Gastric intestinal metaplasia and early gastric cancer in the west: a changing paradigm

Abstract

Gastric cancer remains the fifth leading cancer diagnosis worldwide, and it is the third leading cause of cancer-related mortality. The incidence of gastric cancer within the United States, however, has remained substantially lower than elsewhere, which has led to a lack of screening and surveillance in clinical practice. Patients with known premalignant lesions, such as gastric intestinal metaplasia, which can increase the risk of gastric cancer by as much as 6-fold, might benefit from surveillance guidelines to detect gastric cancer at an earlier, potentially curative stage. Chro-moendoscopy with optical magnification, narrow-band imaging, and other image-enhanced endoscopic techniques are commercially available to assist in the diagnosis of premalignant gastric lesions and early gastric cancer. Furthermore, endoscopic mucosal resection and endoscopic submucosal dissection have become more widely available and offer potentially curative endoscopic resection for dysplastic lesions of the stomach and early gastric cancers, which is an alternative to traditional surgical resection.

Keywords: Early gastric cancer; endoscopic submucosal dissection; esophagogastroduodenoscopy; gastric intestinal metaplasia; staging.

Figures

Figure 1

An esophagogastroduodenoscopy was undertaken to evaluate for gastric intestinal metaplasia and dysplasia in a patient with suspected autoimmune metaplastic atrophic gastritis (antiparietal cell antibody was positive). Note the overall paucity of rugal folds seen on the endoscopic images. Multiple cold biopsies were obtained from the antrum (A), incisura (B), and lesser curve (C) of the stomach, which are the typical “hot spots” for early gastric cancer. Other biopsies were obtained from other areas of the body and fundus to evaluate for autoimmune gastritis. Narrow-band imaging (D) and chromoendoscopy (E) using 0.8% indigo carmine were used to survey for dysplasia, which was not found. Histopathology demonstrated focal intestinal metaplasia in the background of likely autoimmune metaplastic atrophic gastritis.

Figure 1

An esophagogastroduodenoscopy was undertaken to evaluate for gastric intestinal metaplasia and dysplasia in a patient with suspected autoimmune metaplastic atrophic gastritis (antiparietal cell antibody was positive). Note the overall paucity of rugal folds seen on the endoscopic images. Multiple cold biopsies were obtained from the antrum (A), incisura (B), and lesser curve (C) of the stomach, which are the typical “hot spots” for early gastric cancer. Other biopsies were obtained from other areas of the body and fundus to evaluate for autoimmune gastritis. Narrow-band imaging (D) and chromoendoscopy (E) using 0.8% indigo carmine were used to survey for dysplasia, which was not found. Histopathology demonstrated focal intestinal metaplasia in the background of likely autoimmune metaplastic atrophic gastritis.

Figure 2

An 8-mm nodule was found in a gastric body. Narrow-band imaging (A) demonstrated an irregular capillary pattern with thickened vessels suggestive of dysplasia. Cap- and band-assisted endoscopic mucosal resection (B) was performed with complete resection (C) of the lesion. The mucosal defect was closed with endoclips (D). The specimen was resected as a single piece (E), and it was affixed to a foam board with pins (not shown) and delivered for tissue fixation and staining. Low-power histopathology (20x magnification using hematoxylin and eosin staining) showed resection of the mucosa and submucosa with deep and lateral margins negative for dysplasia (F).

Figure 2

High-power histopathology (200x magnification using hematoxylin and eosin staining) of the resected gastric lesion showed low-grade dysplasia and intestinal metaplasia on a background of chronic inflammation (G). Helicobacter pylori infection was not identified. An Alcian blue stain highlighted goblet cells (H) indicative of intestinal metaplasia.

Figure 3

An area of severe dysplasia, measuring approximately 2.5 cm, was identified along the posterior wall of the antrum and involved approximately one-third of the prepyloric channel (A). This lesion was too large to remove by endoscopic mucosal resection in a single piece; as such, endoscopic submucosal dissection was performed. The circumference of the lesion was marked (B), and circumferential incision followed by submucosal dissection (C) was performed. Exposed submucosal vessels were treated with atraumatic coagulating forceps (D) and endoclips (E) to reduce the risk of delayed bleeding. The resected specimen was affixed to a foam board and sent for histopathologic tissue fixation (F). Complete endoscopic resection was achieved with negative circumferential and deep margins on histopathology.