Duodenal Gastric Metaplasia Research Articles

Duodenal Gastric Metaplasia and Duodenal Neuroendocrine Neoplasms: More Than a Simple Coincidence?

Background: Duodenal gastric metaplasia (DGM) is considered a precancerous lesion. No data are available regarding its possible role as a risk factor for duodenal neuroendocrine neoplasms (dNENs). Aims: To assess the prevalence of DGM in a cohort of dNENs. Methods: Subgroup analysis of a retrospective study including dNEN patients who underwent surgical resection between 2000 and 2019 and were observed at eight Italian tertiary referral centers. Results: 109 dNEN patients were evaluated. Signs of DGM associated with the presence of dNEN were reported in 14 patients (12.8%). Among these patients, nine (64.4%) had a dNEN of the superior part of the duodenum, one (7.1%) a periampullary lesion, three (21.4%) a dNEN located in the second portion of the duodenum, with a different localization distribution compared to patients without DGM (p = 0.0332). Ten were G1, three G2, and in one patient the Ki67 was not available. In the group with DGM, six patients (35.7%) were classified at stage I, five (28.6%) at stage II, three (21.4%) at stage III, and no one at stage IV. In the group without DGM, 20 patients (31%) were at stage I, 15 (15%) at stage II, 42 (44%) at stage III, and 19 (20%) at stage IV (p = 0.0236). At the end of the study, three patients died because of disease progression. Conclusions: our findings might suggest that DGM could represent a feature associated with the occurrence of dNEN, especially for forms of the superior part of the duodenum, which should be kept in mind in the endoscopic follow up of patients with DGM. Interestingly, dNEN inside DGM showed a more favorable staging, with no patients in stage IV. The actual relationship and the clinical relevance of this possible association require further clarification.

McCune Albright Syndrome: Gastrointestinal Polyps and Platelet Dysfunction over 12 Years

Background and Objective: Gastrointestinal (GI) polyps with unknown malignant potential and a platelet storage pool deficiency that increases the risk of severe intraoperative and other types of bleeding have been identified in McCune-Albright syndrome (MAS). The natural course of these disorders has not been well characterized. The aim of this study was to report the follow-up of GI polyps and platelet dysfunction (PD) in a cohort of 28 patients with MAS. Methods: Twenty-eight patients with MAS (15 females) were included. Endoscopic screening for GI polyps was undertaken in 14 subjects and 19 were tested for PD. Results: Six subjects (5 males) were diagnosed with GI polyps at a median age of 23 (range 15–43) years, and were monitored for a median period of 8 (range 4.5–11.5) years. At endoscopic follow-up, the 4 patients with hamartomatous polyps at first endoscopy had either normal findings (n = 2), or duodenal gastric metaplasia (n = 2). Two patients with caecal polyps were identified. Of 8 subjects with a platelet storage pool deficiency, 5 required transfusions during surgery, and subsequent platelet cover in 2 markedly reduced intraoperative blood loss. Conclusions: New polyps with uncertain malignant potential are diagnosed after long term follow-up in MAS. Platelet cover reduces the need for red blood cell transfusion during orthopaedic surgery and may be useful to reduce non-operative bleeding events. We recommend regular upper and lower endoscopy and screening for PD in all MAS patients.

Gastric Focal Neutrophil Infiltration and Wide Duodenal Gastric Foveolar Metaplasia Are Histologic Discriminative Markers for Crohn’s Disease and Behçet’s Disease

Background/Aims: Behçet’s disease (BD) with intestinal lesions and Crohn’s disease (CD) share clinical features. However, no report has compared the 2 diseases with regard to lesions of the upper gastrointestinal tract (UGT). We aimed to evaluate endoscopic and histologic findings of UGT in CD and BD. Methods: We retrospectively assessed the endoscopic records and biopsy samples of 84 Helicobacter pylori-negative patients (50 CD, 34 BD). In duodenal samples, MUC5AC immunohistochemical analysis was performed to identify gastric foveolar metaplasia. Results: In endoscopic findings, bamboo joint-like appearance (17/50 CD, 0/34 BD) and erosions (14/50 CD, 2/34 BD) were significantly more frequent in CD gastric lesions (p < 0.001, and p = 0.012). In histologic findings of stomach, focal neutrophil infiltration in lamina propria (15/48 CD, 1/34 BD) was significantly more frequent in CD (p < 0.001). In that of duodenum, wide gastric foveolar metaplasia (19/49 CD, 1/34 BD) was significantly more frequent in CD duodenal lesions (p = 0.013). The mean maximum width of the gastric foveolar metaplasia was 114.0 ± 10.6 and 29.5 ± 4.5 μm for CD and BD respectively (p = 0.003). Conclusions: In H. pylori-negative patients, gastric focal neutrophil infiltration and wide duodenal gastric foveolar metaplasia were important for distinguishing CD from BD.

