Incidence of Gastric Neoplasms Arising from Autoimmune Metaplastic Atrophic Gastritis: A Systematic Review and Case Reports

Abstract

Autoimmune metaplastic atrophic gastritis (AMAG) is associated with an increased risk of gastric neoplasms. This study aimed to systematically analyze the incidence rate of gastric cancer (GC), low-grade dysplasia (LGD) and type-1 gastric neuroendocrine tumor (gNETs) development in AMAG adults. Studies on AMAG patients reporting the incidence of gastric neoplasms was identified through a systematic search in PUBMED and EMBASE. Study quality was assessed using the Joanna Briggs Institute quality assessment tool. Incidence rates of GC, LGD and type-1 gNETs were examined by meta-analysis. Thirteen studies met eligibility criteria. Incidence rate of gastric cancer calculated from the pooled data was 0.14% per person-year in both single-center studies and national registration studies. Meta-analysis showed a relative risk of 11.05 (95% CI: 6.39-19.11) for gastric cancer development in AMAG patients. The calculated pooled gastric LGD and type-1 gNETs incidence rates were 0.52% and 0.83% per person-year, respectively. As for experience from our center, we presented three distinctive cases of gastric neoplasm arising from the background of AMAG. This study underscores the potential for malignant transformation of precancerous lesions and reiterates the importance of careful esophagogastroduodenoscopy screening.

Keywords: autoimmune metaplastic atrophic gastritis; dysplasia; gastric cancer; gastric hyperplastic polyps; neuroendocrine tumor; pernicious anemia.

Figure 1

Flow chart of study selection.

Figure 2

Gastric cancer relative risk of the eight studies with active follow-up in AMAG patients [9,10,11,13,14,15,16,18].

Figure 3

Gastric LGD incidence rates in AMAG patients [9,10,11,14,16].

Figure 4

Incidence rates of type-1 gNETs in AMAG patients [9,10,11,15].

Figure 5

Adenocarcinoma and type-1 gNET arising from the background of AMAG. (A) Protruding lesion in the upper corpus, (B) white nodule in the lower corpus, (C) ME-NBI observation of the nodule showing clear demarcation line with irregular microvessels and microstructure on the surface, (D) immunohistochemical stain for Synaptophysin in the protruding lesion (×4), (E) HE stain of the white nodule in the lower corpus showing early well-differentiated adenocarcinoma (×4).

Figure 6

Malignant transformation of a GHP arising from the background of AMAG. (A) EGD showing multiple gastric hyperplastic polyps, (B,C) pathology revealing moderately differentiated adenocarcinoma at the tip of one of the GHPs (yellow square, HE stain; (B) ×4; and (C) ×20).

Figure 7

Signet-ring-cell carcinoma arising from AMAG. (A) White light and (B) NBI showed a depressed lesion in the corpus, and (C) pathology revealed signet-ring-cell carcinoma (HE stain, (C) ×10).