Nature of the inflammatory cell infiltrate in duodenitis.

Counts of lamina propria and intraepithelial cells, lymphoid and polymorphonuclear, have been performed on semithin sections of endoscopic biopsies from the duodenum of patients with ulcer-associated duodenitis, with non-specific duodenitis, and from controls. In both types of duodenitis there were significant increases in lamina propria counts of plasma cells, lymphocytes and eosinophils, and in intraepithelial lymphocyte counts, when compared with controls. In control specimens, neutrophil polymorphs were very infrequent but a substantial neutrophil polymorph infiltration of the epithelium and lamina propria was present in both types of duodenitis. In biopsies from areas of duodenitis scanning electron microscopy showed the presence of cells, which are probably neutrophil polymorphs, on the luminal surface of the mucosa. Abnormalities in cell counts were present only in biopsies taken from visually inflamed areas of the duodenal bulb. These values returned to normal after healing of duodenitis with cimetidine. This study highlights the complex nature of the mucosal cellular infiltrate in in duodenitis, particularly the striking increase in polymorphonuclear leucocytes. Histopathological features of ulcer-associated and non-specific duodenitis are identical.     

The pattern of involvement of the gastric mucosa in lymphocytic gastritis is predictive of the presence of duodenal pathology

AIM: To determine whether the pattern of involvement of the gastric mucosa in lymphocytic gastritis is predictive of the presence or absence of duodenal pathology. METHODS: 50 cases (M:F, 26:24; median age 57 years) diagnosed as lymphocytic gastritis between 1986 and 1998 with concurrent duodenal (D2) biopsies were identified from a computer search of the pathology records and validated by counting gastric intraepithelial lymphocytes. Gastric and duodenal intraepithelial lymphocyte counts were performed on haematoxylin and eosin (H&E) and anti-CD3 stained sections. D2 biopsies were assessed for villous atrophy and chronic inflammatory cell infiltration by subjective grading, and gastritis was classified and graded according to the updated Sydney system. A case was designated corpus predominant when the corpus chronic inflammation grade exceeded that of the antrum. If it was less, then the case was antrum predominant, and if they were equal it was diffuse (pan-) gastritis. The ratio between the corpus and antral intraepithelial lymphocyte count in individual patients was calculated. RESULTS: Of 50 cases of lymphocytic gastritis, 21 were classified as corpus predominant. With one exception (a case of mild villous atrophy), all were accompanied by normal duodenal morphology. Cases with a corpus predominant gastritis had median duodenal intraepithelial lymphocyte counts of 19 (H&E) and 14.1 (CD3), whereas 29 subjects with an antrum predominant or diffuse gastritis had median counts of 39.9 (H&E) and 37.9 (CD3). Fifteen of these 29 cases (52%) showed villous atrophy; all were graded as moderate or severe. Patients with any degree of villous atrophy had a mean corpus/antrum intraepithelial lymphocyte ratio (H&E) of 0.59 (representing antral predominance), while those with normal duodenal morphology had a ratio of 2.39 (p < 0.0001). CONCLUSIONS: The pattern of involvement of gastric mucosa in lymphocytic gastritis is closely related to the associated duodenal pathology. Those with the corpus predominant form are unlikely to have duodenal pathology, while those with an antral predominant or diffuse form should have distal duodenal biopsies taken to exclude villous atrophy.     

Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis.

Biopsy specimens of gastric and duodenal mucosa from 290 patients were examined histologically for metaplasia and Campylobacter pyloridis. Estimates of pH on samples of fasting gastric juice from 55 of the patients were performed, and mucosal biopsy specimens from 33 patients were also cultured for C pyloridis. Active duodenitis was seen in 34 duodenal biopsy specimens. Thirty (88%) of the patients with active duodenitis had both greater than 5% gastric metaplasia in the duodenal specimen and C pyloridis associated gastritis. These two factors coexisted in only 0.43% of patients with no duodenal inflammation. When C pyloridis were seen histologically in duodenal biopsy specimens they were confined to areas of gastric metaplasia and never occurred in the absence of a polymorph infiltrate. Of the 55 patients with measurements of gastric juice pH, gastric metaplasia was present in the duodenum in 20 of 42 with a pH of less than 2.5, and in 0 of 13 with a pH of greater than 2.5. These results suggest that acid induced gastric metaplasia in the duodenum and C pyloridis associated gastritis may be synergistic in the pathogenesis of duodenitis; the metaplastic gastric epithelium allows C pyloridis to colonise the duodenal mucosa, where it produces an acute inflammatory response.     

