Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Pathol Int. 2010 Apr;60(4):298-304. doi: 10.1111/j.1440-1827.2010.02523.x.
The pathogenesis of reddish streaks in the intact stomach is unclear. Sixty-three functional dyspeptic patients with gastric reddish streaks were recruited for the study. Fifty-five patients (group I) had only reddish streaks while nine patients (group II) had additional lesions such as reddish patches or spots randomly scattered throughout the stomach. Updated Sydney system and parameters of reactive gastropathy were used to score the biopsy specimens from reddish streaks separately. Helicobacter pylori infection rate was found to be markedly lower in group I than group II patients (13% vs 89%, P < 0.001). H. pylori-infected patients had higher scores for acute and chronic inflammation (P < 0.001) and foveolar hyperplasia (P < 0.005) than non-infected patients, while other parameters for gastritis and gastropathy were similar between infected and non-infected patients. In H. pylori-non-infected patients all biopsy specimens had at least one histological feature of reactive gastropathy. Bile reflux was observed in 54% of patients (34/63). Only 7.9% used non-steroidal anti-inflammatory drugs and 4.9% drank alcohol. The present data indicate that the fundamental histological features of gastric reddish streaks are reactive gastropathy with low H. pylori infection, and are probably enterogastric reflux related in etiology. Coincidental H. pylori infection increased acute and chronic inflammatory cell infiltration, and enhanced the grade of foveolar hyperplasia.
胃内完整黏膜出现红斑的发病机制尚不清楚。本研究共纳入 63 例功能性消化不良伴胃内红斑患者。55 例（I 组）患者仅表现为红斑，9 例（II 组）患者胃内红斑伴有随机分布的红斑斑片或斑点等其他病变。分别采用悉尼系统和反应性胃黏膜病变的参数对红斑处活检标本进行评分。I 组患者 H. pylori 感染率显著低于 II 组（13%比 89%，P<0.001）。与非感染患者相比，H. pylori 感染患者的急性和慢性炎症（P<0.001）和腺窝增生（P<0.005）评分更高，而胃炎和胃病的其他参数在感染和非感染患者之间相似。在 H. pylori 非感染患者中，所有活检标本均至少存在一项反应性胃黏膜病变的组织学特征。胆汁反流见于 54%的患者（34/63）。仅 7.9%的患者使用非甾体抗炎药，4.9%的患者饮酒。本研究数据表明，胃内红斑的基本组织学特征为低 H. pylori 感染的反应性胃黏膜病变，可能与肠-胃反流有关。偶然的 H. pylori 感染增加了急性和慢性炎症细胞浸润，并增强了腺窝增生的程度。
