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Radiographically diagnosed antral gastritis: findings in patients with and without Helicobacter pylori infection

Departments of ¹ Radiology and ² Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA

Correspondence: Marc S Levine, MD, Department of Radiology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA

	Abstract

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The purpose of this study was to characterize the radiographic findings of antral gastritis and to determine whether there are differences in the appearance of antral gastritis in patients with and without Helicobacter pylori infection. A search of radiology, endoscopy and pathology files revealed 90 patients with antral gastritis on double contrast upper gastrointestinal tract studies who had endoscopy with testing for H. pylori. The barium studies were evaluated to further characterize the findings of antral gastritis without knowledge of the H. pylori status of the patients or of the endoscopy or pathology findings. The radiographic findings of antral gastritis included thickened folds in 67 patients (74%), polypoid antral gastritis (a subset of patients with thickened folds) in 6 (9%), antral erosions in 21 (23%), enlarged areae gastricae in 14 (16%), crenulation of the lesser curvature in 4 (4%), mucosal nodularity in 2 (2%), a hypertrophied antral-pyloric fold in 2 (2%) and antral striae in 1 (1%). 43 patients (48%) with antral gastritis were H. pylori positive and 47 patients (52%) were H. pylori negative. Thickened folds were detected in 39 H. pylori-positive patients (91%) with antral gastritis vs 28 H. pylori-negative patients (60%) (p<0.001); polypoid gastritis in 6 H. pylori-positive patients (14%) vs 0 H. pylori-negative patients (p<0.05); enlarged areae gastricae in 14 H. pylori-positive patients (33%) vs 0 H. pylori-negative patients (p<0.0001); and antral erosions in 2 H. pylori-positive patients (5%) vs 19 H. pylori-negative patients (40%) (p<0.0001). Our experience suggests that antral gastritis caused by H. pylori infection is associated with characteristic features on double contrast studies (including thickened folds, polypoid gastritis and enlarged areae gastricae) and that this condition is rarely associated with antral erosions. Thus, radiologists can often suggest whether the patient's gastritis is caused by H. pylori on the basis of radiographic findings.

	Introduction

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Since its original description as a distinct radiographic entity by Berg in 1952 [1], antral gastritis has been recognized as a common condition manifested by a spectrum of findings on double contrast upper gastrointestinal (GI) tract examinations, including thickened rugal folds [1–3], crenulation of the lesser curvature of the distal antrum [2, 4, 5], mucosal nodularity [2, 3, 5], erosions [6–8], antral striae [9], enlarged areae gastricae [2, 3, 10] and a hypertrophied antral-pyloric fold [11, 12]. Although antral gastritis has been diagnosed with considerable frequency on double contrast barium studies, the cause of this condition is often uncertain. Various factors have been implicated in the development of antral gastritis, including alcohol, tobacco, coffee, and aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) [3, 13–18]. Helicobacter pylori has also been recognized as a major cause of gastritis [19]; the antrum is reported to be the most common site of inflammation in these patients [20]. However, to our knowledge little has been written in the radiological literature about the frequency of the various radiographic findings of antral gastritis or their relationship to H. pylori infection. The purpose of this investigation, therefore, was to further characterize the findings of antral gastritis on double contrast barium studies and also to determine whether there are differences in the appearance of antral gastritis in patients with and without underlying H. pylori infection.

	Materials and methods

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A computerized search of the radiology archives at our hospital revealed 1500 cases of antral gastritis diagnosed on double contrast upper GI tract examinations during a 6-year period from 1995–2000. A review of the radiological reports revealed that 103 of these patients also had known or suspected gastric neoplasms or prior gastric surgery, thus these cases were excluded from the analysis. A subsequent review of the endoscopy and pathology files at our hospital revealed that 90 of the remaining 1397 patients had undergone upper endoscopy with testing for H. pylori (CLOtest alone in 32 patients, thiazine stains alone in 32 and CLOtest and thiazine stains in 26) within 6 months of the barium studies (mean interval 3 months). Patients were considered to be H. pylori positive if the CLOtest and/or two or more antral biopsy specimens within 3 cm from the pylorus with thiazine stains for H. pylori were positive for this infection [21]. We relied on endoscopic testing rather than a urea breath test or serum antibody test to determine the H. pylori status of the patients, as endoscopy is considered to be an extremely accurate technique for diagnosing this infection [21]. The presence or absence of H. pylori served as the gold standard for the 90 patients in our study group because of known discrepancies between the endoscopic and histological findings of antral gastritis [22].