The Helicobacter (Campylobacter) pylori-colonized duodenal mucosa and gastric metaplasia

Biopsies were obtained from non-ulcerated sites of the duodenum from 100 dyspeptic patients. Helicobacter (Campylobacter) pylori was cultivated from 19 of these biopsies. Active chronic duodenitis (ACD) was found in 17 biopsies and more than 5% gastric metaplasia in 20 biopsies. H. pylori as well as ACD occurred with a significantly increased frequency when more than 5% gastric metaplasia was found in the duodenal biopsies. H. pylori on metaplastic tissue without ACD was, however, seen in two cases. H. pylori was cultivated from 9% and ACD was found in 5% of the biopsies with less than 5% gastric metaplasia. Gastric metaplasia in the duodenum was found significantly more frequently in patients with endoscopic duodenitis or duodenal ulceration than in patients with normal endoscopy. No association between gastric metaplasia in the duodenum and gastric pH or serum antibodies against H. pylori was seen. This study indicates that there is an established, but not exclusive, connection between gastric metaplasia and the colonization of the duodenum by H. pylori, the most important role being played by the antral gastric mucosa rather than the duodenum.     

Gastric epithelium in the duodenum: its association with Helicobacter pylori and inflammation.

Duodenal biopsy specimens from 471 adults and 47 children were examined to determine the prevalence and distribution of gastric epithelium in the duodenal bulb in relation to age, gender, gastroduodenal inflammation, smoking, alcohol and consumption of nonsteroidal anti-inflammatory drugs (NSAID). Gastric metaplasia was present in the anterior wall duodenal biopsy specimen in 31%, was significantly less common in patients under 17 than in adults, and was more common in males than females. In sixty two adults who underwent multiple radial duodenal biopsy gastric metaplasia was randomly distributed around the duodenal circumference; sixty three per cent of the patients with gastric metaplasia found on multiple biopsy were detected by just the anterior biopsy. Gastric metaplasia was not obviously associated with alcohol, cigarette, or NSAID consumption. While the presence of gastric metaplasia was associated with adulthood, male sex, and low fasting gastric juice pH, its extent was associated with active duodenitis and Helicobacter-associated gastritis. On logistic regression, gastric metaplasia in the duodenum and gastric Helicobacter pylori were independent predictors of active duodenitis, but were not significantly associated with inactive duodenal inflammation. H pylori was observed in duodenal biopsy specimens from 32 patients, all with active duodenitis; bacteria were present only on foci of gastric metaplasia, and were more likely to be seen when the metaplasia was extensive. It is proposed that inflammatory injury to the duodenal mucosa by H pylori may stimulate the development of further gastric metaplasia, and that the area of duodenum susceptible to colonisation with H pylori may therefore increase progressively until mucosal integrity is compromised and ulceration supervenes.     

Lysozyme-rich mucus metaplasia in duodenal crypts supersedes Paneth cells in celiac disease

Lysozyme is as an innate enzyme with potent antibacterial properties found in Paneth cells in normal duodenal crypts. Since celiac disease concurs with an abnormal duodenal microbiota we explored the expression of lysozyme in this disease. Fifty-three duodenal biopsies were stained with anti-lysozyme: 15 had normal duodenal mucosa (NDM), 7 chronic active duodenitis (CAD), 3 borderline (BL), 17 subtotal villous atrophy (SVA) and 11 total villous atrophy (TVA). NDM showed lysozyme-positive Paneth cells arranged in “Indian file” in 93.3%. In contrast, lysozyme-positive mucus metaplasia in crypts (LPMMC) replacing Paneth cells was found in 71.5% in CAD, in 96.4% in SVA/TVA, and in 2 cases with B. In 19.3% cases with BL/SVA/TVA, LPMMC replaced all Paneth cells in all crypts in entire sections. In crypts and villi, lysozyme-positive goblet cells (LPGC) were found in 92.8%. Changes were more frequent in the duodenal bulb than in pars descendens. In normal duodenal mucosa, absorptive enterocytes and goblet cells migrate from stem cells upwards, while Paneth cells migrate downwards, towards the base of the crypts. In celiac disease stem cells seem to have been re-programmed, as the normal production of Paneth cells in the crypts was replaced by lysozyme-producing mucus cells. LPMMC and LPGC in celiac disease might mirror an antimicrobial adaptation of stem cells to signals generated by pathogenic duodenal bacteria. The molecular mechanism(s) behind the abrogation of Paneth cells in duodenal crypts and its substitution by LPMMC in celiac disease remains to be elucidated.     

