Schmitt J, de Korwin J D, Faure G, Duprez A
Service de Médecine H, Hôpital Central, Nancy.
Ann Gastroenterol Hepatol (Paris). 1991 Oct;27(5):219-21.
To determine the relationship of microscopic chronic antral gastritis to Helicobacter pylori, 69 consecutive patients were studied. In a prospective longitudinal study, at least 2 successive gastroscopies with antral biopsies were performed (177 investigations on the whole). Sixty six of the 69 patients were treated with various therapeutic regimens i.e. antiulcer drugs and/or antibiotics. The type and intensity of inflammation (as based on whole inflammatory infiltrate density, polymorphonuclear cells presence or absence and IgA and IgM plasma cells counts) were correlated with H. pylori status (Giemsa staining and/or biopsy culture). The presence of the organism (Hp) and the gastritis were significantly correlated (high grade of whole inflammatory infiltrate Hp + ve: 98/109 90 p. cent, Hp-ve: 9/61 15 p. cent, p less than 0.001--presence of neutrophil PMNC Hp + ve: 80/109 73 p. cent, Hp-ve: 1/61 2 p. cent; p less than 0.001--IgA and IgM plasma cells respectively Hp + ve: 7.6 +/- 6.6, 10.6 +/- 7.1, Hp-ve 1.9 +/- 2.9, 4.2 +/- 4.5; p less than 0.005). Clearance and/or eradication of H. pylori after antibiotic treatment were associated with the disappearance of chronic gastritis activity and a statistically significant decrease of whole inflammatory infiltrate density (p less than 0.001) and IgA (p less than 0.005) and IgM (p less than 0.01) plasma cells counts. Mucosal inflammation was unchanged in case of H. pylori persistence and inflammation worsening occurred in case of infection relapse. H. pylori gastric mucosa colonization seemed to be responsible for the antral chronic inflammation associated with its presence. This study documents that antral chronic gastritis is a microbial disease associated with infection by H. pylori, against which there is an inflammatory response characterized by a significant mucosal infiltration with granulocytes and IgA and IgM secreting plasma cells.
为了确定微观慢性胃窦炎与幽门螺杆菌的关系，对69例连续患者进行了研究。在一项前瞻性纵向研究中，至少进行了2次连续的胃镜检查并取胃窦活检（总共177次检查）。69例患者中的66例接受了各种治疗方案，即抗溃疡药物和/或抗生素治疗。炎症的类型和强度（基于整个炎症浸润密度、多形核细胞的有无以及IgA和IgM浆细胞计数）与幽门螺杆菌状态（吉姆萨染色和/或活检培养）相关。该生物体（Hp）的存在与胃炎显著相关（整个炎症浸润程度高，Hp阳性：98/109，90%；Hp阴性：9/61，15%；p<0.001——中性粒细胞PMNCHp阳性：80/109，73%；Hp阴性：1/61，2%；p<0.001——IgA和IgM浆细胞，Hp阳性分别为：7.6±6.6，10.6±7.1；Hp阴性为1.9±2.9，4.2±4.5；p<0.005）。抗生素治疗后幽门螺杆菌的清除和/或根除与慢性胃炎活动的消失以及整个炎症浸润密度（p<0.001）、IgA（p<0.005）和IgM（p<0.01）浆细胞计数的统计学显著降低相关。如果幽门螺杆菌持续存在，黏膜炎症无变化；如果感染复发，则炎症会加重。幽门螺杆菌在胃黏膜的定植似乎是与其存在相关的胃窦慢性炎症的原因。这项研究证明胃窦慢性胃炎是一种与幽门螺杆菌感染相关的微生物疾病，针对这种感染存在一种炎症反应，其特征是黏膜有大量粒细胞浸润以及分泌IgA和IgM的浆细胞浸润。
