, Kraaz W, Loof L, Smolka A, Karlsson A, Karlsson-Parra A.
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
Gastroenterology 1992 Sep;103(3):934-42 Abstract quote
The presence of autoimmune gastritis was investigated in 54 women with postpartum thyroiditis. Parietal cell antibodies (PCA) specific against H+, K(+)-adenosine triphosphatase (EC 188.8.131.52) were found in 18 women during pregnancy; in 10 of them, a 2-9-fold increase in the PCA level was observed in the postpartum period.
At a 5-year follow-up, the initially PCA-positive women still had elevated antibody levels. Hypergastrinemia and low pepsinogen levels were noted in 4 women. In 2 of these women low serum vitamin B12 levels had developed. In 6 of 9 PCA-positive women examined by gastroscopy, biopsy specimens from the gastric body mucosa contained mononuclear cells, mainly T lymphocytes (CD3+) and macrophages (Leu-M3+) combined with an aberrant epithelial expression of HLA-DR. In four patients with chronic gastritis, all parietal cells, as defined by a specific monoclonal antibody, were found to have immunoglobulin G (IgG) deposits by a double-immunostaining method. Three of them had microscopic evidence of atrophy, whereas in 1 patient the body mucosa was intact. In 1 further patient with intact glands at histological examination, the basolateral membrane of some oxyntic glands was coated with IgG.
The selective in situ deposition of antibodies associated with histologically intact parietal cells may support the concept that specific autoantibodies participate in the early pathogenesis of parietal cell destruction.
PATHOGENESIS CHARACTERIZATION MICROSATELLITE INSTABILITY
Infrequency of microsatellite instability in complete and incomplete gastric intestinal metaplasia.
Garay J, Bravo JC, Correa P, Schneider BG.
Hum Pathol. 2004 Jan;35(1):102-6. Abstract quote
Chronic inflammation may be associated with microsatellite instability (MSI). To test the hypothesis that MSI frequently occurs in gastric intestinal metaplasia, we examined gastric biopsies from 58 subjects from an area of high risk for gastric cancer. These were selected to have 2 types of intestinal metaplasia: complete (31 subjects) and incomplete or mixed-type (27 subjects). None of the subjects had gastric cancer, but 95% had chronic inflammation with Helicobacter pylori. We used laser capture microdissection to retrieve metaplastic glands to compare with lymphocytes microdissected from the adjacent gastric mucosae in the same subjects.
We performed microsatellite analysis using 6 microsatellite loci, including BAT26. None of the cases were found to have reproducible MSI, and only 1 case showed loss of heterozygosity at 1 marker, D3S1067. To test the sensitivity of our assay, we mixed templates to produce bands of different mobility and found that we could detect an aberrant microsatellite pattern if only 2% of the DNA showed that pattern.
Our results indicate that MSI is a rare event in intestinal metaplasia in subjects who do not have gastric cancer.
Gastric PDX-1 expression in pancreatic metaplasia and endocrine cell hyperplasia in atrophic corpus gastritis.
Buettner M, Dimmler A, Magener A, Brabletz T, Stolte M, Kirchner T, Faller G.
1Institute of Pathology, University of Erlangen-Nuremberg, Erlangen, Germany.
Mod Pathol. 2004 Jan;17(1):56-61 Abstract quote.
The homeodomain transcription factor PDX-1 plays a key role in endocrine and exocrine differentiation processes of the pancreas. PDX-1 is also essential for differentiation of endocrine cells in the gastric antrum.
The role of PDX-1 in the pathogenesis of endocrine cell hyperplasia and pancreatic metaplasia in corpus and fundus gastritis has not been evaluated. By immunohistochemistry and double-immunofluorescence, we investigated the expression of PDX-1 in 10 tissue specimens with normal human gastric mucosa, nonatrophic and atrophic gastritis and in pancreatic metaplasia, respectively. In normal corpus mucosa and in nonatrophic corpus gastritis, PDX-1 was mainly absent. In pancreatic metaplasia, PDX-1 was found in metaplastic cells and in adjacent gastric glands. In contrast to normal gastric corpus mucosa, PDX-1 could be strongly detected in the cytoplasm of the parietal cells surrounding metaplastic areas. Furthermore, PDX-1 expression was found in hyperplastic endocrine cells and in the surrounding gastric glands in chronic atrophic gastritis. Hyperplastic endocrine cells coexpressed the beta-subunit of the gastric H,K-ATPase.