The endoscopically abnormal duodenum in patients with dyspepsia: biopsy findings in 60 cases

Biopsies from 60 patients with dyspepsia and endoscopically abnormal first part of duodenum were examined. The main endoscopic findings were duodenitis (35 cases), chronic ulceration (eight) and abnormal mucosal patterns (17). The latter included mucosal atrophy, thickening, irregularity, nodularity and polypoid formation. The main histological findings were duodenitis (40), gastric metaplasia (42) and gastric heterotopia (seven). The first two were commonly seen together. Heterotopia was not associated with inflammation. Good correlation existed between endoscopic and histological findings.     

Role ofHelicobacter pylori in gastritis and duodenitis in man

AlthoughHelicobacter pylori is now accepted as the major aetiological factor in chronic gastritis in man, many of the factors which determine its pathogenicity are unknown. The organism has adapted to survive in the low-pH environment of the stomach, partly through its ability to buffer hydrogen ion by the hydrolysis of urea and by the presence of lectins on its surface, which bind to gastric mucosa and epithelial cells. After attachment, harmful toxins and enzymes have access to the gastric cells and cellular damage and an immune response ensues. In patients with duodenal ulceration,Helicobacter pylori-related gastritis predominantly affects the gastric antrum and has a high prevalence. Excessive gastrin production has been suggested as a potential aetiological factor linking infection with duodenal ulcer development. Perhaps more important is the association between gastric metaplasia of the duodenal epithelium, which is correlated with acid load and is more extreme inH. pylori positive patients with duodenitis. Organisms may subsequently spread from the gastric antrum into areas of gastric metaplasia in the duodenal bulb, leading to areas of chronic duodenitis and ultimately frank ulceration. It should not be overlooked, however, that other factors such as genetic predisposition, blood group, stress, drugs and smoking all have a role to play in the outcome, given the comparatively small number of patients in the general population infected withH. pylori who develop ulcer disease.     

Role ofHelicobacter pylori in gastritis and duodenitis in man

AlthoughHelicobacter pylori is now accepted as the major aetiological factor in chronic gastritis in man, many of the factors which determine its pathogenicity are unknown. The organism has adapted to survive in the low-pH environment of the stomach, partly through its ability to buffer hydrogen ion by the hydrolysis of urea and by the presence of lectins on its surface, which bind to gastric mucosa and epithelial cells. After attachment, harmful toxins and enzymes have access to the gastric cells and cellular damage and an immune response ensues. In patients with duodenal ulceration,Helicobacter pylori-related gastritis predominantly affects the gastric antrum and has a high prevalence. Excessive gastrin production has been suggested as a potential aetiological factor linking infection with duodenal ulcer development. Perhaps more important is the association between gastric metaplasia of the duodenal epithelium, which is correlated with acid load and is more extreme inH. pylori positive patients with duodenitis. Organisms may subsequently spread from the gastric antrum into areas of gastric metaplasia in the duodenal bulb, leading to areas of chronic duodenitis and ultimately frank ulceration. It should not be overlooked, however, that other factors such as genetic predisposition, blood group, stress, drugs and smoking all have a role to play in the outcome, given the comparatively small number of patients in the general population infected withH. pylori who develop ulcer disease.     

