Margarita Topalovski

Magnification chromoendoscopy for the detection of intestinal metaplasia and dysplasia in Barrett’s oesophagus

Background: The presence of intestinal metaplasia (IM) in the columnar lined distal oesophagus defines Barrett’s oesophagus with the risk of future malignant transformation. The distribution of both IM and dysplasia (low grade (LGD) and high grade (HGD)) within the columnar lined oesophagus is patchy and mosaic requiring random biopsies. Techniques that could help target areas of high yield within Barrett’s mucosa would be helpful. Aim: To study the utility of high magnification chromoendoscopy (MCE) in the detection of IM, LGD, and HGD in patients with Barrett’s oesophagus. Methods: Consecutive patients detected with columnar mucosa in the distal oesophagus were studied using an Olympus magnification endoscope (GIF-Q16OZ, 115×). The distal oesophagus was sprayed with indigo carmine solution and the oesophageal columnar mucosa patterns were noted under high magnification and targeted for biopsy. All biopsies were read by pathologists blinded to the endoscopic findings. Results: Eighty patients with suspected Barrett’s oesophagus (that is, columnar lined distal oesophagus) were studied: mean age 62.7 years (range 35–81). Mean length of columnar mucosa was 3.7 cm (range 0.5–17). Three types of mucosal patterns were noted within the columnar mucosa after spraying indigo carmine and using MCE: ridged/villous pattern, circular pattern, and irregular/distorted pattern. The yield of IM on target biopsies according to the patterns was: ridged/villous 57/62 (97%) and circular 2/12 (17%). Six patients had an irregular/distorted pattern and all had HGD on biopsy (6/6 (100%)). Eighteen patients had LGD on target biopsies; all had the ridged/villous pattern. All patients with long segment Barrett’s were identified using MCE whereas 23/28 patients (82%) with short segment Barrett’s had the ridged/villous pattern. Conclusions: MCE helps visually identify areas with IM and HGD having specific patterns but not patients with LGD (appear similar to IM). MCE may be a useful clinical tool for the increased detection of patients with IM as well as for surveillance of patients for the detection of HGD. If these preliminary results are validated, MCE would help identify high yield areas, potentially eliminating the need for random biopsies.

Relative risk of dysplasia for patients with intestinal metaplasia in the distal oesophagus and in the gastric cardia

BACKGROUND Biopsy specimens obtained from the gastro-oesophageal junction can reveal intestinal metaplasia in patients presenting for routine upper endoscopy. The site of biopsy may play a critical role in determining the dysplasia risk of a patient. AIMS To evaluate prospectively the dysplasia risk in patients with intestinal metaplasia of the distal oesophagus or within the gastric cardia. METHODS Patients with short segment Barretts oesophagus (SSBO) and cardia intestinal metaplasia (CIM) were followed prospectively. RESULTS 177 patients with SSBO were identified (mean age 62 years, range 38–82; 91% whites). Twenty prevalence cases of dysplasia in SSBO were detected: 17 low grade dysplasia (LGD), three high grade dysplasia (HGD). Seventy six patients with CIM were identified (mean age 67 years, range 37–81; 81% whites). A single prevalence case of LGD in CIM was detected. During follow up of 78 SSBO and 34 CIM patients, dysplasia developed in nine (seven LGD, two HGD) with SSBO and in one (LGD) with CIM. There were significant differences between the two groups with respect to age, ethnicity, dysplasia prevalence, and incidence. Time to dysplasia progression was significantly longer in CIM compared with SSBO patients. Of the five patients with SSBO and HGD, one developed adenocarcinoma of the oesophagus on follow up. No HGD or cancers have been detected over this time period in CIM patients. CONCLUSIONS The dysplasia risk is significantly greater in SSBO than in CIM patients, indicating two potentially different clinical processes. Future studies should separate SSBO from CIM in order to enhance the understanding of the pathophysiology and malignant potential of each entity.

