Gastritis and Erosions in the Pyloric Sphincteric Cylinder #

Holsti (l931) stated that inflammatory alterations of gastritis usually affected the mucosa, but that changes also occurred in the deeper layers of the wall in 66 percent of cases, and even the serous layer might be involved. He performed detailed histological studies of the intramural ganglia in gastric resection specimens affected by chronic gastritis (in the absence of peptic ulceration). Compared with normal controls, the ganglia of gastritis showed marked changes affecting the periganglionar, capsular and intraganglionar structures. The outstanding feature was an increase in connective tissue both in the periganglionar and intraganglionar regions, coupled with intraganglionar infiltration of inflammatory cells and degeneration of ganglion cells; in some ganglia hardly a single normal cell was seen. The changes were more marked in Auerbach's than in Meissner's plexus and more advanced in the pyloric than in the fundic zone. The intensity of the condition varied from case to case, from ganglion to ganglion, and even from one part of a ganglion to another. The spatial spread of the process was uneven, but two components of the wall, namely the mucosa and Auerbach's plexuses, were always involved.

Schindler et al. (l937) pointed out that at that time the normal histological picture of the gastric mucosa was still being debated. Specimens for examination were rarely obtained from healthy stomachs as postmortem changes altered the picture and healthy stomachs were not resected. Minor histological changes did not indicate active disease but were the normal reaction to external irritants, such as hot or cold food; those changes were not due to chronic gastritis. Gastroscopy could be carried out in normal persons, and on the basis of systematic gastroscopic investigations it was suggested that chronic gastritis could be divided into 3 types: superficial, atrophic and hypertrophic. Demonstrating the mucosal folds by means of radiological relief techniques was of little value in the diagnosis of chronic gastritis.

Golden (l937) defined gastritis as inflammation of the gastric wall of unknown etiology, which began in and might be limited to the mucosa, but which frequently extended to the deeper layers and even to the serosa. It could be generalized, but was often patchy and not infrequently it was limited to, or had its maximum effect in, the antrum. The term "antrum" was used synonymously with the canalis egestorius as described by Forssell (l913), while antral systole and diastole indicated contraction and relaxation of the canalis respectively. As the canalis egestorius was the most important part of the stomach as far as motility was concerned, inflammatory change here could be expected to produce serious disturbances in gastric motive function.

Golden (l937) agreed with Schindler et al. (l937) and other previous authors that in many cases of gastritis the change in the mucous membrane could not be demonstrated by radiology, and the condition could only be diagnosed by gastroscopy. In other cases, however, the canalis exhibited motility disorders which were readily apparent during the radiological examination; in some there was absence of contraction (absence of "antral systole"), while in others a greater or lesser degree of "antral" spasm was seen. The spasm could vary from marked contraction to failure of full relaxation of the canalis. Involvement of the deeper layers of the wall by inflammatory infiltration and fibrosis could hamper or prevent normal movements of the muscularis mucosae and consequently of the mucosal folds (Chaps. 2, 13); as a result the folds failed to change in direction as they normally did during antral systole, causing them to appear exaggerated. These features enabled Golden (l937) to make a radiological diagnosis of "antral gastritis and spasm" in appropriate cases. The prepyloric narrowing was sometimes associated with mucosal erosions which at that time were only demonstrable by gastroscopy or histological examination.

In histological studies of 100 partial gastrectomy specimens, Magnus (l946) found that inflammatory gastritis affecting the pyloric region consisted of two types. The first type, acute erosive pyloric gastritis, was characterized by polymorphonuclear infiltration of the mucosa, with lesser numbers of lymphocytes, plasma cells and eosinophils. The glandular epithelium showed degenerative changes, there was capillary hyperaemia with mucosal oedema, and erosions were visible on the surface. The typical erosion had the size of a pin's head and involved only the superficial part of the mucosa, i.e. it did not extend through the mucosa and muscularis mucosae into the submucosa; erosions varied in number from a few to over a hundred in individual cases. The second type, chronic atrophic gastritis, was characterized by atrophy of the glandular parenchyma, fibrosis in the mucosa and submucosa, intense infiltration of the interstitial tissue by plasma cells and lymphocytes, and intestinal metaplasia of the gastric epithelium. There was a transition from acute erosive to chronic atrophic pyloric gastritis, and the two types were sometimes found together.