Villous Duodenal Polyp With Foveolar Gastric Metaplasia in a Patient With Recently Resected Papillary Clear Cell Carcinoma: A Case Report

Duodenal foveolar gastric metaplasia is of well-known clinical occurrence, yet involvement in the form of a villous mass is of rare representation. Foveolar gastric metaplasia (FGM) usually seen as polyps on endoscopy has a benign clinical course and is diagnosed through biopsy. We report a case of FGM of the duodenum in a patient undergoing screening for possible metastatic papillary renal cell carcinoma. An 84-year-old African American male was referred to our gastroenterology clinic for incidental radiological findings concerning for gastric and duodenal malignancy. The patient had surveillance CT abdomen with contrast following robotic assisted nephrectomy for right renal cell carcinoma done 6 months earlier. The CT abdomen revealed a heterogeneously enhancing mass involving the distal stomach and extending into the duodenum. It also revealed subtle enhancing liver lesions. The CT findings were not present on radiological images prior to the nephrectomy. The patient denied any abdominal pain, nausea, vomiting, or early satiety. However, the patient reported losing 20-30 pounds over the past 3 years. Upper endoscopy performed revealed a large circumferential villous mass in the duodenal bulb with no signs of active bleeding. Biopsies of the mass were taken endoscopically. Pathological interpretation revealed gastric foveolar mucosa with benign vascular proliferation and no neoplasm identified. The patient was offered an endoscopic ultrasound for further evaluation of the duodenal mass and the hepatic lesions to rule out malignancy. However, the patient refused the procedure and was accepting of death should the procedure yield findings consistent with malignancy. FGM is known for its benign pathology and involvement of the duodenum. Our case signifies the relative rarity of FGM presenting as a villous mass of the duodenum. Narrow band imaging and endoscopic ultrasonography are techniques used frequently to better evaluate duodenal FGM. Given reported cases of renal cell carcinoma presenting as metastasis with gastric polyps and in other cases with concomitant duodenal papillary carcinoma, we raise the question of the correlation between papillary renal cell carcinoma and FGM of the duodenum in this patient.1900_A Figure 1 No Caption available.1900_B Figure 2 No Caption available.1900_C Figure 3 No Caption available.

Correction: The different pathogenesis of sporadic adenoma and adenocarcinoma in non-ampullary lesions of the proximal and distal duodenum.

[This corrects the article DOI: 10.18632/oncotarget.17051.].

The different pathogeneses of sporadic adenoma and adenocarcinoma in non-ampullary lesions of the proximal and distal duodenum.

Non-ampullary duodenal adenoma with activation of Wnt/β-catenin signalling is common in familial adenomatous polyposis (FAP) patients, whereas sporadic non-ampullary adenoma is uncommon. The adenoma-carcinoma sequence similar to colon cancer is associated with duodenal tumors in FAP, but not always in sporadic tumors. We obtained 37 non-ampullary duodenal tumors, including 25 adenomas and 12 adenocarcinomas, were obtained from biopsies and endoscopic resections. We performed immunohistochemistry for β-catenin, the hallmark of Wnt activation, and aldehyde dehydrogenase 1 (ALDH1), a putative cancer stem cell marker. In non-ampullary lesions, abnormal nuclear localization of β-catenin was observed in 21 (84.0%) of 25 adenomas and 4 (33.3%) of 12 adenocarcinomas. In the proximal duodenum, nuclear β-catenin was less frequent in both adenomas and adenocarcinomas. Gastric duodenal metaplasia (GDM) was observed only in the proximal duodenum. All adenomas with GDM were the gastric foveolar and pyloric gland types, and showed only membranous β-catenin. The intestinal-type adenomas had nuclear β-catenin in the proximal and distal duodenum. ALDH1-positive cells were more frequent in adenocarcinomas than adenomas. Nuclear β-catenin accumulation frequently occurred in ALDH1-positive cells in adenoma, but not in adenocarcinoma. In the non-ampullary proximal duodenum, Wnt/β-catenin pathway activation was more closely associated with adenomas than adenocarcinomas, and while it might cooperate with ALDH1 in adenoma, it does not in adenocarcinoma. The pathogenesis thus may differ between sporadic adenoma and adenocarcinoma of non-ampullary duodenal lesions, especially in the proximal and distal duodenum.

