Lesions Arising in the Setting of Autoimmune Metaplastic Atrophic Gastritis (AMAG) in an Urban Tertiary Care Setting
JY Park, T Cornish, D Lam-Himlin, C Shi, E Montgomery. Johns Hopkins Hospital, Baltimore, MD
Background: Autoimmune Metaplastic Atrophic Gastritis (AMAG) is an early manifestation of pernicious anemia, preceding the hematological changes of pernicious anemia by years to decades. Autoimmune atrophic gastritis manifests in 1 to 5% of the general population. It has been associated with the development of intestinal metaplasia and neoplastic lesions. Pyloric gland adenoma (PGA) is a newly recognized lesion that is highly associated with AMAG. We investigated the presence of PGA and other lesions arising in the setting of AMAG in our urban tertiary care center.
Design: We searched all non-consultation gastric biopsies from 1988 to 2008 using our laboratory information system and further analyzed the histopathologic features of all cases coded as AMAG. In addition, we further selected cases that had been confirmed as AMAG by immunohistochemical staining (IHC) for the body of the stomach (negative gastrin) and the presence of linear and nodular ECL-cell hyperplasia (chromogranin). All polyps and/or neoplastic lesions from this subset were reviewed.
Results: The gastric biopsies (n=54,814) were from 45.5% male (M) and 54.5% female (F) patients comprising 66.4% white, 23.6% African American (AA) and 10% other (non-white Hispanic, Asian, etc.) patients. Gastritis as a general category accounted for 69.3% of gastric biopsies; AMAG was diagnosed in 619 cases of which 527 cases from 380 patients had confirmatory IHC. Based on these cases, AMAG occurred in 0.7% of biopsies with a 2:1 F:M ratio. It was diagnosed in 0.7% of gastric biopsies from white patients, and in 0.8% of gastric biopsies from AA patients. For white males and females the average age was 68.6 and 63.9, respectively; for AA males and females the average age was 64.6 and 62.6, respectively. A review of polyps and/or other neoplastic lesions showed 147 polyps (107 hyperplastic, 15 inflammatory, 11 gastric adenomas, intestinal type, 11 oxyntic gland pseudopolyps, and 3 PGAs), 9 adenocarcinomas, 3 lymphomas, and 23 carcinoids. One of the PGAs had been previously diagnosed as a gastric hyperplastic polyp with changes indefinite for dysplasia.
Conclusions: Consistent with recent epidemiologic surveys of pernicious anemia, the histopathologic diagnosis of AMAG occurs with similar frequency in AA and white patients. The review of prior cases has revealed a single case of PGA that was not previously recognized. Although PGA is strongly associated with AMAG, the current investigation reveals that even in the setting of AMAG, PGA is a rare entity.
Monday, March 22, 2010 1:00 PM
Poster Session II # 74, Monday Afternoon