MacDonald and Rubin (l967) found that gastric suction biopsy studies of gastritis had been disappointing; blind suction biopsy often missed the pyloric mucosal zone and specimens of pyloric mucosa were seldom obtained. Examination of the entire length of gastrectomy specimens by means of the Swiss roll technique afforded better results. For a variety of reasons the definition and classification of chronic gastritis remained unsatisfactory. Correlation between the radiological mucosal fold pattern and histological findings was poor.

Studies by Gear et al. (l97l), (Chap. 29), showed that ulcers of the body of the stomach were associated with more extensive and more severe gastritis than ulcers of the prepyloric region. In the latter gastritis was usually localized to the distal stomach, it was often superficial and showed little evidence of atrophic change or metaplasia. The fact that gastritis persisted in spite of healing of the gastric ulceration, indicated that it was the basic disease process and not simply a zonal change secondary to the ulcer. By means of fibreoptic gastroscopy Whitehead et al. (l972) obtained fresh, multiple full- thickness biopsy specimens from all parts of the gastric mucosa in a large number of patients. They proposed a classification of chronic gastritis applicable to all zones of the mucosa, based on the following features: First, the mucosal type had to be established, e.g. pyloric mucosa had to be differentiated from pseudopyloric metaplasia of body mucosa. Second, the grade had to be determined; chronic atrophic gastritis (in which there was atrophy of tubules) could be subdivided into mild, moderate and severe grades. Third, the stage of activity had to be established; both superficial and atrophic gastritis could be either active or quiescent. Fourth, the presence and type of metaplasia had to be determined; it was acknowledged that difficulties could arise in recognizing mucosal type when severe gastritis was associated with metaplasia or atrophy. In their classification the degree of atrophy, rather than the degree of chronic cellular infiltration, was graded. It was also established that intestinal metaplasia nearly always occurred in mucosa which was the site of atrophic gastritis.

Strickland and Mackay (l973) reviewed the nature of chronic atrophic gastritis in relation to the structure and function of the pyloric antrum, where "antrum" was equated with the pyloric mucosal zone. Two distinct types of atrophic gastritis were recognized. In Type A, tests for parietal cell autoantibody and intrinsic factor antibody were positive; there was sparing of antral mucosa, with diffuse changes in the corpus, and severe impairment of gastric secretion. In Type B, parietal cell autoantibody and intrinsic factor antibody reactions were negative; there was definite antral involvement with focal changes in the corpus, and moderate impairment of gastric secretion. Benign gastric ulceration of the corpus was found to be associated with Type B atrophic gastritis; the more proximally the ulcer was located in the stomach, the more extensive the gastritis and the more severe the impairment of acid secretion proved to be. Chronic atrophic gastritis persisted after ulcer healing, supporting the view that gastric ulcer originated from chronic gastritis.

Rao et al. (l975) stated that the term chronic gastritis carried different connotations for the clinician, the pathologist and the radiologist. Previously little attention had been given to determining the degree of chronic cellular infiltration involving the full thickness of the gastric mucosa. They supported the use of terms which described the morphological abnormalities found in mucosal biopsies, namely the degree of cellular infiltration of the whole mucosa and the presence or absence of atrophy. A simple descriptive classification of chronic gastritis into mild, moderately severe and severe grades, with or without atrophy or metaplasia, was recommended. Mucosal biopsies in 241 patients with a variety of upper abdominal conditions showed chronic gastritis in 184. Only 3 of the patients were diagnosed as true superficial gastritis, where the cellular infiltration was limited to the lamina propria between the pits.

Op den Orth and Dekker (l976) described erosions as superfical mucosal defects which did not penetrate the muscularis mucosae. A flat erosion was a mucosal defect without reaction in the adjacent parts, while a varioliform or complete erosion indicated a mucosal defect surrounded by an elevated zone; the elevated zone had been variously interpreted as a circular contraction of the muscularis mucosae, oedema, leucocytic infiltration, or fibrosis. It was pointed out that erosions could occur as solitary lesions or in combination with other upper gastro-intestinal pathology, e.g. gastric or duodenal ulceration; whether a gastric erosion itself ever developed into a gastric ulcer was controversial. Because of the raised zone surrounding it, an erosion could be visualized fairly easily with double-contrast radiography as a tiny, constant fleck of barium surrounded by a radiolucent halo; some erosions tended to be linear rather than circular. In some cases erosions in the prepyloric area were associated with prominent or irregular mucosal folds; the radiographic diagnosis of erosions was found to be reliable, and correlated well with their endoscopic demonstration.

