From the Department of Pathology, Montefiore Medical Center, Bronx, New York (Choudhuri, Castrodad-Rodriguez, Panarelli).
The Department of Pathology, University of Michigan, Ann Arbor (Hall, Westerhoff).
Arch Pathol Lab Med. 2021 Dec 1;145(12):1536-1543. doi: 10.5858/arpa.2020-0615-OA.
CONTEXT.—: Helicobacter pylori-associated and autoimmune gastritis may coexist in a subset of patients who require treatment for both disorders.
OBJECTIVE.—: To delineate findings that identify autoimmune gastritis in the background of H pylori infection.
DESIGN.—: We examined cases of (1) patients with H pylori-associated gastritis who had successful eradication therapy and subsequent biopsies diagnostic of autoimmune gastritis and (2) H pylori-associated gastritis wherein pathologists noted features of autoimmune gastritis during original interpretation. Control patients underwent H pylori eradication but lacked evidence of autoimmune gastritis or H pylori infection after 10 years of follow-up.
RESULTS.—: Eight subjects had H pylori-associated gastritis followed by H pylori-negative sampling that showed autoimmune gastritis. Review of original samples showed full-thickness inflammation of oxyntic mucosa in 8 of 8 and oxyntic gland loss in 7 of 8 cases. Enterochromaffin-like (ECL) cell hyperplasia, pyloric metaplasia, and intestinal metaplasia were present in 4 of 8 (80% of 5 tested cases), 4 of 8, and 3 of 8 cases, respectively. Features of autoimmune gastritis were noted at the time of their original H pylori diagnosis in 11 study subjects. Ten of 11 samples displayed full-thickness inflammation of oxyntic mucosa and/or partial loss of oxyntic glands, 8 of 11 had ECL cell hyperplasia (all tested cases), 6 of 11 showed pyloric metaplasia, and 4 of 11 harbored intestinal metaplasia. Except for full-thickness oxyntic mucosa inflammation, these features were absent in control cases.
CONCLUSIONS.—: Full-thickness inflammation combined with oxyntic gland loss and ECL cell hyperplasia may help to identify autoimmune gastritis in patients with concomitant H pylori infection.
在需要同时治疗两种疾病的患者中，幽门螺杆菌相关性胃炎和自身免疫性胃炎可能同时存在。
描述在幽门螺杆菌感染背景下识别自身免疫性胃炎的发现。
我们研究了（1）成功根除治疗后随后活检诊断为自身免疫性胃炎的幽门螺杆菌相关性胃炎患者和（2）在最初解释期间病理学家注意到自身免疫性胃炎特征的幽门螺杆菌相关性胃炎患者。对照患者接受了幽门螺杆菌根除治疗，但在 10 年随访后没有自身免疫性胃炎或幽门螺杆菌感染的证据。
8 例患者有幽门螺杆菌相关性胃炎，随后进行了幽门螺杆菌阴性取样，显示自身免疫性胃炎。对原始样本的回顾显示，8 例中有 8 例全层胃窦黏膜炎症，7 例中有 7 例胃窦腺丧失。4 例（5 例检测病例的 80%）、4 例和 3 例分别存在肠嗜铬样（ECL）细胞增生、幽门化生和肠化生。在 11 例研究对象的幽门螺杆菌诊断时就注意到自身免疫性胃炎的特征。11 例样本中有 10 例显示全层胃窦黏膜炎症和/或部分胃窦腺丧失，8 例有 ECL 细胞增生（所有检测病例），6 例有幽门化生，4 例有肠化生。除全层胃窦黏膜炎症外，这些特征在对照组中不存在。
全层炎症伴胃窦腺丧失和 ECL 细胞增生可能有助于在伴有幽门螺杆菌感染的患者中识别自身免疫性胃炎。