Helicobacter pyloriInfection and Duodenal Gastric Metaplasia in Healthy Young Adults

Duodenal ulcers occur relatively frequently in adolescents, like in adults, and may relate to Helicobacter pylori infection and duodenal gastric metaplasia (DGM). This study investigated the association between H. pylori infection and DGM in healthy adults aged 20-29. Between 1995 and 2005, endoscopic biopsies of the duodenum, antrum and body were taken from healthy, young volunteers, who were first-year medical students, faculty staff, residents, and research assistants of Gyeongsang National University in Jinju, Korea. Urease tests were performed and the extent of DGM and histopathological grades according to the Updated Sydney System were determined. In total, 662 subjects were enrolled (429 males and 233 females). The median age was 22.3 years. The overall incidence of DGM was 11.5% but DGM was more frequent in males (15.4%) than in females (4.3%) (p<0.0001). While H. pylori positivity rates changed significantly during the 1995-2005 period (p<0.01), the incidences of DGM did not. DGM was observed in 7.2% and 14.9% of subjects who were and were not colonized with H. pylori, respectively. DGM was also associated with less severe chronic gastritis and the absence of active gastritis in both the antrum and body, and the absence of follicles in the antrum (p<0.05). These findings suggested that DGM is not rare in healthy young adults and is unrelated to gastric H. pylori infection.

DoesHelicobacter pyloriNot Relate to Duodenal Gastric Metaplasia in Healthy Young Adults?

Does<i>Helicobacter pylori</i>Not Relate to Duodenal Gastric Metaplasia in Healthy Young Adults?

Histopathological Findings in Duodenal Biopsy of a Mexican Children Population with Gastritis by Helicobacter Pylori

Introduction: Chronic inflammation and duodenal gastric metaplasia (DGM) increase with the presence of Helicobacter pylori (Hp). DGM is considered the earliest change in the development of duodenal ulcer in children with Hp gastritis. Until now, histopathological duodenal changes in children with Hp associated gastritis had not been studied in Mexico, where there is a high gastric Hp prevalence. Objective: This study aims to describe the histopathological findings of duodenal biopsy in a Mexican children population with Hp-associated gastritis. Materials and Methods: This cross-sectional, retrospective and analytical study examined, using light microscopy, the gastric and duodenal biopsies from a consecutive series of cases of children with and without Hp gastritis, received from 2000 to 2007. In the duodenal biopsy, active or non-active chronic duodenitis and DGM were observed. The DGM was highlighted with alcian blue/PAS stain. Results: 306 patients with a histopathological diagnosis of chronic gastritis, 95 with Hp and 211 without Hp, are included in this study. The frequency of chronic duodenitis in patients with chronic gastritis by Hp is 100%. We found the highest gastric Hp frequency (p 0.05) between Hp-associated chronic gastritis and the following: alteration of villus height/crypt depth ratios, damage to surface enterocytes, loss of brush border, and duodenal ulcer. Conclusions: In the Mexican children population with and without Hp chronic gastritis studied, chronic duodenitis is a very common histopathological finding. The DGM is related to the presence and density of gastric Hp. To confirm DGM, an ancillary method could be used in the endoscopic duodenal biopsy.