We conclude that PDX-1 represents a candidate switch factor for glandular exocrine and endocrine transdifferentiation in chronic gastritis and that an impaired parietal cell differentiation might play a key role in disturbed gastric morphogenic processes.
HISTOLOGICAL TYPES CHARACTERIZATION GENERAL
The histopathological spectrum of type A gastritis.
Eidt S, Oberhuber G, Schneider A, Stolte M.
Institute of Pathology, Klinikum Bayreuth, Germany.
Pathol Res Pract 1996 Feb;192(2):101-6 Abstract quote
It has been recently shown that type A gastritis can be histologically diagnosed in the preatrophic stage.
In order to evaluate whether parietal cell atrophy in AG might correlate with other histopathological findings in the antral and body mucosa, we retrospectively investigated 171 consecutive cases of histologically diagnosed preatrophic (active) or atrophic type A gastritis (H&E, Warthin-Starry).
The prevalences of intestinal metaplasia (75% vs 44.4%) and micronodular hyperplasia (86.1% vs 52.4%) of endocrine cells in the oxyntic mucosa were significantly higher of parietal cell atrophy was present (p < 0.001 and p < 0.0001, respectively), whereas the prevalence of nodular lymphoid aggregates (77.8% vs 48.1%) and of Helicobacter pylori (14.3% vs 1.9%) in the oxyntic mucosa was significantly higher if parietal cell atrophy could not be detected (p < 0.001 and p < 0.01, respectively). In the antral mucosa, altered patterns of the inflammatory reaction could be demonstrated independent of the parietal cell mass possibly caused by impaired gastric acid production.
Our data support the notion that the development of parietal cell atrophy in type A gastritis represents a stepwise process including initial pseudohypertrophy of these cells.
Autoimmune Gastritis: Distinct Histological and Immunohistochemical Findings Before Complete Loss of Oxyntic Glands
Michael Torbenson, M.D., Susan C. Abraham, M.D., John Boitnott, M.D., John H. Yardley, M.D. and Tsung-Teh Wu, M.D., Ph.D.
Division of Gastrointestinal/Liver Pathology, Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
Mod Pathol 2002;15:102-109 Abstract quote
Autoimmune gastritis (AG) can be easily recognized when the histological features are fully developed, but recognizing AG before the complete loss of the oxyntic mucosa is more challenging. One feature of fully developed AG is enterochromaffin cell-like (ECL) hyperplasia, but its presence or absence in earlier stages of AG has not been fully evaluated.
A retrospective study of biopsy specimens from 40 patients was performed; all of the patients were originally diagnosed with possible AG based on the presence of lymphocytic infiltration and damage to oxyntic glands and/or the presence of metaplastic epithelium that disproportionately involved the body mucosa. Nineteen cases had follow-up serological studies for antiparietal cells and/or antiintrinsic factor antibodies: 13 were positive and 6 negative. The remaining 21 cases were indeterminate because of incomplete testing.
The histological findings were similar in the patients who were serologically positive and those who were indeterminate for AG. In all of these cases, the oxyntic mucosa showed lymphoplasmacytic infiltrates within the lamina propria with focal gland infiltration and damage. Sixty-five percent (22/34) of the cases showed intestinal and/or pyloric metaplasia, and 85% (29/34) showed parietal cell pseudohypertrophy. Chromogranin stains were performed in 11 of 13 cases with positive serological markers for AG, and all showed at least linear ECL cell hyperplasia. In contrast, none of the six cases with negative serological studies had linear ECL cell hyperplasia, P < .001.
In conclusion, the following constellation of findings supports a diagnosis of AG before the complete loss of oxyntic mucosa: deep or diffuse lymphoplasmacytic infiltrates within the lamina propria with foci of gland infiltration and damage, epithelial metaplasia, parietal cell pseudohypertrophy, and ECL cell hyperplasia at the linear or greater level.
