Eidt S, Oberhuber G, Schneider A, Stolte M
Institute of Pathology, Klinikum Bayreuth, Germany.
Pathol Res Pract. 1996 Feb;192(2):101-6. doi: 10.1016/S0344-0338(96)80203-2.
It has been recently shown that type A gastritis can be histologically diagnosed in the preatrophic stage. In order to evaluate whether parietal cell atrophy in AG might correlate with other histopathological findings in the antral and body mucosa, we retrospectively investigated 171 consecutive cases of histologically diagnosed preatrophic (active) or atrophic type A gastritis (H&E, Warthin-Starry). The prevalences of intestinal metaplasia (75% vs 44.4%) and micronodular hyperplasia (86.1% vs 52.4%) of endocrine cells in the oxyntic mucosa were significantly higher of parietal cell atrophy was present (p < 0.001 and p < 0.0001, respectively), whereas the prevalence of nodular lymphoid aggregates (77.8% vs 48.1%) and of Helicobacter pylori (14.3% vs 1.9%) in the oxyntic mucosa was significantly higher if parietal cell atrophy could not be detected (p < 0.001 and p < 0.01, respectively). In the antral mucosa, altered patterns of the inflammatory reaction could be demonstrated independent of the parietal cell mass possibly caused by impaired gastric acid production. Our data support the notion that the development of parietal cell atrophy in type A gastritis represents a stepwise process including initial pseudohypertrophy of these cells.
最近研究表明,A型胃炎在萎缩前期即可通过组织学诊断。为了评估自身免疫性胃炎(AG)中壁细胞萎缩是否与胃窦和胃体黏膜的其他组织病理学表现相关,我们回顾性研究了171例经组织学诊断为萎缩前期(活动期)或萎缩性A型胃炎的连续病例(苏木精-伊红染色、Warthin-Starry银染色)。存在壁细胞萎缩时,胃黏膜内分泌细胞肠化生(75%对44.4%)和微结节增生(86.1%对52.4%)的发生率显著更高(分别为p<0.001和p<0.0001),而未检测到壁细胞萎缩时,胃黏膜结节状淋巴样聚集(77.8%对48.1%)和幽门螺杆菌感染(14.3%对1.9%)的发生率显著更高(分别为p<0.001和p<0.01)。在胃窦黏膜中,可证实炎症反应模式的改变与可能由胃酸分泌受损导致的壁细胞数量无关。我们的数据支持这样一种观点,即A型胃炎中壁细胞萎缩的发展是一个逐步的过程,包括这些细胞最初的假性肥大。