The barium studies from these 90 cases were evaluated by an experienced GI radiologist who had no knowledge of the H. pylori status of the patients or of the endoscopic or pathological findings. The quality of the double contrast studies was rated as excellent in 67 patients (74%), good in 17 (19%) and fair in 6 (7%). In all cases, the reviewer agreed with the original radiological diagnosis of antral gastritis. The images from these examinations were evaluated to characterize the findings of antral gastritis, including: thickened folds (defined as folds 5 mm or greater in width) [2, 3]; erosions (defined as "varioliform" when central punctate or slit-like collections were surrounded by radiolucent mounds of oedema and as "incomplete" when the central barium collections were not surrounded by mounds of oedema) [6–8]; mucosal nodularity; crenulation (defined as irregularity or pleating) of the lesser curvature [4, 5]; enlarged areae gastricae (defined as areae gastricae 4 mm or greater in diameter) [2]; antral striae (defined as transverse striations in the antrum) [9]; and a hypertrophied antral-pyloric fold (defined as a single lobulated fold that extended from the lesser curvature of the distal antrum into the pylorus or base of the duodenal bulb) [11, 12]. A subset of patients with thickened folds was considered to have polypoid antral gastritis (defined as markedly thickened, lobulated folds 10 mm or greater in width). In all cases, measurements were obtained from digital images on a computer workstation, using a standard 12 mm barium tablet from an index image in one case as the reference. We recognize that the effect of magnification on our measurements depended on the height of the fluoroscopy tower above the examination table. However, the degree of magnification was in no way related to patient selection, so this variable should have no significant effect on our findings.

The radiographic findings were then stratified on the basis of the H. pylori status of the patients to determine whether there were differences in the frequency of these findings in patients with and without H. pylori infection. A statistical analysis of the data was performed using a Fisher's Exact test.

Endoscopy reports were available for review in 57 of the 90 cases; the reports were reviewed to determine whether there were visible endoscopic signs of gastritis. Endoscopy biopsy specimens were obtained in 77 cases; pathology reports were also reviewed to determine whether there were pathological findings of gastritis. It should be noted that endoscopy biopsy specimens were obtained in some patients who had normal endoscopy findings to evaluate for histological evidence of gastritis or H. pylori infection. Finally, the radiological and endoscopic findings were correlated with the pathology findings.

Our Institutional Review Board approved all aspects of this retrospective study and did not require informed consent for patients included in the study.

	Results

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Clinical findings
Mean age was 53.5 years (range 21–82 years). There were 48 men and 42 women. Presenting symptoms included epigastric pain or dyspepsia in 70 patients, reflux symptoms in 13, early satiety in 4 and dysphagia in 3.

Radiographic findings
The most common radiographic finding was thickened folds (Figure 1), which were detected in 67 patients (74%). The mean width of the thickened folds was 5.8 mm (range 5–15 mm; SD 0.5 cm). The folds were irregular in 55 patients (82%) and straight in the remaining 12 (18%). The thickened folds involved the antrum alone in 49 patients (73%) and the antrum and body in 18 (27%). 6 (9%) of these 67 patients had markedly thickened, lobulated folds (i.e. polypoid antral gastritis) (Figure 2) which had a mean width of 13 mm (range 10–15 mm; SD 1.0 cm).

View larger version (116K): [in this window] [in a new window]   Figure 1. 88-year-old woman with antral gastritis. Supine oblique image from double contrast study shows mildly thickened, scalloped folds (black arrows) in the antrum. Note transverse orientation of folds. Some barium precipitates (white arrows) are also seen in the antrum. Endoscopy revealed moderate inflammation of the antrum, and biopsy specimens from this region confirmed the presence of antral gastritis. This patient was Helicobacter pylori positive and had no history of non-steroidal anti-inflammatory drug use.

View larger version (122K): [in this window] [in a new window]   Figure 2. 38-year-old woman with polypoid antral gastritis. Supine oblique image from double contrast study shows markedly thickened, lobulated folds (arrows) in the antrum. Endoscopy revealed severe inflammation of the antrum, and biopsy specimens from this region confirmed the presence of antral gastritis. All of our patients with polypoid antral gastritis were Helicobacter pylori positive.

