GASTROENTEROLOGY
1992;103:1113-1123
CORRESPONDENCE Readers are encouraged to write Letters to the Editor concerning articles that have been published in GASTROENTEROLOGY. Short, general comments are also considered, but use of the Correspondence Section for publication of original data in preliminary form is not encouraged. Letters should be typewritten double-spaced and submitted in triplicate.
The Sydney System and Chronic Gastritis Dear Sir: We read with interest the critique presented by Correa and Yardley’ along with the accompanying editorial* concerning the Sydney system of classifying chronic gastritis. We agree with Rubin’s comments favoring a clinicopathologic approach to the diagnosis of gastritis rather than a complex histological classification. In this regard, we propose that the greatest value could be obtained from a biopsy by providing a uniform and a comprehensive description of histological parameters. These data could then be analyzed for histopathologic patterns based on current knowledge and correlated with clinical data to achieve the best possible overall diagnosis. As our understanding of histological patterns and clinical parameters evolves, the baseline data would then be available on older biopsies to allow reclassification. It is far more useful, clinically and conceptually, to divide in a geographical way the extent of the gastritis present. Therefore, we would propose the adoption of a standardized “gastritis reporting form” such as the one described below: 1. Distribution: Antrum
Incisura
Corpus
Pangastric
2. Atrophy: Absent
Present a. If present, intestinal
metaplasia: Absent
Present 3. Inflammation: a. Distribution: Superficial
Epithelial
Superficial & deep
infiltration
b. Type: Eosinophils
Lymphocytes
Granulomas
Neutrophils
4. Dysplasia Present
Absent a. If present: Mild
Severe
Moderate
5. Foveolar Hyperplasia Present
Absent 6. Helicobacter
pylori Absent
Present
Not evaluated
a. If present: Antrum 7. Other Morphological 8. Interpretive
Corpus
Both
Findings
Comments
To classify chronic gastritis as suggested by the authors, a systematic way of obtaining biopsy specimens in very much the same way that specimens are obtained in a patient with Barrett’s esoph-
agus (four quadrant biopsies every 2-3 cm) should be promoted. In the stomach, four quadrant specimens could be obtained every 4-5 cm starting from the pyloric end in order to best differentiate diffuse from multifocal gastritis. GEORGE YOUNGBERG.M.D. Chief, Surgical Pathology VA Medical Center Johnson City, Tennessee 37614-0622 1.
Correa P, Yardley JH. Grading and classification of chronic gastritis: one American response to the Sydney system. Gastroenterology 1992;102:355-359, of chronic gastritis: an 2. Rubin CE. Histological classification iconoclastic view. Gastroenterology 1992:102:360-361.
Some German Remarks on ‘One American Response to the Sydney System’ Dear Sir: Recently, GASTROENTEROLOGY published two papers from the New World’,’ in which many of the points made were not in line with the facts in the Old (European) World.3 Correa and Yardley’ claim that autoimmune gastritis limited to the oxyntic mucosa is found almost exclusively in Scandinavian populations. We are unable to confirm this. In 1990, in our own referred material, for example, we identified autoimmune gastritis in 296 patients, which represents 3% of all cases of gastritis diagnosed annually in material, predominantly gastroenterological-histological, obtained from approximately 80,000 patients a year. Additionally, Correa and Yardley maintain that duodenal and pyloric peptic ulcers are accompanied by a chronic gastritis limited to the antrum. From the German point of view, this claim, too, is incorrect. On the one hand, Helicobacter pylori-induced gastritis is not-as the German surgeon Konjetzny correctly noted in the 1920s4-gastritis accompanying the ulcer, but its underlying disease, which means that the ulcers, which are a sequela of gastritis, can be cured by eradicating H. pylori. On the other hand, an H. pylori-induced gastritis in the oxyntic mucosa can readily be found in patients with duodenal ulcers, too,” which, as was clear even before the rediscovery of H. pylori,’ is only insignificantly less severe and less active than the gastritis that represents the underlying disease of gastric ulcer.” This is possibly a result of the fact that the zone of corporeal mucosa in patients with pyloric gastritis and a duodenal ulcer compared with the zone of antral mucosa is considerably larger than in patients with gastric ulcers secondary to H. pylori-induced gastritis,‘.I0 which means that more of the ammonia produced by H. pylori is neutralized by the gastric acid and can thus do less damage to the mucosa.11-13 The claim made by Correa and Yardley to the effect that the intestinal metaplasia is not part of diffuse antral gastritis also cannot be allowed to go unchallenged. In our material comprising 2-3 forceps biopsy specimens taken from the antrum in each of 996 patients with duodenal ulcers, we have identified intestinal metaplasia in 15.6 / .l4The incidence of intestinal metaplasia increases Oo with increasing age of the patient15 and with increasing severity of gastritis.‘” Also, forms of therapy directed toward gastric acid lead to an increase in the incidence of intestinal metaplasia of the antral mucosa in patients with duodenal ulcers. Thus, vagotomy and
1992;103:1113-1123
CORRESPONDENCE Readers are encouraged to write Letters to the Editor concerning articles that have been published in GASTROENTEROLOGY. Short, general comments are also considered, but use of the Correspondence Section for publication of original data in preliminary form is not encouraged. Letters should be typewritten double-spaced and submitted in triplicate.