FOXP3‐expressing CD4+ T‐cell Numbers Increase in Areas of Duodenal Gastric Metaplasia and are Associated to CD4+ T‐cell Aggregates in the Duodenum of Helicobacter pylori‐infected Duodenal Ulcer Patients

We have previously demonstrated that Helicobacter pylori infection is associated with an increased number of CD4(+)CD25(high) regulatory T cells in the gastric and duodenal mucosa. In this study, we determined the number and localization of CD4(+) cells expressing the regulatory T-cell-specific transcription factor FOXP3 in the antrum and duodenum of duodenal ulcer patients, asymptomatic carriers, and uninfected individuals. We also determined gene expression levels of FOXP3 as well as anti- and proinflammatory cytokines before and after H. pylori eradication. Cellular FOXP3 expression was studied by immunofluorescence and flow cytometry, and transcription levels of FOXP3, interleukin (IL)-10, transforming growth factor-beta, CD4, and interferon-gamma were analyzed by real-time reverse transcription-polymerase chain reaction. We found an increased (6-fold) frequency of CD4(+)FOXP3(+) T cells in H. pylori-infected gastric mucosa; interestingly 26% of these cells did not co-express CD25. The increase of FOXP3-expressing T cells in the antrum of infected individuals was dependent on the presence of H. pylori, since eradication therapy resulted in 4-fold lower levels of FOXP3 and IL-10 mRNA in the antrum. Furthermore, higher numbers of CD4(+)FOXP3(+) T cells were found in areas of duodenal gastric metaplasia in the duodenum of duodenal ulcer patients compared to duodenal gastric metaplasia of asymptomatic individuals and healthy mucosa in both patient groups. In duodenal ulcer patients, the CD4(+)FOXP3(+) T cells were more highly associated to aggregates in the duodenal mucosa. The numbers of CD4(+)FOXP3(+) T cells are increased and localized in CD4(+) T-cell aggregates in areas of duodenal gastric metaplasia in duodenal ulcer patients.

Gastric duodenal metaplasia in duodenal adenomas

Backgound: In cases of known aetiology, gastric duodenal metaplasia (GMD) is a reversible lesion. In cases of unknown aetiology, the fate of GMD remains elusive. GMD was recently found in...

Clinical Significance of Widespread Gastric Metaplasia in the Duodenal Bulb

All the risk factors of peptic ulcer disease are not thoroughly understood. To assess duodenal gastric metaplasia (DGM) in relation to Helicobacter pylori status and endoscopy findings with special reference to the effects of highly selective vagotomy. The study population consisted of 1056 adult patients and an additional 154 patients who had had a highly selective vagotomy. Their clinical and endoscopy records as well as the histology of gastric and duodenal biopsies were evaluated retrospectively. H. pylori infection had been determined by serology and culture. Widespread (more than 20%) DGM was strongly associated with H. pylori positive duodenal ulcer disease (in 59.7% of patients). The prevalence of DGM diminished progressively the more proximally the ulcer was located in the stomach, and was 2.5% in proximal gastric ulcers patients. In vagotomized patients, the prevalence of widespread DGM (8.4% of patients, median 14 years after operation and the majority still H. pylori positive) was close to that of patients with H. pylori gastritis without peptic ulcer disease (4.5%). Widespread DGM is an indicator for an increased risk of duodenal ulcer among H. pylori positive patients and it could be used to select patients for eradication therapy.

Helicobacter heilmannii infection of the antrum and duodenal bulb

A 66-year-old male farmer pre-sented at the Unit of Gastroenterology,Policlinico Hospital, University of Bari,Bari, Italy, with a 1-year history of dys-phagia upon both solid and liquid foodintake, belching, occasional vomiting,and weight loss. His medical history in-cluded pulmonary emphysema, surgeryfor inguinal hernia, and hypertension.Endoscopy revealed the presence ofchronic esophagitis, hiatal hernia, andantral erosions. The bulb was hyper-emic. The mucosa of the remainingduodenum appeared normal. Multiplebiopsy specimens were taken from theesophagus, gastric body and antrum,and the duodenal bulb. The esophagealhistology revealed epithelial acanthosiswithout gastric and intestinal metapla-sia. Histology showed moderate chronicantral gastritis, as demonstrated by anincreased number of lymphocytes andplasma cells in the lamina propria withseveral polymorphonuclear cells (Fig. 1).The gastric body histology was normal.The duodenal bulb showed a chronicinflammation associated with small fociof gastric metaplasia. Gram-stainedsmears of sections of the gastric antrumand duodenal gastric metaplasia revealedseveral gram-negative, tightly coiled,spiral-shaped bacteria resembling

Evidence for acid-induced loss of Cdx2 expression in duodenal gastric metaplasia.

