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Gastric Lesions in Patients With Autoimmune Metaplastic Atrophic Gastritis (AMAG) in a Tertiary Care Setting

Park, Jason Y. MD, PhD*; Cornish, Toby C. MD, PhD; Lam-Himlin, Dora MD; Shi, Chanjuan MD, PhD§; Montgomery, Elizabeth MD

The American Journal of Surgical Pathology: November 2010 - Volume 34 - Issue 11 - p 1591-1598
doi: 10.1097/PAS.0b013e3181f623af
Original Articles

Autoimmune metaplastic atrophic gastritis (AMAG) is an early manifestation of pernicious anemia that precedes the hematologic changes by years to decades. It is associated with metaplastic changes and neoplasms, including pyloric gland adenomas (PGAs). We investigated the frequency of PGAs and other lesions in all nonconsultation gastric biopsies and resections (1988 to 2008) diagnosed as AMAG. We further selected cases confirmed as AMAG by immunohistochemical identification of the gastric body (negative gastrin) and linear and nodular enterochromaffin-like cell hyperplasia (chromogranin). From this subset, all polyps and neoplasms were reviewed. We identified a total of 41,245 patients with gastric biopsies or resections from 46.7% males and 53.3% females comprising patients self-identified as 67.0% white, 23.6% African-American, 1.4% Asian, 0.8% non-White Hispanic, and 7.2% other or unknown. AMAG was diagnosed in 461 patients (1.1%), and had the following percentages based on race: 1.1% White, 1.3% African-American, 1.4% Asian, and 2.7% non-White Hispanic. The female:male ratio was 2:1 with an overall median age at presentation of 67.0 years. Of the 461 patients with AMAG, 143 had endoscopically identifiable lesions. These lesions (n=240) consisted of 179 polyps (138 hyperplastic polyps, 20 oxyntic mucosa pseudopolyps, 18 intestinal-type gastric adenomas, and 3 PGAs), 46 well-differentiated neuroendocrine neoplasms (carcinoid), 1 gastrointestinal stromal tumor, 3 lymphomas, and 11 adenocarcinomas. In summary, AMAG occurred with similar frequency across all racial groups. Although PGAs are associated with AMAG, they remain rare in the setting of AMAG.

*Department of Pathology, University of Texas Southwestern Medical Center and Children's Medical Center, Dallas, TX

Department of Pathology, Johns Hopkins Hospital, Johns Hopkins University, Baltimore, MD

Department of Pathology, Mayo Clinic, Scottsdale, AZ

§Department of Pathology, Vanderbilt University, Nashville, TN

Correspondence: Jason Y. Park, MD, PhD, Department of Pathology, Children's Medical Center, 1935 Medical District Drive, Dallas, TX (e-mail: jaspar@childrens.com).

© 2010 Lippincott Williams & Wilkins, Inc.