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Review
. 2021 Oct;161(4):1325-1332.e7.
doi: 10.1053/j.gastro.2021.06.078. Epub 2021 Aug 26.

AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review

Affiliations
Review

AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review

Shailja C Shah et al. Gastroenterology. 2021 Oct.

Abstract

Description: The purpose of this Clinical Practice Update Expert Review is to provide clinicians with guidance on the diagnosis and management of atrophic gastritis, a common preneoplastic condition of the stomach, with a primary focus on atrophic gastritis due to chronic Helicobacter pylori infection-the most common etiology-or due to autoimmunity. To date, clinical guidance for best practices related to the diagnosis and management of atrophic gastritis remains very limited in the United States, which leads to poor recognition of this preneoplastic condition and suboptimal risk stratification. In addition, there is heterogeneity in the definitions of atrophic gastritis, autoimmune gastritis, pernicious anemia, and gastric neoplasia in the literature, which has led to confusion in clinical practice and research. Accordingly, the primary objective of this Clinical Practice Update is to provide clinicians with a framework for the diagnosis and management of atrophic gastritis. By focusing on atrophic gastritis, this Clinical Practice Update is intended to complement the 2020 American Gastroenterological Association Institute guidelines on the management of gastric intestinal metaplasia. These recent guidelines did not specifically discuss the diagnosis and management of atrophic gastritis. Providers should recognize, however, that a diagnosis of intestinal metaplasia on gastric histopathology implies the diagnosis of atrophic gastritis because intestinal metaplasia occurs in underlying atrophic mucosa, although this is often not distinctly noted on histopathologic reports. Nevertheless, atrophic gastritis represents an important stage with distinct histopathologic alterations in the multistep cascade of gastric cancer pathogenesis.

Methods: The Best Practice Advice statements presented herein were developed from a combination of available evidence from published literature and consensus-based expert opinion. No formal rating of the strength or quality of the evidence was carried out. These statements are meant to provide practical advice to clinicians practicing in the United States. Best Practice Advice Statements BEST PRACTICE ADVICE 1: Atrophic gastritis is defined as the loss of gastric glands, with or without metaplasia, in the setting of chronic inflammation mainly due to Helicobacter pylori infection or autoimmunity. Regardless of the etiology, the diagnosis of atrophic gastritis should be confirmed by histopathology. BEST PRACTICE ADVICE 2: Providers should be aware that the presence of intestinal metaplasia on gastric histology almost invariably implies the diagnosis of atrophic gastritis. There should be a coordinated effort between gastroenterologists and pathologists to improve the consistency of documenting the extent and severity of atrophic gastritis, particularly if marked atrophy is present. BEST PRACTICE ADVICE 3: Providers should recognize typical endoscopic features of atrophic gastritis, which include pale appearance of gastric mucosa, increased visibility of vasculature due to thinning of the gastric mucosa, and loss of gastric folds, and, if with concomitant intestinal metaplasia, light blue crests and white opaque fields. Because these mucosal changes are often subtle, techniques to optimize evaluation of the gastric mucosa should be performed. BEST PRACTICE ADVICE 4: When endoscopic features of atrophic gastritis are present, providers should assess the extent endoscopically. Providers should obtain biopsies from the suspected atrophic/metaplastic areas for histopathological confirmation and risk stratification; at a minimum, biopsies from the body and antrum/incisura should be obtained and placed in separately labeled jars. Targeted biopsies should additionally be obtained from any other mucosal abnormalities. BEST PRACTICE ADVICE 5: In patients with histology compatible with autoimmune gastritis, providers should consider checking antiparietal cell antibodies and anti-intrinsic factor antibodies to assist with the diagnosis. Providers should also evaluate for anemia due to vitamin B-12 and iron deficiencies. BEST PRACTICE ADVICE 6: All individuals with atrophic gastritis should be assessed for H pylori infection. If positive, treatment of H pylori should be administered and successful eradication should be confirmed using nonserological testing modalities. BEST PRACTICE ADVICE 7: The optimal endoscopic surveillance interval for patients with atrophic gastritis is not well-defined and should be decided based on individual risk assessment and shared decision making. A surveillance endoscopy every 3 years should be considered in individuals with advanced atrophic gastritis, defined based on anatomic extent and histologic grade. BEST PRACTICE ADVICE 8: The optimal surveillance interval for individuals with autoimmune gastritis is unclear. Interval endoscopic surveillance should be considered based on individualized assessment and shared decision making. BEST PRACTICE ADVICE 9: Providers should recognize pernicious anemia as a late-stage manifestation of autoimmune gastritis that is characterized by vitamin B-12 deficiency and macrocytic anemia. Patients with a new diagnosis of pernicious anemia who have not had a recent endoscopy should undergo endoscopy with topographical biopsies to confirm corpus-predominant atrophic gastritis for risk stratification and to rule out prevalent gastric neoplasia, including neuroendocrine tumors. BEST PRACTICE ADVICE 10: Individuals with autoimmune gastritis should be screened for type 1 gastric neuroendocrine tumors with upper endoscopy. Small neuroendocrine tumors should be removed endoscopically, followed by surveillance endoscopy every 1-2 years, depending on the burden of neuroendocrine tumors. BEST PRACTICE ADVICE 11: Providers should evaluate for iron and vitamin B-12 deficiencies in patients with atrophic gastritis irrespective of etiology, especially if corpus-predominant. Likewise, in patients with unexplained iron or vitamin B-12 deficiency, atrophic gastritis should be considered in the differential diagnosis and appropriate diagnostic evaluation pursued. BEST PRACTICE ADVICE 12: In patients with autoimmune gastritis, providers should recognize that concomitant autoimmune disorders, particularly autoimmune thyroid disease, are common. Screening for autoimmune thyroid disease should be performed.