Roesch (l978) pointed out that gastric erosions occurred very commonly and were often multiple. In the acute type the epithelial defect was not surrounded by inflammatory reaction, while the chronic type had an elevated, bulging border. Only the chronic type was detectable radiologically, presenting as a small fleck with a surrounding halo. Endoscopy showed that almost 60 percent of chronic erosions occurred in the antral region, and that they were often associated with prominent mucosal folds. Radiological demonstration of these bead-like prepyloric folds was highly suspicious of chronic erosions, even in the absence of a central punctate barium-filled depression. Where erosions were followed-up for 5 years or longer, the transformation of multiple antral erosions into hyperplastic folds could often be seen.

Morson and Dawson (l979) reiterated that the most accurate diagnosis of gastritis was made on biopsies taken under direct vision through a fibrescope. Their classification, which was made on histological grounds, entailed 3 types, namely chronic superfical gastritis, atrophic gastritis (both of which might be either active or quiescent), and gastric atrophy. Active superficial gastritis might be accompanied by small erosions. In atrophic gastritis the essential feature was not the increase in inflammatory cells in the lamina propria, but the reduction or atrophy of the deep glands, accompanied by intestinal metaplasia in the "antrum". Attention was drawn to the fact that in both superficial and atrophic gastritis, submucous fibrosis and thickening of the muscularis externa had been reported, giving rise to "antral" deformity which was recognizable radiologically.

Freise et al. (l979) did four year follow-up studies in 64 patients with gastric erosions. The most common site of multiple erosions was the "antral" region. Erosions were frequently seen in combination with other upper gastrointestinal conditions such as gastric or duodenal ulceration or hiatus hernia. In 10 percent of cases chain-like multiple erosions developed into a persistent, prominent gastric mucosal fold, usually in the "antrum". When such a fold was seen, it could be taken to be the result of a chain of erosions. There was no evidence that erosions led to chronic gastric ulceration, polyps or malignancy.

Karvonen et al. (l983) classified erosions according to their endoscopic morphology. In the complete type there was a surrounding elevated border; incomplete or flat erosions were surrounded by a red halo, and haemorrhagic erosions were punctate bleeding spots. In 86 percent of 117 patients with gastric erosions (but without other upper gastrointestinal pathology), the lesions occurred only in the antral or prepyloric part of the stomach, and in the majority of patients presented as multiple erosions. Some showed features of both the complete and incomplete types, and were characterized by their location on prominent prepyloric mucosal folds. Nesland and Berstad (l985) noted a specific endoscopic appearance, consisting of standing prepyloric mucosal folds, redness and erosions, in a considerable number of patients presenting with dyspepsia; they called the condition erosive prepyloric changes (EPC) and divided it into three grades on the basis of the endoscopic features. In grade 1 there were standing mucosal folds, independent of peristalsis, running either transversely or longitudinally in the "antral" lumen. In grade 2 the same appearance was seen with red spots or streaks situated on top of the folds. In grade 3 the previous 2 appearances were associated with macroscopic erosions, described as white, fibrin-covered spots with red halos. EPC grades 2 and 3 were found in 26 percent of 1001 consecutive patients examined endoscopically. After excluding all patients with ulcer, carcinoma, post- operative conditions and upper gastro-intestinal bleeding, a group of 651 patients with non-ulcer dyspepsia remained; EPC grades 2 or 3 were seen in 210. In a group of 34 asymptomatic volunteers, grade 2 was found in 5 cases and grade 3 in one case. The frequency of grades 2 and 3 of erosive prepyloric changes appeared to be higher in non- ulcer dyspepsia than in patients with peptic ulceration and also varied with age. The highest frequency encountered was 52 percent, in patients with non-ulcer dyspepsia in the 40 to 49 year age group. The entity prepyloric erosive changes probably represented a form of antral gastritis. It might have a bearing on the radiological diagnosis of antral gastritis. Although the redness and often also the erosions were not visible radiologically, the permanent and coarse mucosal folds should be evident.

