Jevremovic Dragan, Torbenson Michael, Murray Joseph A, Burgart Lawrence J, Abraham Susan C
Department of Pathology, Mayo Clinic, Rochester, MN 55905, USA.
Am J Surg Pathol. 2006 Nov;30(11):1412-9. doi: 10.1097/01.pas.0000213337.25111.37.
The 2 major recognized forms of atrophic gastritis are autoimmune and environmental atrophic gastritis. These differ in their topographical distribution in the stomach, histologic features, and etiology. Autoimmune atrophic gastritis results from immune-mediated destruction of specialized oxyntic glands, is restricted to the body and fundus, and shows characteristic neuroendocrine hyperplasia. Environmental atrophic gastritis is associated with long-standing Helicobacter pylori infection and preferentially involves antrum and transition zone mucosa. In this study, we describe a distinctive form of atrophic gastritis that differs markedly from both of these classic variants. This gastritis is characterized by: (1) intense mucosal inflammatory infiltrates, persisting even into the phase of severe glandular atrophy, (2) pangastric distribution with diffuse involvement of both body and antrum, (3) lack of association with H. pylori, and (4) lack of neuroendocrine hyperplasia. The 8 patients presented ranged from 1 to 75 years and showed a slight female predominance (5F:3M). All had systemic autoimmune and/or connective tissue diseases including autoimmune enterocolitis (4 cases), systemic lupus erythematosus, refractory sprue, autoimmune hemolytic anemia, and disabling fibromyalgia. Positive serum autoimmune markers were documented in 7 of 8 (87%) patients, but serologies for antiparietal cell and anti-intrinsic factor antibodies were undertaken in only 1 patient each and were negative. We propose that the distinctive histology of this form of atrophic pangastritis and its association with systemic autoimmune disease suggests an autoimmune process directed against multiple cell lineages in the stomach. The development of multifocal low-grade dysplasia in 1 patient, a 19-year-old woman, suggests that this condition might have neoplastic potential.
萎缩性胃炎的两种主要公认形式是自身免疫性萎缩性胃炎和环境性萎缩性胃炎。它们在胃内的分布部位、组织学特征和病因方面存在差异。自身免疫性萎缩性胃炎是由免疫介导的特殊泌酸腺破坏引起的，局限于胃体和胃底，并表现出特征性的神经内分泌增生。环境性萎缩性胃炎与长期幽门螺杆菌感染有关，主要累及胃窦和移行区黏膜。在本研究中，我们描述了一种与这两种经典类型明显不同的独特萎缩性胃炎形式。这种胃炎的特征为：（1）即使在严重腺体萎缩阶段仍存在强烈的黏膜炎症浸润；（2）全胃分布，胃体和胃窦均弥漫受累；（3）与幽门螺杆菌无关；（4）无神经内分泌增生。所报告的8例患者年龄在1岁至75岁之间，女性略占优势（5例女性：3例男性）。所有患者均患有系统性自身免疫性和/或结缔组织疾病，包括自身免疫性小肠结肠炎（4例）、系统性红斑狼疮、难治性口炎性腹泻、自身免疫性溶血性贫血和致残性纤维肌痛。8例患者中有7例（87%）血清自身免疫标志物呈阳性，但仅对1例患者进行了抗壁细胞抗体和抗内因子抗体的血清学检测，结果均为阴性。我们认为，这种萎缩性全胃炎的独特组织学表现及其与系统性自身免疫性疾病的关联提示存在针对胃内多种细胞谱系的自身免疫过程。1例19岁女性患者发生多灶性低级别发育异常，提示这种情况可能具有肿瘤发生潜能。