Prospective Evaluation of Intestinal Metaplasia and Dysplasia Within the Cardia of Patients with Barrett's Esophagus

The prevalence of cardia versus noncardiagastric intestinal metaplasia in patients with Barrettsesophagus was assessed prospectively. Four-quadrantbiopsies were obtained from the cardia from 119consecutive patients with Barretts esophagus and 64control patients. Gastric surveillance biopsies wereobtained in 108 of the Barretts patients and 58 controlpatients. There was a significantly greater prevalence of cardia intestinal metaplasia inshort-segment Barretts (10.2%), but not traditionalBarretts (3.3%), compared to control patients (0%) (P= 0.009). Dysplastic changes were significantly morefrequent in the metaplastic epithelium within theesophagus than in the cardia (P < 0.0001). Asignificantly greater prevalence of noncardia intestinalmetaplasia compared to cardia intestinal metaplasia wasfound in each of the three groups of patients;however, the prevalence of noncardia intestinalmetaplasia between short-segment, traditional, andcontrol patients was not significantly different. Cardiaintestinal metaplasia was an infrequent finding inpatients with Barretts esophagus and appears to developindependently from that in the remainder of thestomach.

Yield of intestinal metaplasia in patients with suspected short-segment Barrett's esophagus (SSBE) on repeat endoscopy.

Biopsies from short segments of columnar appearing mucosa in the distal esophagus often fail to reveal intestinal metaplasia (IM). The yield of IM on repeat upper endoscopy (EGD) and biopsy in these patients is not known. Our aim was to prospectively evaluate the yield of IM on repeat EGD in patients with suspected SSBE (negative for IM on first EGD). Forty-three patients with suspected SSBE underwent repeat EGD with biopsy. This included 42 men and 1 woman, mean age 53 years (range: 45–90) with a mean columnar mucosa length of 1.26 cm (range: 0.5–2.5). On repeat EGD, 10 of 43 patients (23.2%) had evidence of IM. There was no statistically significant difference between the patients with proven SSBE on repeat EGD compared to those with persistent negative IM with regards to age, ethnicity, length of columnar mucosa, GERD symptoms, and hiatal hernia size. In conclusion, more than 20% of patients with suspected SSBE have evidence of IM (ie, proven SSBE) on repeat EGD. Thus repeat EGD with biopsy may be warranted in patients with tongues of columnar mucosa in the distal esophagus but no IM on the first biopsy to confirm the diagnosis of SSBE.

Helicobacter pylori eradication dramatically improves inflammation in the gastric cardia.

OBJECTIVES:Inflammation of the gastric cardia, i.e., “carditis,” has been associated with Helicobacter pylori (H. pylori) infection; however, some investigators believe carditis to be a histological marker for gastroesophageal reflux disease. The aim of this study was to investigate the role of H. pylori eradication on the grade of carditis scored according to the updated Sydney classification.METHODS:Consecutive patients presenting for upper endoscopy underwent systematic gastric biopsies (eight antral, 12 corpus, and four cardia). Patients with H. pylori infection and carditis were identified and followed prospectively before and after H. pylori treatment. At pretreatment and, on average, 2 yr after eradication of H. pylori, the degree of inflammation in the gastric cardia and H. pylori status were blindly assessed by a single pathologist.RESULTS:A total of 31 patients with H. pylori infection and carditis were identified. The mean age was 70 yr (range: 37–81 yr); all were male. Four were African-American and 27 were Caucasian. All patients were treated with standard anti-H. pylori therapy, including a proton pump inhibitor in combination with two antibiotics for 2 wk. Eradication of H. pylori was successful in 23 patients (group I), whereas eight patients had persistent infection (group II). Patients were followed after eradication therapy for a mean of 23.2 months (range: 6–48 months). After eradication therapy, there was a significant decrease (p < 0.0001) in the carditis scores (activity and inflammation scores) in group I, whereas the scores remained unchanged in group II patients. In both groups, there were no significant changes in the degree of intestinal metaplasia or atrophy. There were four patients with intestinal metaplasia, and one with atrophy.CONCLUSIONS:There is a dramatic improvement in the degree of inflammation and activity scores in the gastric cardia of patients with successful H. pylori eradication compared to those with persistent infection. By fulfilling one of Kochs postulates (i.e., improvement in the disease after cure of the possible etiological organism), these data support H. pylori as being the etiological agent for carditis in this group of patients.

Detection of Cardia Intestinal Metaplasia: Do the Biopsy Number and Location Matter?

