Guidelines recommend that whenever Helicobacter pylori infection is identified and treated, eradication testing should be offered to the patient.[3]Chey WD, Howden CW, Moss SF, et al. ACG clinical guideline: treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2024 Sep 1;119(9):1730-53.
https://journals.lww.com/ajg/fulltext/2024/09000/acg_clinical_guideline__treatment_of_helicobacter.13.aspx
http://www.ncbi.nlm.nih.gov/pubmed/39626064?tool=bestpractice.com
[107]Gupta S, Li D, El Serag HB, et al. AGA clinical practice guidelines on management of gastric intestinal metaplasia. Gastroenterology. 2020 Feb;158(3):693-702.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7340330
Testing for eradication of H pylori may be performed using urea breath test, fecal antigen test, or biopsy-based testing.[3]Chey WD, Howden CW, Moss SF, et al. ACG clinical guideline: treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2024 Sep 1;119(9):1730-53.
https://journals.lww.com/ajg/fulltext/2024/09000/acg_clinical_guideline__treatment_of_helicobacter.13.aspx
http://www.ncbi.nlm.nih.gov/pubmed/39626064?tool=bestpractice.com
One study has demonstrated that serologic biomarkers such as pepsinogens I and II, gastrin-17, and H pylori IgA/IgG antibodies (markers of gastric mucosal status) show a high degree of accuracy as a noninvasive method to diagnose corpus atrophy, a common occurrence in the general population, although the clinical role of these markers is unclear at present.[108]Storskrubb T, Aro P, Ronkainen J, et al. Serum biomarkers provide an accurate method for diagnosis of atrophic gastritis in a general population: the Kalixanda study. Scand J Gastroenterol. 2008;43(12):1448-55.
http://www.ncbi.nlm.nih.gov/pubmed/18663663?tool=bestpractice.com
[109]van Marrewijk CJ, van Oijen MG, Paloheimo LI, et al. Influence of gastric mucosal status on success of stepwise acid suppressive therapy for dyspepsia. Aliment Pharmacol Ther. 2009 Jul;30(1):82-9.
http://www.ncbi.nlm.nih.gov/pubmed/19309389?tool=bestpractice.com
Patients with nonsteroidal anti-inflammatory drug (NSAID)/alcohol-associated erosive gastritis refractory to symptomatic therapy may require a follow-up endoscopy with biopsy.[43]Park WG, Shaheen NJ, Cohen J, et al. Quality indicators for EGD. Gastrointest Endosc. 2015 Jan;81(1):17-30.
http://www.ncbi.nlm.nih.gov/pubmed/25480101?tool=bestpractice.com
Patients with diffuse atrophic gastritis and vitamin B12 deficiency should have close follow-up with tests for serum vitamin B12 levels, methylmalonic acid levels, or homocysteine levels to determine response to treatment.[31]Toh BH, van Driel IR, Gleeson PA. Pernicious anemia. N Engl J Med. 1997 Nov 13;337(20):1441-8.
http://www.ncbi.nlm.nih.gov/pubmed/9358143?tool=bestpractice.com
At present, there is no definitive treatment for atrophic gastritis; however, monitoring these patients for gastric intestinal metaplasia is important. Patients should be risk stratified to determine surveillance intervals, with recommendations stating that patients with advanced atrophic gastritis should undergo endoscopic surveillance every 3 years.[110]Pimentel-Nunes P, Libânio 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 Apr;51(4):365-88.
https://www.thieme-connect.de/products/ejournals/abstract/10.1055/a-0859-1883
http://www.ncbi.nlm.nih.gov/pubmed/30841008?tool=bestpractice.com
The risk of gastric adenocarcinoma and carcinoid tumors with atrophic gastritis and/or autoimmune gastritis is uncertain; however, atrophic pangastritis, severe intestinal metaplasia of the body of the stomach, and age >50 years all increase the risk for developing gastric neoplastic lesions in patients with atrophic gastritis.[111]Vannella L, Lahner E, Osborn J, et al. Risk factors for progression to gastric neoplastic lesions in patients with atrophic gastritis. Aliment Pharmacol Ther. 2010 May;31(9):1042-50.
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2010.04268.x/full
http://www.ncbi.nlm.nih.gov/pubmed/20175768?tool=bestpractice.com
One study examined 929 patients with chronic atrophic gastritis undergoing at least three screening upper endoscopies followed for 36-129 months. Low-grade intraepitheial metaplasia developed in 75 (8.1%) patients, high-grade intraepithelial neoplasia developed in eight (0.9%) patients, and gastric cancer developed in 14 (1.5%) patients.[112]Sun L, Jin X, Huang L, et al. Risk of progression in patients with chronic atrophic gastritis: a retrospective study. Front Oncol. 2022 Aug 1;12:942091.
https://pmc.ncbi.nlm.nih.gov/articles/PMC9377336
http://www.ncbi.nlm.nih.gov/pubmed/35978825?tool=bestpractice.com