VARIANTS ATROPHIC AUTOIMMUNE PANGASTRITIS
- Atrophic Autoimmune Pangastritis: A Distinctive Form of Antral and Fundic Gastritis Associated With Systemic Autoimmune Disease.
Departments of *Pathology double daggerGastroenterology and Hepatology, Mayo Clinic, Rochester, MN daggerDepartment of Pathology, The Johns Hopkins Hospital, Baltimore, MD section signHospital Pathology Associates, P.A., Abbott NW Hospital, Minneapolis, MN.
- Am J Surg Pathol. 2006 Nov;30(11):1412-1419. Abstract quote
The 2 major recognized forms of atrophic gastritis are autoimmune and environmental atrophic gastritis. These differ in their topographical distribution in the stomach, histologic features, and etiology. Autoimmune atrophic gastritis results from immune-mediated destruction of specialized oxyntic glands, is restricted to the body and fundus, and shows characteristic neuroendocrine hyperplasia. Environmental atrophic gastritis is associated with long-standing Helicobacter pylori infection and preferentially involves antrum and transition zone mucosa.
In this study, we describe a distinctive form of atrophic gastritis that differs markedly from both of these classic variants. This gastritis is characterized by: (1) intense mucosal inflammatory infiltrates, persisting even into the phase of severe glandular atrophy, (2) pangastric distribution with diffuse involvement of both body and antrum, (3) lack of association with H. pylori, and (4) lack of neuroendocrine hyperplasia. The 8 patients presented ranged from 1 to 75 years and showed a slight female predominance (5F:3M).
All had systemic autoimmune and/or connective tissue diseases including autoimmune enterocolitis (4 cases), systemic lupus erythematosus, refractory sprue, autoimmune hemolytic anemia, and disabling fibromyalgia. Positive serum autoimmune markers were documented in 7 of 8 (87%) patients, but serologies for antiparietal cell and anti-intrinsic factor antibodies were undertaken in only 1 patient each and were negative.
We propose that the distinctive histology of this form of atrophic pangastritis and its association with systemic autoimmune disease suggests an autoimmune process directed against multiple cell lineages in the stomach. The development of multifocal low-grade dysplasia in 1 patient, a 19-year-old woman, suggests that this condition might have neoplastic potential.
Active autoimmune gastritis without total atrophy of the glands.
Stolte M, Baumann K, Bethke B, Ritter M, Lauer E, Eidt H.
Institut fur Pathologie, Klinikum Bayreuth, Bundesrepublik Deutschland.
Z Gastroenterol 1992 Oct;30(10):729-35 Abstract quote
To date, autoimmune gastritis has been diagnosed for the most part only when total atrophy of the oxyntic glands is detected.
On the basis of 40 patients without total atrophy of the glands, and with parietal cell antibodies in the serum, we show that the diagnosis of type A gastritis is also possible in the pre-atrophic stage.
The histological criteria for the diagnosis of active autoimmune gastritis without total atrophy of the glands are 1. usually dense, diffuse locally emphasized lymphocytic infiltration of the lamina propria between the glands in the oxyntic mucosa, 2. focal destruction of individual glands in the corpus of the stomach by lymphocytes, and 3. reactive pseudohypertrophy of the parietal cells.
A comparison with a group of patients with autoimmune gastritis and total atrophy of the glands shows that in active autoimmune gastritis, too, women are more frequently affected than men (in both groups, the sex ratio is approximately 3:1). Patients without atrophy of the glands are, on average, about 12 years younger than those with "burnt out" type A gastritis (average age 69.98:57.80 years). While in the case of burnt out type A gastritis, no colonisation with Helicobacter pylori was to be found, such colonisation was demonstrated for the corpus mucosa in 22.5%, and for the antral mucosa in 15.0%. In 27.5% a minimal or low-grade inactive superficial gastritis, as may be seen after eradication of Helicobacter pylori, was additionally diagnosed in the antrum.
A knowledge of the histological appearance of the pre-atrophic stage of type A gastritis might be of importance for the possible prevention of pernicious anaemia.
ENDOCRINE CELL GROWTHS
Endocrine cell growths in atrophic body gastritis. Critical evaluation of a histological classification.
