Abstract and Introduction
Abstract
Purpose of Review: The majority of problems in interpreting gastritis remain Helicobacter related, but their nature has changed. The present review covers gastritis historically through cancer risk staging systems.
Recent Findings: Key points to remember are: Helicobacter is associated with several forms of gastritis; in the present review, I am focusing on the two ends of the disease, 'Helicobacter pylori infection', that starts with antral predominant gastritis but can continue to oxyntic predominant disease with atrophy; the role Helicobacter pylori plays in autoimmune gastritis with pernicious anemia remains unresolved; gastritis staging systems for cancer risk, namely Baylor and Operative Link on Gastritis Assessment, are currently available.
Summary: As most gastric carcinomas arise on a background of atrophic gastritis, and the risk increases with the extent of atrophy, an index of atrophy location and extent could be useful in predicting patients at greatest risk for carcinoma. It is now possible to stage patients for cancer risk. Nonetheless, in a field such as gastritis in which many issues remain unresolved, a classification or staging system that is more descriptive will likely prove more useful.
Recent Findings: Key points to remember are: Helicobacter is associated with several forms of gastritis; in the present review, I am focusing on the two ends of the disease, 'Helicobacter pylori infection', that starts with antral predominant gastritis but can continue to oxyntic predominant disease with atrophy; the role Helicobacter pylori plays in autoimmune gastritis with pernicious anemia remains unresolved; gastritis staging systems for cancer risk, namely Baylor and Operative Link on Gastritis Assessment, are currently available.
Summary: As most gastric carcinomas arise on a background of atrophic gastritis, and the risk increases with the extent of atrophy, an index of atrophy location and extent could be useful in predicting patients at greatest risk for carcinoma. It is now possible to stage patients for cancer risk. Nonetheless, in a field such as gastritis in which many issues remain unresolved, a classification or staging system that is more descriptive will likely prove more useful.
Introduction
As the development of gastric carcinoma is an unpredictable process, recognizing the presence and extent of gastritis with associated atrophy can help identify patients with different gastric cancer risk. The present review is an overview of our approach to gastritis, including the most recently described histology-based gastritis staging systems, the Baylor System[1] and Operative Link on Gastritis Assessment (OLGA) System.[2,3•]
Atrophic Body Gastritis in Patients With Autoimmune Thyroid Disease
An Underdiagnosed Association
Marco Centanni, MD; Massimo Marignani, MD; Lucilla Gargano, MD; Vito D. Corleto, MD; Alessandro Casini, MD; Gianfranco Delle Fave, MD; Mario Andreoli, MD; Bruno Annibale, MD
Arch Intern Med. 1999;159:1726-1730.
Background Atrophic body gastritis (ABG) has never been histologically characterized in patients with autoimmune thyroid disease (AITD), and its prevalence may be substantially different from that previously assessed based on only indirect evidence.
Objective To detect and characterize the presence of ABG in patients with AITD.
Methods Sixty-two patients with AITD (5 men and 57 women), aged between 21 and 74 years, have been screened for the presence of ABG by assaying serum gastrin levels. Patients with hypergastrinemia underwent gastroscopy followed by the histological examination of multiple biopsy specimens. The diagnosis of ABG was based on hypergastrinemia and pentagastrin-resistent achlorhydria, confirmed by histological examination.
Results Twenty-two (35%) of 62 patients had hypergastrinemia (mean ± SEM gastrin level, 1070 ± 288 pmol/L). The diagnosis of ABG has been histologically confirmed in all 22 patients, and the score of atrophy was moderate to severe. In group A (patients aged 20-40 years; n=21), 6 patients (29%) had ABG, compared with 11 patients (37%) in group B (patients aged 41-60 years; n=30) and 5 patients (45%) in group C (patients aged 61-80 years; n=11). Antiparietal cell antibodies were detected in only 68% (15/22) of patients with ABG. Anemia was observed in 82% (18/22) of patients with AITD and ABG but only in 22% (9/40) of patients without ABG (P<.0001).