Keywords: Atrophic Gastritis; Best Practice; Early Cancer Detection; Endoscopy; Gastric Cancer; Gastric Intestinal Metaplasia; Helicobacter pylori; Screening; Surveillance.

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Conflict of interest statement

Conflicts of interest

This author disclosed the following: Shailja C. Shah serves as a consultant for Phathom Pharmaceuticals. The remaining authors disclose no conflicts.

Figures

Figure 1.
Figure 1.
Histopathologic features of normal gastric mucosa, chronic AG, and gastric NET. (A) Normal gastric oxyntic mucosa, characterized by short foveolae (pits) and tightly packed, straight glands. The glands are primarily lined by parietal (pink) cells, which predominate in the upper two-thirds, and by chief (purple) cells at the base. (B) Normal antral mucosa, with wider foveolae and loosely packed glands, primarily lined by mucus-secreting cells. (C, D) H pylori–associated AG. (C) Corpus mucosa with chronic inflammation, moderate loss of oxyntic glands, pseudopyloric metaplasia (asterisks), and IM (thick arrow). Remaining parietal cells (thin arrows) are forming short, disorganized glands. In marked oxyntic atrophy (not shown), there may be complete absence of parietal and chief cells, making the histologic findings indistinguishable from those of antral atrophy. (D) Antral mucosa with shrunk, vanishing glands (thin arrows) and foci of IM (thick arrows) surrounded by fibromuscular tissue in the lamina propria. (E, F) Oxyntic mucosa showing fully developed autoimmune gastritis. (E) Complete absence of parietal and chief cells replaced by pseudopyloric (asterisks) and intestinal (arrow) metaplasia, in a background of chronic inflammation. In this case, glands with pseudopyloric metaplasia show ECL cell hyperplasia, highlighted in (F) with chromogranin A stain. Linear (thin arrows) and micronodular (thick arrow) ECL cell hyperplasia are observed. In earlier stages of autoimmune gastritis, the destruction of oxyntic glands by infiltrating lymphocytes (not shown) and the corpus-predominant pattern of inflammatory and atrophic changes strongly suggests this condition. (G, H) Gastric type 1 ECL cell NET. (G) The tumor is composed of well-differentiated cells with monomorphic round nuclei, arranged in small nests (arrows) infiltrating the lamina propria. The neuroendocrine differentiation is confirmed using chromogranin A stain (H).
Figure 2.
Figure 2.
Typical endoscopic appearance of chronic AG, IM, and gastric NET. Characteristic endoscopic features of chronic AG include pale appearance of mucosa, loss of gastric rugal folds, and prominence of submucosal blood vessels due to thinning of the atrophied gastric epithelium, as shown in (A) HD-WLE and (B) NBI. Changes representing IM are frequently found in chronic AG (CG). On HD-WLE, the areas with IM typically appear mildly nodular (C). On magnifying NBI (D), characteristic signs of IM include the LBC (white arrowhead) and white opaque field (WOF, yellow arrowhead) (or white opaque substance [WOS]). The LBC sign refers to the fine, blue-white lines on the crests of the epithelial surface, which correspond to histologic finding of the brush border (microvilli). The WOF (or WOS) is caused by light scattering at microscopic lipid droplets that accumulate in the mucosa of IM. Both LBC and WOF/WOS signs are best visualized using magnifying NBI. IM in the flat gastric mucosa is shown in (E) (nonmagnifying NBI image). (F, G) Magnified views of IM (white square [E]) with and without NBI, respectively, with abundant LBCs visible in (G). Note that areas of IM with LBC coexist with non-IM mucosa (right upper corner of [G]). (H) and (I) demonstrate endoscopic appearance of gastric NETs on HD-WLE (H) and near-focus NBI (I).
Figure 3.
Figure 3.
Algorithm for clinical management of AG.

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