BACKGROUND AND AIM:Presence of intestinal metaplasia in the gastric cardia (cardia intestinal metaplasia, CIM) has been reported in 5–34% of patients undergoing upper endoscopy and is a topic of interest given the rising incidence of cancer in this location. The aim of this article is to determine the prevalence of CIM in biopsies obtained from two separate locations within the gastric cardia.METHODS:Patients presenting to the endoscopy unit for upper endoscopy for any symptoms were invited to participate in the study. The biopsy protocol included: eight biopsies from the gastric cardia, four from upper cardia (forceps across the squamocolumnar junction), four from lower cardia (within 1 cm of upper cardia), and four each from the gastric body and antrum. All cardia biopsies were stained with hematoxylin and eosin (H&E) and alcian blue at pH 2.5 for the presence of goblet cells and the body/antrum biopsies were stained with Steiner silver stain for Helicobacter pylori detection. In patients testing negative for H. pylori by histology, a serology test was performed.RESULTS:Sixty-five patients have been evaluated by this protocol; median age 54 yr (range: 34–81 yr), 63 males, 53 Caucasians, and 12 African Americans. The detection of CIM was as follows: upper cardia only, 7, both upper and lower cardia, 5, and lower cardia only, 7. Thus, CIM was detected in 12 patients (18%) in the upper cardia biopsies, in 12 patients (18%) in the lower cardia; overall prevalence of CIM was 29% (19 patients). Fifty-eight percent of CIM patients tested positive for H. pylori by either histology or serology. The addition of serology allowed for the detection of eight additional H. pylori-positive CIM patients.CONCLUSIONS:The prevalence of CIM in this study was similar (18%, four biopsies) at each location; however, if both locations were considered (eight biopsies), the prevalence increased to 29%. Thus, CIM prevalence may vary depending on the number of biopsies obtained as well as on the location of biopsies. Use of additional testing detects more patients who are H. pylori positive and should be performed if association of CIM with H. pylori is contemplated. Future endoscopic studies of the gastric cardia should specify the location of biopsies, the number of biopsies obtained, and the tests used to diagnose H. pylori.

Spectrum of intestinal metaplasia in the upper foregut: inter-relationships and associated features

Spectrum of intestinal metaplasia in the upper foregut: inter-relationships and associated features

Inflammation & intestinal metaplasia in the gastric cardia of patients presenting for upper endoscopy

Inflammation & intestinal metaplasia in the gastric cardia of patients presenting for upper endoscopy

Location of dysplasia and cancer in patients with Barrett's esophagus

Surveillance of patients with Barretts esophagus is undertaken for the detection of dysplasia and adenocarcinoma. This involves obtaining random biopsies from the entire Barretts segment. The preferential location of dysplasia/cancer either proximally or distally within the Barretts segment in not clear and if clarified may assist in surveillance programs. Aim: To determine the location of dysplasia/cancer in patients with Barretts esophagus. Methods: Patients with Barretts esophagus (2=:3cms length) diagnosed with low grade dysplasia (LGD), high grade dysplasia (HGD) or cancer (CA) were identified from a well defined prospectively followed group of patients with Barretts esophagus all having undegone a similar biopsy protocol-4 quadrant, every -2 cms. The location of biopsies revealing dysplasia/cancer in these patients was classified as proximal/distalif dysplasia/cancer were diagnosed in biopsy specimens from both proximal & distal Barretts segments; distal only -dysplasia/cancer only in the distal biopsy specimens; proximal only -dysplasia/cancer only in the proximal biopsy specimens. The patient demographics and the length of Barretts were also recorded. Results: Sixty-five patients (all white males) with Barretts esophagus and LGD,HGD,and/or CA were studied; mean age 61.4 years (range:30-80 yrs), mean Barretts length 7.7 ems (range:3-19 cms) These patients have undergone a total of 198 EGDlbx sessions revealing dysplasia/cancer. Location of dysplasia/cancer is as follows (table): Conclusions: Dysplasia, including HGD and CA is distributed throughout the entire length of the segment (ie.both proximally & distally) in more than half of patients with dysplasia/cancer within Barretts esophagus thus necessitating the need for surveillance biopsies from the entire Barretts esophagus. The concept that cancer occurs distally in patients with Barretts esophagus is probably incorrect.