Duodenal bulb biopsy findings for patients with non-ulcer dyspepsia with or without Campylobacter pylori gastritis

Duodenal bulb biopsy specimens from 85 patients with non-ulcer dyspepsia (30 of whom had normal stomachs and 52 of whom had Campylobacter pylori gastritis) were examined for the presence and amount of gastric surface epithelial metaplasia (using both the hematoxylin and eosin stain and the Alcian blue-periodic acid-Schiff method), acute inflammation, and C. pylori (using the Giemsa stain). Gastric metaplasia occurred in the duodenal bulb in 61% of patients with gastric C. pylori and in an identical percentage for those who lacked C. pylori gastritis. For patients with gastric metaplasia, foci of metaplastic cells were seen in 70% of their bulb biopsy fragments. The Alcian blue-periodic acid-Schiff stain was superior to the hematoxylin and eosin stain for detecting gastric metaplasia. Only one of 33 patients without gastric C. pylori had gastritis and duodenitis. Fourteen of 52 (27%) patients with C. pylori gastritis had duodenitis; C. pylori was seen in the duodenal biopsy specimens from 13 of these patients. The organisms were often few, requiring oil immersion microscopy for detection. Each patient with duodenitis had gastric metaplasia, but some of these metaplastic foci were not inflamed. When present in the duodenum of patients with C. pylori gastritis, gastric metaplasia, acute inflammation, and C. pylori are typically patchy. Hence, several biopsy fragments of the duodenal bulb would be required for studies designed to determine the effectiveness of compounds used to treat C. pylori duodenitis.     

Helicobacter-associated duodenitis and gastric metaplasia in duodenal ulcer patients.

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.     

Quantitation of intraepithelial lymphocytes in human duodenum: what is normal?

BACKGROUND: An increase in intraepithelial lymphocytes (IELs) is mandatory for the histological diagnosis of coeliac disease (CD). Currently, duodenal biopsies are used almost exclusively to establish the diagnosis, yet published work continues to cite an upper limit of 40 lymphocytes/100 epithelial cells, a figure derived from jejunal biopsies over 30 years ago. Aim: To establish the normal range for IEL counts in distal duodenal biopsies. MATERIALS/METHODS: Twenty subjects (seven men, 13 women; median age, 34 years; range, 20-65) with a normal sugar permeability test and concurrent distal duodenal biopsies were identified. The number of IELs and epithelial cell nuclei in an uninterrupted length of surface (villous) epithelium (> 500 cells) was counted. An image analysis system was used to assess villous architecture by calculating the villous height to crypt depth ratio. RESULTS: The range of IEL counts in 20 subjects was 1.8-26/100 villous epithelial cells, with a mean value of 11 and SD of 6.8. The mean villous to crypt ratio was 1.82 (SD, 0.38; range, 1.22-2.46). There was no correlation between IEL counts and villous to crypt ratio (Spearman rank correlation, -0.066; p = 0.80). CONCLUSIONS: These results suggest that 25 IELs/100 epithelial cells (mean +2 SD) should be taken as the upper limit of the normal range for duodenal mucosa.     

An examination of the relationship between the endoscopic appearance of duodenitis and the histological findings in patients with epigastric pain

The endoscopic appearance of duodenitis is a common finding in patients undergoing endoscopy because of epigastric pain however, the relationship of the visual findings to histology is poorly defined. We set out to ascertain if there was a correlation between the endoscopic and histological appearances of the duodenal mucosa. Consecutive patients with epigastric pain referred for diagnostic gastroduodenoscopy were studied. The visual appearances of 'duodenitis' (erythema, erosions and sub-epithelial haemorrhage) were reported independently by two endoscopists. Duodenal biopsies were taken and assessed for: neutrophil infiltrate, mononuclear infiltrate, gastric metaplasia, villous atrophy and a breach in the mucosa. H pylori status was determined. Of the 93 patients with endoscopic features of duodenitis an increase in histological markers of inflammation was found in 75 (81%). However, histological inflammation was absent or minimal in 68 (73%). Conversely, biopsies from normal-looking mucosa revealed histological evidence of inflammation in 26 (27%). For patients with the endoscopic features of duodenitis the positive & negative predictive value for neutrophilic infiltrate was 39% and 98% respectively. Biopsies from erosions confirmed a breach in the mucosa in only 2 of 40 patients. Neutrophilic infiltrate occurred with NSAI ingestion and infection with H pylori. The endoscopic appearance of the duodenal mucosa is unreliable in determining the presence of histological inflammation. The endoscopic appearance of 'erosions' is not usually associated with a mucosal breach.     