Bordi C, Annibale B, Azzoni C, Marignani M, Ferraro G, Antonelli G, D'Adda T, D'Ambra G, Delle Fave G.
Department of Anatomic Pathology, University of Parma, Italy.
J Pathol 1997 Jul;182(3):339-46 Abstract quote
The aim of the present study was to evaluate the correspondence of the classification of non-antral endocrine cell growths proposed by Solcia and co-workers with clinical features and non-endocrine mucosal changes.
For this purpose, 94 cases of newly diagnosed atrophic body gastritis were investigated using endoscopic biopsies and compared with 18 control subjects. The patients were subdivided into the following four groups according to the most severe pattern of endocrine cell proliferation found in the body mucosa, as shown by chromogranin A immunostaining: group 1, normal pattern (7 cases, 7.5 per cent); group 2, simple hyperplasia (6 cases, 6.5 per cent); group 3, linear hyperplasia (24 cases, 25.8 per cent); group 4; micronodular hyperplasia (56 cases, 60.2 per cent). Adenomatoid hyperplasia was found in only one case, thus precluding further analysis. Patients in groups 1 and 2 had lower acid secretion, higher gastrin level, and higher mean scores in all histopathological variables of chronic gastritis considered by the Sydney system when compared with controls, but did not differ among them in any parameter investigated.
When compared with groups 1 and 2, patients of groups 3 and 4 showed higher values of circulating gastrin, higher scores of glandular atrophy, and lower values of acid secretion and of mononuclear and neutrophil inflammatory cell infiltration. Moreover, group 4 patients differed significantly from those of group 3 in their higher gastrin levels and atrophy scores, and lower scores of neutrophil cell infiltration.
On the basis of these results, it is proposed that for practical purposes the normal and the simple hyperplasia patterns may be incorporated into a single group. It is concluded that this classification in its simplified form, based on a qualitative histological approach, shows clinical relevance without the need to perform expensive, time-consuming morphometric evaluations.
OXYNTIC MUCOSA PSEUDOPOLYPS
Oxyntic mucosa pseudopolyps: a presentation of atrophic autoimmune gastritis.
Krasinskas AM, Abraham SC, Metz DC, Furth EE.
Am J Surg Pathol 2003 Feb;27(2):236-41 Abstract quote
Gastric polyps are often present in the setting of atrophic gastritis. Although the majority of these polyps are nonneoplastic, such as hyperplastic polyps, neoplastic polyps may be present.
We discuss nine cases that illustrate an additional nonneoplastic cause of polyps in atrophic gastritis. Specifically, preserved islands of relatively normal oxyntic mucosa in a background of gastric atrophy may appear polypoid endoscopically. The patients (seven women, two men, mean age 64 years) presented with nonspecific abdominal or reflux symptoms (n = 8) and diarrhea (n = 1). Five of five patients tested were confirmed to have hypergastrinemia, and three of three patients tested had antiparietal cell antibodies.
Biopsies from the gastric body or fundus of our nine patients showed fragments of atrophic mucosa and separate fragments of preserved oxyntic mucosa. Based upon the histologic characteristics of the atrophic fundic and relatively normal antral biopsies, the gastric atrophy appeared to be of autoimmune-type. The relatively preserved oxyntic glands showed parietal cell hypertrophy and focal mild chronic inflammation. The number of polyps observed endoscopically ranged from less than five to multiple/diffuse. Three patients had persistent nodularities in their stomachs for 1, 3, and 7 years of their follow-up. Our study shows that some patients with atrophic gastritis, autoimmune-type, may present with gastric polyps/nodules that represent relatively preserved oxyntic mucosa.
This presentation may be more common than is presently recognized because biopsies of the polyps alone will not show histologic features of atrophic gastritis or reveal the etiology of the polyp itself. Although a limited number of previous studies have suggested this type of polypoid presentation may represent "early" atrophic gastritis, its persistence in three of our patients argues against this hypothesis.
PANCREATIC ACINAR METAPLASIA
Pancreatic acinar cell metaplasia in autoimmune gastritis.
Jhala NC, Montemor M, Jhala D, Lu L, Talley L, Haber MM, Lechago J.