Berstad and Nesland (l985) stated that the three grades of EPC were merely different expressions of the same process. While the superficial mucosal state might regress or progress to another grade, the prominent, standing prepyloric mucosal folds were of a permanent nature. Histological verification was obtained in 88 percent of cases of endoscopically visible grade 3 erosions; they were always accompanied by an element of acute inflammation with infiltration of neutrophil polymorphs. In the vast majority there was an additional chronic inflammatory infiltration of lymphocytes and plasma cells. Intramucosal fibrosis was present in all biopsy specimens. Clinically, EPC appeared to be related to non-ulcer dyspepsia. The symptoms could be suggestive of gastric ulcer, while endoscopy proved the absence of ulceration. The findings supported the theory that EPC was a disease entity of its own, to be differentiated from ulcer disease. The permanent feature of the condition, namely standing mucosal folds, was independent of the ongoing inflammatory activity in the surface layer; whether contractions in the deeper muscular layers contributed to the fold formation was not known.

Berstad and Nesland (l987) reiterated that EPC was an endoscopic diagnosis based on the presence of standing prepyloric folds, with or without different types of erosions. Standing folds were defined as transverse or parallel folds in the prepyloric region, which might run into the pylorus itself and which were independent of peristaltic movements. They did not believe that EPC and peptic ulceration were aspects of the same disease process; EPC could not be considered to be merely a form of antral gastritis.

Hojgaard et al. (l987) pointed out that clinicians, endoscopists and pathologists defined gastritis in different ways. Pathoanatomical gastritis occurred very commonly and the prevalence increased with age. These authors found no correlation between dyspepsia (in patients without peptic ulceration) and endoscopic signs suggesting gastritis, or histological gastritis. It was concluded that gastritis did not seem to constitute a clinical entity in non-ulcer dyspepsia.

Karvonen et al. (l987) studied 130 patients with gastric mucosal erosions, occurring in the absence of peptic ulceration, by endoscopic biopsy; most were located in the "antrum". In their view erosions were inconsistent phenomena, probably with different pathogeneses and etiologies. Some incomplete erosions were associated with abuse of analgesics, but those located on prepyloric mucosal folds appeared to be associated with duodenal ulceration or duodenitis. The study suggested that prepyloric erosions constituted an entity of their own; in most instances the mucosa of the corpus was well preserved despite ageing, the appearance being similar to that of duodenal ulcer disease.

Present Investigations #

Patients and Methods #

During routine upper gastrointestinal barium examinations, a presumptive radiological diagnosis of "antral gastritis" was made from time to time. Most of these patients subsequently had endoscopic investigations (unfortunately biopsies were not taken in all). After a suitable interval the patients' clinical notes were perused and a final diagnosis obtained.

A total of 50 cases who were diagnosed radiologically, and confirmed endoscopically, as chronic "antral" gastritis were studied. The following are examples of the more pronounced cases:

Case Reports #

Case 28.1. G.G., 52 year old male. Radiographic examination showed a moderate degree of constant contraction of the pyloric sphincteric cylinder, with absence of normal, cyclical contraction and relaxation; the contraction fixed the pyloric aperture in the open position (Fig. 28.1). The stomach appeared to be hypertonic; rapid emptying of fluid barium occurred. Endoscopic biopsy of the "antral" region revealed acute on chronic gastritis; no evidence of malignancy was seen. Repeat endoscopic biopsy two months later showed acute on chronic inflammatory reaction in the lamina propria, with eosinophylic infiltration and without evidence of intestinal metaplasia. Stainings for Helicobacter pylori were positive. A third endoscopic biopsy two months after the second, showed chronic gastritis with intestinal metaplasia. Stainings for Helicobacter pylori were negative.

Fig. 28.1. Case G.G. Moderate degree of constant contraction of pyloric sphincteric cylinder (arrows). Cyclical activity absent. Pyloric aperture patent

Case 28.2 J.C., 63 year old male, was a know case of ethanol abuse and liver cirrhosis. Radiographic examination showed a marked degree of constant contraction of the pyloric sphincteric cylinder, which contained prominent, irregular, immobile mucosal folds (Fig. 28.2 A-D).

Fig. 28.2 A-D. Case J.C. Constant contraction of sphincteric cylinder with absent cyclical activity. Irregular, immobile folds in cylinder

Peristaltic waves were normal in the remainder of the stomach, but stopped abruptly at the commencement of the cylinder, which showed total absence of cyclical contraction and relaxation. Endoscopy revealed chronic "antral" gastritis; a few small erosions were noted in the first part of the duodenum.