Conclusions In the patients with AITD studied, about one third had ABG, which was diagnosed also in young patients; the measurement of gastrin levels represented the most reliable tool in the diagnosis of ABG; and the presence of anemia, even microcytic, was suggestive of undiagnosed ABG.
From the Departments of Experimental Medicine and Pathology (Drs Centanni, Gargano, Casini, and Andreoli), Gastroenterology (Drs Marignani, Delle Fave, and Annibale), and Cell Biotechnology and Hematology (Dr Corleto), University of Rome "La Sapienza"; and Institute of Experimental Medicine, Consiglio Nazionale Delle Ricerche (Drs Centanni and Andreoli), Rome, Italy.
Abstract
Dyspepsia is a common clinical problem. Its causes include peptic ulcer disease, gastroesophageal reflux, and functional (nonulcer) dyspepsia. A detailed clinical description of pain does not reliably differentiate the cause. Approximately 80% of gastroscopies are performed for the investigation of dyspepsia. "Gastritis" is diagnosed endoscopically in 59% of all stomachs, although in only 3% are the changes severe. Pathologic examination of unselected gastric biopsy specimens reveals that abnormalities are present in 62–73%, but there is only a weak correlation between endoscopic and histologic findings. For these reasons, it is recommended that endoscopic examination should always be accompanied by biopsy. Ideally, biopsies should be taken in a systematic fashion to include sampling of antrum and corpus. Recent evidence suggests that gastric infection by Helicobacter pylori initially presents as a superficial gastritis. Later it may become atrophic with development of intestinal metaplasia. The onset of atrophic changes may be related to the duration of infection, the strain of the infecting organism, associated dietary factors, or as-yet undefined host factors related to immunity. Persistent superficial gastritis predisposes to duodenal ulcer and gastric mucosa–associated lymphoid tissue lymphoma. Atrophic gastritis predisposes to gastric ulcer and adenocarcinoma. Evidence is accumulating that in some patients, pernicious anemia may be an end result of H. pylori–induced atrophic gastritis. Reactive gastropathy is a relatively common finding in gastric biopsies; in most instances it is associated with either reflux of duodenal contents or therapy with nonsteroidal anti-inflammatory drugs. Lymphocytic gastritis, eosinophilic gastritis, and the gastritis associated with Crohn's disease are distinct morphologic entities. Lymphocytic gastritis and eosinophilic gastritis have a variety of clinical associations. Carditis is a controversial topic: currently opinions are divided as to whether it is the result of gastroesophageal reflux or a proximal extension of H. pylori infection from the remainder of the stomach.
Keywords:
Atrophic gastritis, Carditis, Gastric cardia, Gastric Crohn's disease, Gastritis, Helicobacter, Lymphocytic gastritis, Pernicious anemia, Proton pump inhibitors, Reactive gastropathy
od Pathol 2003;16(4):325–341
Gastritis and Carditis
David A Owen M.B.1
1University of British Columbia, Vancouver, British Columbia, Canada
Correspondence: David A. Owen, M.B., Dept. of Pathology and Laboratory Medicine, Vancouver General Hospital, 855 West 12th Avenue, Vancouver, B.C. Canada V5Z 1M9; fax: (604) 875-4797; e-mail: dowen@vanhosp.bc.ca.
Accepted 8 January 2003.