Department of Pathology, Baylor College of Medicine, Houston, Tex, USA.
Arch Pathol Lab Med. 2003 Jul;127(7):854-7. Abstract quote
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.
CHARACTERIZATION SPECIAL STAINS IMMUNOPEROXIDASE
Fundic argyrophil cell hyperplasia in atrophic gastritis: a search for a sensitive diagnostic method.
Belaiche J, Delwaide J, Vivario M, Gast P, Louis E, Boniver J.
Department of Gastroenterology, University of Liege, CHU Sart Tilman, Belgium.
Acta Gastroenterol Belg 1993 Jan-Feb;56(1):11-7 Abstract quote.
Hypergastrinemia induces argyrophil cell hyperplasia in oxyntic mucosa (FACH) in patients with non-antral atrophic gastritis, with or without pernicious anemia. This proliferation favours the development of carcinoid tumours.
In order to determine the most usual appropriate method to document FACH, we have studied 29 consecutive fundic biopsies from 26 patients with fundic chronic gastritis. The study encompassed gastrinemia levels, standard histology permitting the classification of chronic gastritis, demonstration of FACH by Grimelius stain, immunohistochemical studies using NSE, chromogranin A and by electron microscopy. The FACH was classified for each stain as slight, moderate or severe. The study displayed a relationship between the grade of gastritis and the density of argyrophil endocrine cells in oxyntic mucosa assessed by Grimelius stain (p < 0.0001) and chromogranin A (P < 0.01). There was also a relationship between the serum gastrin level and the density of argyrophil endocrine cells detected by these two stains (p < 0.001). A highly significant correlation was observed between Grimelius stain and chromogranin A (p < 0.0001). On the other hand, no significant correlation was noted with either NSE or electron microscopy.
We conclude that Grimelius stain and immunohistochemical studies against chromogranin A were the best methods for the demonstration of FACH in atrophic gastritis. One of these two techniques is sufficient in current practice for defining the patients at risk for subsequent surveillance.
DIFFERENTIAL DIAGNOSIS KEY DIFFERENTIATING FEATURES CHRONIC SUPERFICIAL GASTRITIS
Long-term observation of subjects with normal mucosa and with superficial gastritis: results of 23--27 years' follow-up examinations.
Ihamaki T, Saukkonen M, Siurala M.
Scand J Gastroenterol 1978;13(7):771-5 Abstract quote
261 subjects with a normal body mucosa or with superficial gastritis used as controls for an atrophic gastritis series have been followed up for 23--27 years. Of them, 41 died during the earlier and 63 during the present follow-up period. In all, 141 subjects were reexamined in 1976--1977 and 16 answered a questionnaire. None of the subjects had gastric carcinoma or an adenomatous polyp. One patient diagnosed and reported earlier had died of gastric carcinoma during the present period of observation.
Of the subjects with normal body mucosa 58% had developed superficial and 14% atrophic gastritis. Of those with superficial body gastritis 42% had developed atrophic gastritis and 18% showed an improvement of the gastritic changes. It should be noted, however, that earlier examinations were performed with blind biopsy and the present with direct vision gastroscopic biopsy.
The state of the antral and body mucosa was similar in 53%, antral changes dominated in 33% and the changes in the body in 14%. Intestinal metaplasia was found in 36%, atypical epithelium in 6%, parietal cell antibodies in 0.5% and intrinsic factor antibodies in 0.5%. The fasting serum gastrin level was above 100 ng/ml in 10%. Only 2 cases fulfilled the morphological, functional and immunological criteria of type A gastritis.
The present controls differed from the atrophic gastritis series in that the topography of gastritis was different and in that the incidence of metaplasia, atypia, gastric antibodies and high serum gastrin levels was markedly lower.
FOCALLY ENHANCED GASTRITIS The Clinical Significance of Focally Enhanced Gastritis.
Xin W, Greenson JK.
Department of Pathology, University of Michigan Health System, Ann Arbor, MI.
