Unique endoscopic and histological findings of early gastric cancer with surrounding map-like redness detected 10 years after successful Helicobacter pylori eradication

We are indebted to Helena Popiel, Instructor of the Center for International Education and Research of Tokyo Medical University, for her editorial review of the manuscript.

The MAPS II guidelines state that patients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk of developing gastric adenocarcinoma, and therefore should undergo surveillance endoscopy [1]. In fact, it is well established that IM is associated with intestinal-type gastric adenocarcinoma [2] [3]. Recently, map-like redness, which is specifically observed after Helicobacter pylori eradication, has been shown to indicate IM histologically and to be an independent risk factor for post-eradication gastric adenocarcinoma [4] [5].

We report the case of a 64-year-old man who underwent successful H. pylori eradication therapy 10 years previously. Esophagogastroduodenoscopy (EGD) prior to H. pylori eradication showed atrophic mucosa with a visible vascular pattern in the lesser curvature of the gastric body ([Fig. 1 a]). An EGD 5 years after eradication therapy again displayed atrophic mucosa in the lesser curvature of the gastric body; however, the vascular pattern was less prominent than before H. pylori eradication ([Fig. 1 b]). A further EGD 10 years after eradication therapy displayed a 10-mm depressed lesion in the lesser curvature of the lower gastric body, which was histologically diagnosed as a tubular adenocarcinoma ([Fig. 1 c]). Although map-like redness was observed around the gastric adenocarcinoma, the mucosal atrophy and vascular patterns were unclear. The gastric adenocarcinoma was successfully resected en bloc by endoscopic submucosal dissection (ESD) ([Video 1]).

Fig. 1 Endoscopic images from the lesser curvature of the gastric body during progression over 10 years after Helicobacter pylori eradication therapy showing: a before H. pylori eradication therapy, atrophic mucosa with a visible vascular pattern; b 5 years after H. pylori eradication, a less prominent vascular pattern, although atrophic mucosa is still observed; c 10 years after H. pylori eradication therapy, a 10-mm depressed lesion that was histologically diagnosed as a tubular adenocarcinoma (yellow arrows), with map-like redness present around the gastric cancer, but unclear mucosal atrophy and vascular patterns.

Video 1 Unique endoscopic and histological findings of early gastric cancer with surrounding map-like redness detected 10 years after successful Helicobacter pylori eradication.

The tumor was histologically diagnosed as a well-differentiated adenocarcinoma limited to the mucosal layer, and curative resection was achieved. IM and almost normal gastric fundic glands were observed in patches of the background mucosa of the tumor ([Fig. 2] and [Fig. 3]).

Fig. 2 Endoscopic submucosal dissection of the lesion showing: a, b endoscopic images: a before marking; b after marking around the lesion; c the macroscopic appearance of the resected specimen; d the formalin-fixed and sectioned specimen. Histological images of a section from the region connecting the yellow and red dots are shown in [Fig. 3].

Fig. 3 Histological images (all stained with hematoxylin and eosin) of a section from the region connecting the yellow and red dots shown in [Fig. 2] showing: a panoramic view; b, c, d magnified images (original magnification × 200) of: b, c intestinal metaplasia and almost normal gastric fundic glands in patches within the green and blue boxes; d a well-differentiated adenocarcinoma limited to the mucosal layer in the orange box indicated in part a.

This case suggested that the histological difference between improvement in gastric mucosal atrophy upon H. pylori eradication and IM represents endoscopic map-like redness. Therefore, map-like redness may not be observed in the early period after H. pylori eradication, so care should be taken not to underestimate the risk of gastric adenocarcinoma when performing surveillance EGDs.

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Competing interests

The authors declare that they have no conflict of interest.

Acknowledgments

We are indebted to Helena Popiel, Instructor of the Center for International Education and Research of Tokyo Medical University, for her editorial review of the manuscript.

• References

• 1 Pimentel-Nunes P, Libanio D, Marcos-Pinto R. et al. Management of epithelial precancerous conditions and lesions in the stomach (MAPS II): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG), European Society of Pathology (ESP), and Sociedade Portuguesa de Endoscopia Digestiva (SPED) guideline update 2019. Endoscopy 2019; 51: 365-388
• 2 Goldenring JR, Nam KT, Wang TC. et al. Spasmolytic polypeptide-expressing metaplasia and intestinal metaplasia: time for reevaluation of metaplasias and the origins of gastric cancer. Gastroenterology 2010; 138: 2207-2210
• 3 Radyk MD, Burclaff J, Willet SG. et al. Metaplastic cells in the stomach arise, independently of stem cells, via dedifferentiation or transdifferentiation of chief cells. Gastroenterology 2018; 154: 839-843
• 4 Nagata N, Shimbo T, Akiyama J. et al. Predictability of gastric intestinal metaplasia by mottled patchy erythema seen on endoscopy. Gastroenterology Res 2011; 4: 203-209
• 5 Majima A, Dohi O, Takayama S. et al. Linked color imaging identifies important risk factors associated with gastric cancer after successful eradication of Helicobacter pylori. Gastrointest Endosc 2019; 90: 763-769

Publication History

Article published online:
03 February 2023