Case 28.3 L.M., 50 year old female. Radiographic examination showed pronounced, constant contraction of the pyloric sphincteric cylinder; occasionally a minor degree of relaxation occurred, but cyclical contraction and relaxation was absent and most of the time the appearance remained as illustrated (Fig. 28.3). Prominent circular and irregular mucosal folds which appreared to be immobile, were present in the contracted cylinder. A concave indentation was seen in the base of the duodenal bulb. Endoscopy revealed a number of mucosal erosions as well as an appearance of severe "antral" gastritis. This was still present at a second endoscopy 8 months later, indicating chronicity.

Fig. 28.3. Case L.M. Constant contraction of sphincteric cylinder (arrows), with prominent irregular, static mucosal folds

Case 28.4 C.C., 36 year old female. Radiographic examination showed the pyloric sphincteric cylinder to be markedly contracted most of the time; at such times it contained longitudinal mucosal folds (Fig. 28.4A). Occasionally it relaxed to a certain extent, when a fold changed in direction to become circular (Fig. 28.4B); relaxation was never complete and cyclical activity was absent. Endoscopy revealed an erosion on the lesser curvature side of the pyloric region; touching the mucosa caused haemorrhage. The endoscopic diagnosis was erosive antral gastritis.

A
Fig. 28.4. A Case C.C. Marked contraction of sphincteric cylinder, with longitudinal mucosal folds B Case C.C. Some relaxation of cylinder. A mucosal fold has changed in direction to become circular. Cyclical activity absent	B

Case 28.5 J.M., 45 year old male. The pyloric sphincteric cylinder remained partially contracted throughout the radiographic examination, with complete absence of normal, cyclical contraction and relaxation. At least one prominent, circumferential mucosal fold, which did not change in position, was present in the partially contracted cylinder (Fig. 28.5). Initially it was difficult to distinguish between a permanent, circumferential mucosal fold and a prepyloric septum. Endoscopy revealed prominent, thickened prepyloric mucosal folds with an abnormal, whitish, granular surface. Endoscopic biopsy showed lymphocytic and plasma cell infiltration of the lamina propria; in some areas atypical epithelium, presumably due to inflmmatory change, was seen. The endoscopic diagnosis was chronic "antral" gastritis.

Fig. 28.5. Case J.M. Partial contraction of sphincteric cylinder, with absent cyclical activity. Prominent static, circular mucosal fold in cylinder (arrow)

Discussion #

A brief review of the literature shows that many aspects of gastritis are still controversial; even its definition is contentious. It has been stated that clinicians, pathologists and endoscopists defined "gastritis" in different ways (Hojgaard et al. l987). Others held that the term "chronic gastritis" had different connotations for the clinician, the pathologist and radiologist (Rao et al. l975). Authors differ on the subdivision of gastritis into various types and grades. It is agreed, however, that the diagnosis in the intact stomach can only be made by means of endoscopy, biopsy and microscopy. As the deeper layers of the wall are also involved in many instances, a full investigation would entail histologic examination of resection specimens.

The cases quoted here show that certain radiologically recognizable alterations may be associated with chronic "antral" gastritis, perhaps more correctly termed chronic gastritis affecting the pyloric sphincteric cylinder. (One of the cases was diagnosed as erosive haemorrhagic gastritis). The radiologically recognizable alterations are:

1. Partial but constant contraction of the sphincteric cylinder; the degree of contraction was usually described as "moderate" or "marked". In these cases radiologically visible peristaltic waves in the corpus and sinus of the stomach appeared normal, but each wave stopped at the commencement of the partially contracted cylinder. In some cases the cylinder showed minor degrees of contraction and relaxation, but maximal cyclical contraction and relaxation at a rate of 3 cycles per minute was absent in all. The appearance closely resembles that of pylorospasm (Chap. 20).

   In some cases the pyloric aperture was seen to be fixed in the open position as a consequence of partial contraction of the cylinder; this appearance may be associated with duodenogastric reflux (Chap. 27). It is presumed that the lack of cyclical activity of the cylinder may have a bearing on trituration and the emptying of solids (Chap. 18).