Am J Surg Pathol. 2004 Oct;28(10):1347-1351 Abstract quote
Focally enhanced gastritis (FEG) is typified by small collections of lymphocytes and histiocytes surrounding a small group of foveolae or gastric glands, often with infiltrates of neutrophils. Several studies have found that FEG is commonly seen in Crohnâ€™s disease patients with a positive predictive value of 94%. Additional studies have found that FEG is present in up to 20% of pediatric ulcerative colitis patients, suggesting that FEG is a marker for inflammatory bowel disease (IBD) in general.
We reviewed all gastric biopsies from a single calendar year (1999) to study the incidence of FEG and its relationship to IBD. A total of 34 cases of FEG were found among 971 gastric biopsies from 927 patients. Only 4 FEG patients were found to have IBD (2 Crohnâ€™s, 1 ulcerative colitis and 1 chronic colitis, type indeterminate, 11.8%, positive predictive value of 5.9%). Five FEG patients were status post bone marrow transplantation (14.7%). There were no other clinical correlations and gastric histopathology did not predict which patients with FEG had IBD.
We conclude that FEG is not a common histologic finding in our patient population and that the positive predictive value of this finding is much too low to be thought of as a specific marker for IBD. An isolated biopsy diagnosis of FEG should not be interpreted as being suggestive of Crohnâ€™s disease.
PROGNOSIS AND TREATMENT CHARACTERIZATION PROGNOSTIC FACTORS CARCINOID TUMORS
Morphology and pathogenesis of endocrine hyperplasias, precarcinoid lesions, and carcinoids arising in chronic atrophic gastritis.
Solcia E, Fiocca R, Villani L, Gianatti A, Cornaggia M, Chiaravalli A, Curzio M, Capella C.
Dept. of Human Pathology, Ist Medical Faculty, University of Pavia, Italy.
Scand J Gastroenterol Suppl 1991;180:146-59 Abstract quote
The spectrum of endocrine cell changes occurring in 80 cases of body-fundus chronic atrophic gastritis (CAG), mostly type A or multifocal, including various types of hyperplasia, precarcinoid lesions (20 cases), and neoplasia (carcinoid, 24 cases) have been analyzed histologically, histochemically, and ultrastructurally.
Changes associated with gland atrophy, pyloric- or intestinal-type metaplasia, regenerative hyperplasia, and hypergastrinemia have been identified and their neoplastic potential evaluated in the light of their proliferative capacity (bromodeoxyuridine incorporation) and clinicopathologic behavior.
A close link between disseminated precarcinoid lesions of non-tumor mucosa and multiple carcinoids (carcinoidosis) arising in hypergastrinemic type-A CAG is suggested. Hyperplastic changes, including endocrine cell clusters, seem to have no or only minimal neoplastic potential.
TREATMENT HELICOBACTER TREATMENT
Cure of autoimmune gastritis by Helicobacter pylori eradication in a 21-year-old male.
Stolte M, Meier E, Meining A.
Institut fur Pathologie, Klinikum Bayreuth.
Z Gastroenterol 1998 Aug;36(8):641-3 Abstract quote
BACKGROUND: More recent investigations have shown that in some patients Helicobacter pylori (Hp) antibodies can act as antigastric antibodies and lead to atrophic autoimmune gastritis of the oxyntic mucosa. The question thus arises as to whether this form of autoimmune gastritis can be healed by eradicating Hp.
METHODS: Case history of a 21-year-old man with active autoimmune gastritis of the oxyntic mucosa with lymphocytic infiltration of the entire lamina propria, foci of lymphocytic destruction of a number of glands, and hypertrophy of the preserved parietal cells, but no signs of Hp in the Warthin Starry stain. The search for parietal cell antibodies and intrinsic factor antibodies proved negative, while the level of the gastrin in the serum was slightly elevated. Since the presence of Hp IgG antibodies (243 U/ml) was confirmed. Hp eradication therapy was carried out.
RESULTS: 15 months after Hp treatment the Hp IgG antibody titre had decreased to 11 U/ml. The autoimmune gastritis had healed, and autoaggressive inflammatory infiltrates with focal destruction of corpus glands and hypertrophy of the parietal cells were no longer detectable.
CONCLUSIONS: Autoimmune gastritis induced by Hp may possibly be cured with Hp eradication treatment; to confirm this, further controlled prospective studies are needed.
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