Gastric metaplasia in the duodenum (GMD) is characterized by transdifferentiation of intestinal epithelial cells into gastric foveolar cells within the duodenal mucosa. GMD is often associated with duodenal ulceration. Higher duodenal acidity due to increased gastric acid output into the duodenum has been implicated in the development of GMD. Intestinal development and homeostasis are controlled by the homeobox transcription factor Cdx2, which is considered to be the master regulator of intestinal differentiation. Using immunohistochemistry, the present study shows that GMD is associated with loss of expression of Cdx2 and its target gene product sucrase-isomaltase. Quantitative RT-PCR experiments using the intestinal cell line Caco2 revealed that Cdx2 and sucrase-isomaltase were down-regulated and gastric mucins MUC5AC and MUC6 were up-regulated under acidic culture conditions. Thus, it is suggested that increased acid exposure leads to GMD by impairing the transcription of Cdx2 and subsequently that of its intestine-specific target genes.

Duodenal gastric metaplasia and Helicobacter pylori infection in high and low duodenal ulcer-prevalent areas in India.

Previous reports, based on surgery, showed duodenal ulcer (DU) to be more common in the rice-eating areas of southern India than in the northern wheat-eating areas. Does this difference persist? Can it be explained by risk factors other than diet? A total of 20 053 records from patients undergoing endoscopy for dyspepsia, and 590 endoscopy patients from two northern and two southern centers in India were studied prospectively. Records were scrutinized to determine the relative incidence of DU and non-ulcer dyspepsia in wheat- and rice-eating areas. Age, sex, length of history, smoking and medication were recorded. Three antral biopsies and one from each duodenal quadrant were taken. A rapid urease test was carried out on one of the antral biopsies; the others were examined for Helicobacter pylori, gastritis, duodenitis and duodenal gastric metaplasia. The difference in diet-associated prevalence persisted. No differences in smoking, Helicobacter pylori infection or duodenal gastric metaplasia were found between the two regions, but all three were more common in DU than in non-ulcer dyspeptic patients from both dietary areas. The dietary differences between the regions remain the only factor to account for the differences in DU prevalence. A strong interrelationship between duodenal gastric metaplasia and cigarette smoking is demonstrated.

Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa

Background. Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU). Aims. We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions. Patients. A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study. Methods. Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa ( Heliobacter pylori infection was determined only by histology). Results. The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex ( p=0.046), Heliobacter pylori-positive chronic gastritis ( p=0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease ( p<0.001), duodenal ulcer ( p<0.001), and duodenal bulb deformity and scarring in endoscopy ( p<0.001), but not with age ( p=0.7) nor use of nonsteroidal anti-inflammatory drugs ( p=0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1–2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4–36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3–0.8). Conclusions. In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.

A simple method to demonstrate duodenal gastric metaplasia

The diagnosis of duodenal gastric metaplasia (DGM) is based on the demonstration of periodic acid Schiff (PAS) positive mucin in duodenal columnar cells. Recently, groups of duodenal columnar cells were seen to be autofluorescent in haematoxylin and eosin (H&E) stained sections from a patient with DGM. Consecutive archival gastric and duodenal H&E sections from 30 patients with chronic gastritis and DGM (CG+DGM), from 30 with chronic gastritis without DGM (control group I), from 30 with normal gastric and duodenal mucosa (control group II), and from five patients with coeliac disease (control group III) were reviewed on a fluorescent microscope. The surface epithelium of the gastric mucosa in all 95 cases had autofluorescent material. In 31 cases with DGM (including one unreported case in control group I), groups of columnar duodenal cells also had autofluorescent material. In the remaining 64 cases, duodenal columnar cells were not autofluorescent. Results were confirmed with the PAS stain. The method described detected apical mucin secretion in columnar cells, both in the stomach and in the duodenum from patients with DGM. The autofluorescence was induced by eosin (which binds to neutral mucin). Observing H&E stained duodenal biopsies under a fluorescence microscope may be sufficient to confirm DGM or to detect incipient DGM. Despite long observation periods and a long exposure time while photographing, the autofluorescence did not fade away. Because re-cuttings for special staining (PAS) are no longer required when this method is used, both final diagnosing time and laboratory costs can be reduced.