2. Prominent irregular and/or circular mucosal folds showing restricted movements or no movement at all. In view of the restricted movements of the walls of the cylinder it is not surprising that "independent but co-ordinated" movements of the inner mucosal layer should also be curtailed or absent (Chaps. 2, 13). It is surmized that cellular infiltration in the mucosa, submucosa, muscular layers and neuronal elements occurring in chronic gastritis, partially accounts for the restricted movements.

   Theoretically the static, irregular mucosal folds projecting into the lumen should hamper duodenogastric reflux occurring as a result of patency of the pyloric aperture in some cases.

3. A presumptive radiological diagnosis of chronic gastritis affecting the sphincteric cylinder, was only made if the above features occurred in the absence of other pathology in the upper gastrointestinal tract (e.g. gastric ulceration or hiatus hernia).

   According to Nesland and Berstad (l985) and Karvonen et al. (l987), erosive prepyloric change (EPC) was a condition characterized by standing mucosal folds and erosions; it was diagnosed endoscopically and appeared to be an entity of its own. Radiographically a standing mucosal fold may also be recognized, as seen in Fig. 28.5. In this case it concerned a circular fold which failed to change in position. It was associated with lymphocytic and plasma cell infiltration, no mention being made of erosions.

References #

1. Berstad A, Nesland AA. Prepyloric erosions and related changes: review. Scand J Gastroenterol l985, 20, 779-782.
2. Berstad A, Nesland AA. Erosive prepyloric changes: a new entity. Scand J Gastroenterol l987, 22, Suppl 128, 94-100.
3. Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr l913, Suppl 30, 1-265.
4. Freise J, Hofmann R, Gebel M, et al. Follow-up study of chronic gastric erosions. Endoscopy l979, 11, 13-17.
5. Gear MWL, Truelove SC, Whitehead R. Gastric ulcer and gastritis. Gut l97l, 12, 639-645.
6. Golden R. Antral gastritis and spasm. J Amer Med Assoc l937, 109, 1497-1500.
7. Holsti O. On the condition of the intramural ganglia in the stomach in cases of gastritis. Acta Med Scand l93l, 76, 316-342.
8. Holsti O. On the nature of the pylorus affections which simulate ulcus. Acta Med Scand l93l, 76, 343-393.
9. Hojgaard L, Matzen P, Christoffersen P. Gastritis: a clinical entity? Scand J Gastroenterol l987, 22, Suppl 128, 90-93.
10. Karvonen AL, Sipponen P, Lehtola J, et al. Gastric mucosal erosions: an endoscopic, histological and functional study. Scand J Gastroenterol l983, l8, 1051-1056.
11. Karvonen AL, Kekki M, Lehtola J, et al. Prepyloric erosions: an entity of its own among erosive gastric lesions. A morphologic and dynamic study of gastric mucosa in patients with gastric erosions. Scand J Gastroenterol l987, 22, 1095-1101.
12. MacDonald WC, Rubin CE. Gastric biopsy: a critical evaluation. Gastroenterology l967, 53, 143-170.
13. Magnus HA. The pathology of simple gastritis. J Path Bact l946, 58, 431-439.
14. Morson BC, Dawson IMP. Gastrointestinal Pathology. Blackwell Scientific Publications, London 2nd ed, l979, p 91.
15. Nesland AA, Berstad A. Erosive prepyloric changes in persons with and without dyspepsia. Scand J Gastroenterol l985, 20, 222-228.
16. Op den Orth JO, Dekker W. Gastric erosions: radiological and endoscopic aspects. Radiol Clin l976, 45, 88-99.
17. Rao SS, Krasner N, Thomson TJ. Chronic gastritis: a simple classification. J Path l975, 117, 93-96.
18. Roesch W. Erosions of the upper gastrointestinal tract. Clin Gastroenterol l978, 7, 623-634.
19. Schindler R, Ortmayer M, Renshaw JF. Chronic gastritis. J Amer Med Assoc l937, l08, 465-468.
20. Strickland RG, Mackay IR. A reappraisal of the nature and significance of chronic atrophic gastritis. Amer J Dig Dis l973, 18, 426-440.
21. Whitehead R, Truelove SC, Gear WML. The histological diagnosis of chronic gastritis in fibreoptic gastroscope biopsy specimens. J Clin Path l972, 25, 1-11.