View larger version (124K): [in this window] [in a new window]   Figure 3. 41-year-old woman with erosive antral gastritis. Supine oblique spot image from double contrast study shows multiple varioliform erosions in the antrum as punctate collections of barium (arrowheads) surrounded by radiolucent mounds of oedema (arrows). Endoscopy revealed visible signs of antral gastritis, but no biopsy specimens were obtained. Almost all of our patients with antral erosions were Helicobacter pylori negative (including this patient), and nearly half had a history of recent aspirin or other non-steroidal anti-inflammatory drug use.

View larger version (157K): [in this window] [in a new window]   Figure 4. 68-year-old woman with antral gastritis. Supine oblique image from double contrast study shows enlarged areae gastricae (white arrows) in the antrum and body of the stomach as well as a thickened antral fold (black arrow). Endoscopy revealed inflammation of the antrum, and the CLOtest was positive for Helicobacter pylori. All of our patients with enlarged areae gastricae were H. pylori positive.

Radiographic findings in patients with and without H. pylori infection (Table 1)

Correlation between radiographic, endoscopic and pathological findings
57 (74%) of the 77 patients in whom endoscopic biopsy specimens were obtained had biopsy-proven antral gastritis, and 20 (26%) had normal biopsy specimens. We were able to retrieve the endoscopy reports in 40 of the 57 patients with pathologically proven antral gastritis. Endoscopy revealed findings of antral gastritis in 21 (52.5%) of these 40 patients, including mucosal oedema and erythema in 17 patients and mucosal friability in 4. Endoscopy was normal in the remaining 19 patients (47.5%), and these are presumed to represent false negative endoscopic examinations. 28 (49%) of the 57 patients with biopsy-proven antral gastritis were found to be H. pylori positive and 29 (51%) were found to be H. pylori negative.

We were also able to retrieve the endoscopy reports in 17 of the 20 patients with normal biopsy specimens. Endoscopy revealed findings of antral gastritis in 8 (47%) of these 17 patients, with mucosal oedema and erythema in all 8. Endoscopy was normal in the remaining 9 patients (53%). 7 (35%) of the 20 patients with normal biopsy specimens were found to be H. pylori positive and 13 (65%) were found to be H. pylori negative.

	Discussion

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Antral gastritis has long been recognized on barium studies as a common form of gastritis. This condition is important because it may be a cause of dyspepsia, epigastric pain or other upper GI signs or symptoms [23]. The radiographic diagnosis of antral gastritis has traditionally been based on a variety of findings. In our study, however, by far the most common sign of antral gastritis on double contrast upper GI tract examinations was thickened folds (Figures 1 and 2), which were detected in 74% of cases. Other less common findings included antral erosions (Figure 3) and enlarged areae gastricae (Figure 4), which were detected in 23% and 16% of cases, respectively. In contrast, other radiographic findings of antral gastritis were rarely detected in patients with this condition.

Since its discovery in 1983 [24], H. pylori infection has increasingly been recognized as the leading cause of gastritis in the adult population [19]. The prevalence of H. pylori gastritis has been found to be nearly 50% in Americans over the age of 60 years [25]. In our study, nearly 50% of patients with antral gastritis were infected by this organism. We also found a significant association between thickened folds or enlarged areae gastricae on double contrast studies and H. pylori infection (p<0.001 and p<0.0001, respectively) (Figures 1 and 4). Although thickened folds can also be seen in patients without H. pylori infection, more than 90% of patients with H. pylori gastritis had this finding. Our experience therefore suggests that H. pylori gastritis is unlikely in the absence of thickened folds. Furthermore, we found a significant association between H. pylori infection and a subset of patients with thickened folds in whom there was a polypoid form of antral gastritis, characterized by markedly thickened, lobulated antral folds (p<0.05) (Figure 2); all of our patients with polypoid antral gastritis were found to be H. pylori positive. An association between H. pylori infection and polypoid gastritis (not necessarily involving the antrum) has been reported previously in the radiological literature [10]. When this form of gastritis is detected on barium studies, endoscopy and biopsy may be required to rule out non-Hodgkin's lymphoma or other submucosally infiltrating neoplasms. Nevertheless, it is important to be aware of the association between H. pylori infection and polypoid antral gastritis, so that the endoscopist can be alerted to the possibility that the patient may have H. pylori gastritis rather than malignant tumour as the cause of this finding.

When H. pylori gastritis is confirmed in symptomatic patients who have no ulcers or tumour on barium studies or endoscopy (so-called "non-ulcer dyspepsia"), some investigators have found that eradication of the infection is more likely to produce symptomatic benefit than anti-secretory agents alone [26]. However, others have found that eradication of H. pylori in patients with non-ulcer dyspepsia is not likely to relieve symptoms in this group [27]. It therefore remains controversial whether eradication of the infection is the appropriate course of action in H. pylori-positive patients with antral gastritis who have non-ulcer dyspepsia.