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. . Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). . The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.

Gastric metaplasia: a frequently overlooked feature of duodenal biopsy specimens in untreated celiac disease.

Duodenal gastric metaplasia is rarely reported in untreated celiac disease, although it is seen in 60% to 100% of duodenal biopsy specimens in nonceliac patients with histologic duodenitis. The low incidence could represent underreporting, a decreased incidence in pediatric patients generally, or the more distal sampling site that is customary for most biopsy specimens that are obtained to diagnose celiac disease. It could also be a unique feature of the inflammatory reaction that characterizes this disease. The purpose of this study was to examine the incidence of gastric metaplasia in duodenal specimens from children with untreated celiac disease with special reference to patient age and biopsy site. Formalin-fixed paraffin-embedded specimens of duodenal mucosa were selected from the pathology department's archival material. Sections were either stained histochemically or by immunochemical methods, according to an antigen-retrieval protocol. Forty-four duodenal specimens from untreated patients with celiac disease (n = 22) and control subjects of similar age with normal histology (n = 22) were examined. Ten of each were obtained during upper endoscopy from the proximal duodenum (proximal site) and 12 of each by Crosby capsule near the ligament of Treitz (distal site). All specimens from patients with celiac disease exhibited marked villous atrophy. None had been noted to have gastric metaplasia during routine examination of sections stained by hematoxylin and eosin. Fifteen (68%) of 22 of the celiac specimens and 2 of 22 (9%) control specimens contained gastric metaplasia, identified as patches of gastric-type cells containing MUC5AC (gastric mucin), pS2 (gastric trefoil factor) and neutral (periodic acid-Schiff-positive) mucin. Five of the seven celiac specimens that had no metaplasia showed increased numbers of goblet cells expressing gastric markers. The incidence of gastric metaplasia was not different for endoscopic (70%) or capsule (67%) specimens. Sixty-eight percent (7/11) of patients aged less than 3 years had gastric metaplasia. The presence of gastric metaplasia has been previously underreported in celiac disease specimens. Detection would be improved by the routine use of period acid-Schiff/ alcian blue staining. The incidence of gastric metaplasia in celiac disease is not significantly influenced by biopsy site or age at time of the biopsy.

3492 Cap-fitted gastroscopy improves visualisation and targeting of lesions.

Introduction: Adequate visualisation of lesions during gastroscopy (OGD)is essential for diagnosis, biopsy and targeted therapy.The duodenal bulb, D1-D2 junction, cardia and posterior gastric wall are difficult areas to examine because of instability of the endoscope tip or tangential approach. Simple cap-fitted gastroscopy (CF-OGD) improves visualisation by maintaining tip stability in the duodenal bulb and D1-D2 junction, allows manipulation of tangential sites to an "en-face" approach while maintaining a fixed distance between the scope tip and the lesion. Method: A recycled transparent cap from a Wilson-Cook Sixshooter(R) variceal ligator was evaluated prospectively during OGD by a single experienced endoscopist(YCK). Where visualisation or targeting for biopsy or therapy was deemed suboptimal due to endoscope tip instability or tangential approach, the examination was repeated using the same scope fitted with the cap. Results: 17 procedures were deemed necessary for CF-OGD for diagnosis or treatment. Males 9, mean age 62 years (27-89 years). Site of lesion: deformed duodenal bulb 7, D1-D2 junction 5, D2 1, posterior gastric wall 3, incisura 1, cardia 1, pylorus 1. Diagnostic entities: duodenal varix 1, duodenal ulcer 7, gastric ulcer 3, antral cancer 1, Crohn's disease duodenum 1, duodenal polyp 3, gastric polyp 1, duodenal gastric metaplasia 1. Additional procedures: targeted biopsy 7, injection of bleeding DU 3, polypectomy (2.5cm D1 polyp) 1. There were no problems encountered with intubation using the cap or complications. Conclusion: Simple cap-fitted gastroscopy is a useful adjunct to OGD to visualise difficult areas, obtain biopsies and target lesions for therapy.