Loss of alkaline phosphatase activity in duodenal mucosa: a marker for precursors of gastric metaplasia?

Biopsy specimens from duodenal mucosa in 34 patients with upper gastrointestinal symptoms and endoscopically abnormal mucosa (including duodenitis, active duodenal ulcer, and healed duodenal ulcer) and in 9 patients with histologically normal mucosa were examined histologically for gastric metaplasia and endogenous alkaline phosphatase (AP) activity. Using haematoxylin and eosin (H&E) and periodic acid-Schiff (PAS), we found gastric metaplasia in 91.2 per cent (31 out of 34) of patients with altered duodenal mucosa and in 33.3 per cent (3 out of 9) of patients with histologically normal, non-inflamed duodenal mucosa (P less than 0.001). To characterize gastric metaplasia further, histochemical methods for AP activity were applied to duodenal mucosa specimens. No AP activity was detected in complete metaplastic cells, but focal or diffuse loss of AP activity was frequently shown in otherwise normal appearing enterocytes next to metaplastic cell groups. Focal loss of AP activity was also detected in seven out of nine healthy controls (= 77.8 per cent) which appeared normal when stained with H&E. Our results suggest that the loss of AP activity in enterocytes may be an early marker of developing gastric metaplasia or at least a morphological manifestation of cell damage.     

Distribution of carbonic anhydrase I in gastric and duodenal tissue sections

Forty-four sections of normal and abnormal gastric and duodenal tissue were examined by an immunoperoxidase technique for the demonstration of carbonic anhydrase I. The presence of the enzyme in normal gastric parietal and surface epithelial cells was confirmed. The enzyme was also demonstrated in normal and metaplastic intestinal absorptive cells, and in gastric adenocarcinoma of the usual and superficial types. The enzyme was normally absent in antral and Brunner's glands, normal and metaplastic goblet cells, and signet ring tumor cells. Gastritis and duodenitis were associated with a decrease in the staining intensity of the enzyme in surface epithelial cells, suggesting a possible decreased enzyme activity, which may enhance the risk for peptic ulceration in susceptible persons.     

Chronic duodenitis with gastric metaplasia: electron microscopic study including comparison with normal

Dudoenal biopsies from 11 patients with non-ulcer dyspepsia were examined by electron microscopy. Chronic duodenitis with gastric metaplasia was seen in samples from four patients, and areas of normal-looking duodenal mucosa were present in nine. The metaplastic cells were similar to those previously described in association with duodenal ulcers. They usually showed marked morphological differences from the normal duodenal absorptive cells. The microvilli were distorted and reduced in number, the glycocalyx was ill-defined, the cytoplasm filled with mucous globules and the intercellular spaces, in some areas, were widened and contained acute and chronic inflammatory cells.     

Endoscopic and histological changes in upper gastrointestinal tract of patients with chronic renal failure

To evaluate the endoscopic and histological changes in upper gastrointestinal tract of patients with chronic renal failure 50 patients and 50 controls were studied. Upper gastrointestinal endoscopy was done and 2 biopsies each were taken from oesophagus, corpus and antrum of the stomach and duodenum. Sections were stained with haematoxylin & eosin, Alcian blue--Periodic acid Schiff's (pH 2.5), and Loeffler's methylene blue stains. Oesophagus was endoscopically normal in most of the patients. Predominant histological finding was chronic oesophagitis which was significantly higher in patients than controls (47.1% Vs 26%; p<0.05). Significantly higher (p<0.001) number of patients had gastritis, oedema and pale mucosa on endoscopic examination of stomach. Predominant histological changes were mucosal oedema (82.35%), gastritis (23.5%) and increase in number of bi- and multinucleated parietal cells with vacuolation and fragmentation of the cytoplasm (29%). Prevalence of H. pylori was less in patients as controls (35.2% Vs 54%; p< 0.01). Endoscopic examination of duodenum mainly showed duodenitis, pale mucosa, oedema and nodularity. Brunner's gland hyperplasia (82.4%), duodenitis (70.6%) and gastric metaplasia (29.4%) were the main histological features. H. pylori was seen in 5.9% cases of gastric metaplasia in duodenum. Patients with CRF have significant upper gastrointestinal tract abnormalities which mainly occur due to metabolic changes in response to high urea concentration in gastric juice and are not related to H. pylori infection.     