In contrast, H. pylori-negative patients with antral gastritis on double contrast studies were significantly more likely to have antral erosions than H. pylori-positive patients (p<0.0001) (Figure 3). Although gastric erosions may occasionally be seen radiographically in patients with H. pylori infection [28], our data indicate that erosions are much more likely to be encountered in H. pylori-negative patients than in H. pylori-positive patients with antral gastritis. Also, 48% of patients with antral erosions had a documented history of recent aspirin or other NSAID use at the time of the barium study, whereas only 10% with antral erosions were H. pylori positive. We therefore believe that erosive antral gastritis is more likely to be caused by NSAIDs than by H. pylori infection.

An association has previously been reported between recent use of aspirin or other NSAIDs and the development of incomplete, linear or serpiginous erosions in the gastric antrum or body, typically in the region of the greater curvature [29]. In our study, however, only 40% of patients with erosive antral gastritis and a known history of NSAID use were found to have linear erosions. Instead, the majority of patients had varioliform erosions, characterized by punctate or slit-like collections of barium with surrounding mounds of oedema (Figure 3). Our data suggest that NSAIDs should still be considered as a possible cause of the patient's erosive gastritis when the erosions are confined to the antrum and have a varioliform appearance.

Although some authors have found a reasonable correlation between the endoscopic and histological diagnosis of gastritis [30, 31], others have shown that the endoscopic findings of antral gastritis correlate poorly with the histological findings [22]. In our study, visible signs of inflammation were reported at endoscopy in slightly more than 50% of patients with histological antral gastritis, whereas apparent endoscopic findings of antral gastritis were present in nearly 50% of patients with normal biopsy specimens from the antrum. It therefore is important to be aware of the limitations of endoscopy in diagnosing this condition.

In a recent study, Faigel et al [32] found that the presence and degree of antral gastritis on endoscopy biopsy specimens is highly predictive of H. pylori infection. Marked inflammatory changes on biopsy specimens should therefore arouse suspicion of H. pylori infection even if no organisms are seen on histology specimens with special stains for H. pylori. Conversely, special stains for H. pylori showing apparent organisms without associated inflammation should arouse suspicion of false positive special stains for H. pylori. In our study, the discrepancy between the presence or absence of antral gastritis on histology specimens and the findings of the CLOtest or special stains for H. pylori in some cases raises the possibility that these individuals may have had false positive or false negative tests for this infection.

Our study has additional limitations. There was unavoidable selection bias, as we only included patients with radiographically diagnosed antral gastritis who had undergone endoscopy. As a result, our study group contains a highly selected group of patients that was skewed toward those with more severe symptoms who were more likely to have endoscopy; our patient population therefore may not reflect the true spectrum of radiographic findings in all patients with antral gastritis, many of whom are asymptomatic [25]. Because of the frequent lag between the barium study and endoscopy, we also cannot be certain whether some patients without histopathological findings of antral gastritis had false positive radiographic studies or whether the gastritis had healed in the interim. We tried to minimize this problem by only including patients in whom the interval between the barium studies and endoscopy was 6 months or less. Nevertheless, our study is limited by the long mean interval of 3 months between these procedures. Another limitation of our study is the lack of absolute proof of antral gastritis in all cases, as no perfect gold standard exists for this diagnosis. Although 48% of patients with erosive antral gastritis had a history of recent aspirin or other NSAID use, we were unable to determine the frequency of NSAID use in patients with non-erosive antral gastritis, as these individuals were not carefully questioned about their NSAID history at the time of the barium study. Finally, because of logistical problems obtaining clinical follow-up on our patients (the vast majority were seen only as out-patients who had no centralized medical records), we cannot exclude the possibility that some of the H. pylori-negative patients with radiographically diagnosed antral gastritis were initially H. pylori positive and that the organism could have been eradicated from the stomach during the interval between the barium studies and endoscopy.

In conclusion, our experience suggests that antral gastritis caused by H. pylori infection is associated with characteristic features on double contrast studies (including thickened folds, polypoid gastritis and enlarged areae gastricae) and that this condition is rarely associated with antral erosions. Thus, radiologists can often suggest whether the patient's gastritis is caused by H. pylori on the basis of the radiographic findings.

Received for publication March 6, 2002. Accepted for publication May 21, 2002.

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