Collagenous Gastritis: A Case Report, Morphologic Evaluation, and Review
Abstract
Collagenous gastritis is rare; there are only four previous case reports. Histologic features seem to overlap with the other "collagenous enterocolitides"; however, pathologic criteria are not yet established for the diagnosis of collagenous gastritis. We describe an additional case of ostensible collagenous gastritis in a patient who initially presented with celiac sprue and subsequently developed colonic manifestations of mucosal ulcerative colitis. Endoscopic biopsies of the stomach revealed deposition of patchy, very thick bandlike subepithelial collagen in gastric antral mucosa, focal superficial epithelial degeneration, numerous intraepithelial lymphocytes, and a dense lamina propria lymphoplasmacytic infiltrate. Image analysis evaluation of gastric antral biopsies demonstrated a mean thickness of subepithelial collagen of 27.07 
. Morphologic comparison was made with age-matched control groups of 10 patients who had normal gastric mucosal biopsies and 10 patients who had "chronic" gastritis, which revealed mean subepithelial collagen measures of 1.37 and 1.19 , respectively. We compared these morphologic findings with those of all previous case reports of collagenous gastritis and propose a pathologic definition based on the limited combined data. It seems that subepithelial collagen is dramatically thickened in reported cases of collagenous gastritis, with a cumulative mean measure of 36.9 . It is also apparent from this and previous reports that the thickened subepithelial collagen is accompanied by a chronic or chronic active gastritis and sometimes intraepithelial lymphocytes and surface epithelial damage. Recently described associations of lymphocytic gastritis, sprue, and lymphocytic colitis as well as collagenous and lymphocytic colitis suggest a common pathogenesis that empirically may include collagenous gastritis in the same disease spectrum. We propose that collagenous gastritis can be confidently identified by using analogous defined features of collagenous colitis: subepithelial collagen more than 10 in a patchy distribution, lamina propria lymphoplasmacytic infiltrates, intraepithelial lymphocytes, and surface epithelial damage. Collagenous gastritis also seems to have the same spectrum of associated clinical findings as collagenous colitis, including frequent coexistence of celiac sprue, watery diarrhea syndrome, and female predominance.
. Morphologic comparison was made with age-matched control groups of 10 patients who had normal gastric mucosal biopsies and 10 patients who had "chronic" gastritis, which revealed mean subepithelial collagen measures of 1.37 and 1.19 , respectively. We compared these morphologic findings with those of all previous case reports of collagenous gastritis and propose a pathologic definition based on the limited combined data. It seems that subepithelial collagen is dramatically thickened in reported cases of collagenous gastritis, with a cumulative mean measure of 36.9 . It is also apparent from this and previous reports that the thickened subepithelial collagen is accompanied by a chronic or chronic active gastritis and sometimes intraepithelial lymphocytes and surface epithelial damage. Recently described associations of lymphocytic gastritis, sprue, and lymphocytic colitis as well as collagenous and lymphocytic colitis suggest a common pathogenesis that empirically may include collagenous gastritis in the same disease spectrum. We propose that collagenous gastritis can be confidently identified by using analogous defined features of collagenous colitis: subepithelial collagen more than 10 in a patchy distribution, lamina propria lymphoplasmacytic infiltrates, intraepithelial lymphocytes, and surface epithelial damage. Collagenous gastritis also seems to have the same spectrum of associated clinical findings as collagenous colitis, including frequent coexistence of celiac sprue, watery diarrhea syndrome, and female predominance.Keywords:
Celiac sprue, Collagenous colitis, Collagenous gastritis, Lymphocytic colitis, Lymphocytic gastritis, Mucosal ulcerative colitis
Abstract
Background
Tetanus is a serious but vaccine-preventable disease and fatality rate of the disease is high in the neonates and the elderly. The aim of this study was to detect the tetanus antibody prevalence in the over sixty-year age residents of the nursing homes in Bolu.
Methods
A voluntary-based study was done in the residents of two nursing homes in Bolu, Turkey. Blood samples were taken from 71 volunteers residing in there nursing homes. Tetanus IgG antibodies were measured by a commercial ELISA kit.
Results
Among overall subjects, only 11 (15.7 %) had the protective tetanus antibody titers at the time of the study. Totally, 10 subjects were examined in emergency rooms due to trauma or accidents within the last ten years and, four (40%) of them had protective antibody levels. Of the remaining 61 subjects only 7 (11%) had protective antibody levels (p < 0.05) [Relative Risk = 3.49, 95% Confidence Interval 1.24–9.77].
Conclusions
Tetanus antibody level is below the protective level in the majority of the over-sixty-year-age subjects residing in the nursing homes. Each over sixty-year age person in our country should be vaccinated. Until this is accomplished, at least, nursing home residents should be vaccinated during registration.
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