The Sydney System and Chronic Gastritis Dear Sir: We read with interest the critique presented by Correa and Yardley’ along with the accompanying editorial* concerning the Sydney system of classifying chronic gastritis. We agree with Rubin’s comments favoring a clinicopathologic approach to the diagnosis of gastritis rather than a complex histological classification. In this regard, we propose that the greatest value could be obtained from a biopsy by providing a uniform and a comprehensive description of histological parameters. These data could then be analyzed for histopathologic patterns based on current knowledge and correlated with clinical data to achieve the best possible overall diagnosis. As our understanding of histological patterns and clinical parameters evolves, the baseline data would then be available on older biopsies to allow reclassification. It is far more useful, clinically and conceptually, to divide in a geographical way the extent of the gastritis present. Therefore, we would propose the adoption of a standardized “gastritis reporting form” such as the one described below: 1. Distribution: Antrum
Incisura
Corpus
Pangastric
2. Atrophy: Absent
Present a. If present, intestinal
metaplasia: Absent
Present 3. Inflammation: a. Distribution: Superficial
Epithelial
Superficial & deep
infiltration
b. Type: Eosinophils
Lymphocytes
Granulomas
Neutrophils
4. Dysplasia Present
Absent a. If present: Mild
Severe
Moderate
5. Foveolar Hyperplasia Present
Absent 6. Helicobacter
pylori Absent
Present
Not evaluated
a. If present: Antrum 7. Other Morphological 8. Interpretive
Corpus
Both
Findings
Comments
To classify chronic gastritis as suggested by the authors, a systematic way of obtaining biopsy specimens in very much the same way that specimens are obtained in a patient with Barrett’s esoph-
agus (four quadrant biopsies every 2-3 cm) should be promoted. In the stomach, four quadrant specimens could be obtained every 4-5 cm starting from the pyloric end in order to best differentiate diffuse from multifocal gastritis. GEORGE YOUNGBERG.M.D. Chief, Surgical Pathology VA Medical Center Johnson City, Tennessee 37614-0622 1.
Correa P, Yardley JH. Grading and classification of chronic gastritis: one American response to the Sydney system. Gastroenterology 1992;102:355-359, of chronic gastritis: an 2. Rubin CE. Histological classification iconoclastic view. Gastroenterology 1992:102:360-361.
Some German Remarks on ‘One American Response to the Sydney System’ Dear Sir: Recently, GASTROENTEROLOGY published two papers from the New World’,’ in which many of the points made were not in line with the facts in the Old (European) World.3 Correa and Yardley’ claim that autoimmune gastritis limited to the oxyntic mucosa is found almost exclusively in Scandinavian populations. We are unable to confirm this. In 1990, in our own referred material, for example, we identified autoimmune gastritis in 296 patients, which represents 3% of all cases of gastritis diagnosed annually in material, predominantly gastroenterological-histological, obtained from approximately 80,000 patients a year. Additionally, Correa and Yardley maintain that duodenal and pyloric peptic ulcers are accompanied by a chronic gastritis limited to the antrum. From the German point of view, this claim, too, is incorrect. On the one hand, Helicobacter pylori-induced gastritis is not-as the German surgeon Konjetzny correctly noted in the 1920s4-gastritis accompanying the ulcer, but its underlying disease, which means that the ulcers, which are a sequela of gastritis, can be cured by eradicating H. pylori. On the other hand, an H. pylori-induced gastritis in the oxyntic mucosa can readily be found in patients with duodenal ulcers, too,” which, as was clear even before the rediscovery of H. pylori,’ is only insignificantly less severe and less active than the gastritis that represents the underlying disease of gastric ulcer.” This is possibly a result of the fact that the zone of corporeal mucosa in patients with pyloric gastritis and a duodenal ulcer compared with the zone of antral mucosa is considerably larger than in patients with gastric ulcers secondary to H. pylori-induced gastritis,‘.I0 which means that more of the ammonia produced by H. pylori is neutralized by the gastric acid and can thus do less damage to the mucosa.11-13 The claim made by Correa and Yardley to the effect that the intestinal metaplasia is not part of diffuse antral gastritis also cannot be allowed to go unchallenged. In our material comprising 2-3 forceps biopsy specimens taken from the antrum in each of 996 patients with duodenal ulcers, we have identified intestinal metaplasia in 15.6 / .l4The incidence of intestinal metaplasia increases Oo with increasing age of the patient15 and with increasing severity of gastritis.‘” Also, forms of therapy directed toward gastric acid lead to an increase in the incidence of intestinal metaplasia of the antral mucosa in patients with duodenal ulcers. Thus, vagotomy and