Duodenal intraepithelial lymphocytosis with normal villous architecture: common occurrence in H. pylori gastritis.

We have observed expansions of intraepithelial lymphocytes in duodenal biopsies from patients with Helicobacter pylori gastritis. This study was undertaken to prospectively evaluate, unselected, paired gastric and duodenal biopsies from 50 patients with H. pylori gastritis and a comparison group of 30 patients with other types of gastritis (10 autoimmune and 20 reactive) to: (1) quantify duodenal intraepithelial lymphocytes, determine their distribution patterns, epithelial location, and phenotype, and (2) correlate the intraepithelial lymphocyte elevations with various features of gastric and duodenal pathology. Intraepithelial lymphocytes were analyzed with antibodies including CD3, CD8, and TIA-1. A stain for H. pylori was performed on all gastric and duodenal biopsies. Duodenal intraepithelial lymphocytes from patients with H. pylori gastritis (using CD3) ranged from 3 to 42 lymphocytes/100 epithelial cells (mean 18.5) compared to 3 to 18 lymphocytes/100 epithelial cells (mean 6.6) in the comparison group. Intraepithelial lymphocyte elevations were seen in 44% of the duodenal biopsies from patients with H. pylori gastritis (using CD3). Significant differences in the intraepithelial lymphocyte counts between patients with H. pylori gastritis and the comparison group were seen for all three T-cell antigens (P<0.001 for CD3 and CD8 and P<0.002 for TIA-1). Duodenal intraepithelial lymphocytes in the H. pylori+ cases had a latent cytotoxic phenotype, H. pylori was not visualized in any of the duodenal biopsies from patients with H. pylori gastritis, and no patient had clinical evidence of celiac disease. Our study highlights frequent duodenal intraepithelial lymphocytosis in individuals with H. pylori gastritis and the lymphocyte distribution patterns (and numbers) overlapped with those described for celiac disease patients. H. pylori gastritis must be considered as a possible explanation for duodenal intraepithelial lymphocytosis with normal villous architecture, especially when lymphocytosis is patchy, intraepithelial lymphocytes display a 'latent' cytotoxic phenotype, and the clinical findings and serologic profile does not fit celiac disease.     

52例十二指肠粘膜活检组织病理学观察

观察５２例纤维胃镜咬取的十二指肠粘膜标本，组织学显示９８％有慢性炎，８０％为萎缩性炎。按粘膜绒毛高度和萎缩程度分轻、中、重３级。结合临床，中、重度萎缩性十二指肠炎，可作为小肠吸收不良的诊断依据。５２例中，有ＭＧＥ、Ｂｒｕｎｎｅｒ’ｓ腺增生分别为２１％和５０％。组织化学染色证实十二指肠杯状细胞含混合性粘液。     

Prevalence of gastric metaplasia, inflammation, and Campylobacter pylori in the duodenum of members of a normal population

Mucosal biopsies were obtained from 116 asymptomatic volunteers (50% were male; mean age, 46 years; age range, 19-91 years) to study the prevalence of duodenal gastric metaplasia (GM) and its association with inflammation and Campylobacter pylori in a normal population. GM was identified in 25 subjects (22%). Eighty-three subjects (72%) had histologic duodenitis, but in only 10 did the infiltrate include neutrophils (grade 2 duodenitis). C. pylori was found in the stomach in 36 subjects (31%), all of whom had gastritis, but was not identified histologically in the duodenum. There were no significant differences between the overall frequency of duodenitis and either GM or antral C. pylori. Although the frequency of severe (grade 2) duodenitis was not significantly different between those with and those without GM, grade 2 duodenitis was found in 9 of 36 subjects with antral C. pylori but in only 1 of 80 without antral C. pylori (P less than 0.001). These findings suggest that gastric metaplasia is a common finding in the normal population and that grade 1 duodenitis is most likely clinically unimportant, whereas grade 2 duodenitis is usually associated with antral C. pylori.