Avunduk C, Navab F, Hampf F, Coughlin B
Division of Gastroenterology, Baystate Medical Center, Springfield, Massachusetts, USA.
Am J Gastroenterol. 1995 Nov;90(11):1969-73.
Large gastric folds may result from infectious, inflammatory, neoplastic, vascular, and infiltrative disorders involving a part or the entire gastric wall. Helicobacter pylori infection of the gastric mucosa is associated with an active gastritis characterized by infiltration of the mucosa and submucosa with neutrophils, eosinophils, macrophages, and lymphocytes. The purposes of the study were: 1) to study patients with large gastric folds noted on computed tomography, upper gastrointestinal series, or endoscopy, with endoscopy and biopsies and endoscopic ultrasound to determine the prevalence of H. pylori infection and the location of the thickening within the gastric wall; 2) to reexamine H. pylori-infected patients with EUS after antimicrobial therapy to determine whether resolution of the wall thickening accompanied eradication of H. pylori and improvement of histological gastritis.
Thirty-two patients with thickened gastric folds were studied. Eighteen patients had H. pylori infection and were treated with amoxicillin 1 g b.i.d. and omeprazole 40 mg b.i.d. x 14 days. One month after antimicrobial therapy, patients were reexamined by EUS, and gastric biopsies were obtained.
Eighteen of 32 patients had H. pylori infection and gastritis. In the H. pylori-infected patients with gastritis, EUS demonstrated diffuse thickening of the inner three layers (mucosa-lumen interface, deep mucosa, submucosa) without thickening of the 4th and 5th layers of the gastric wall. After antimicrobial therapy and resolution of gastritis, EUS demonstrated concomitant resolution of this thickening and normalization of layers 1-3.
H. pylori gastritis is a common cause of gastric wall thickening. EUS allows intrinsic localization of the gastric wall thickening in patients with large gastric folds and H. pylori infection and documents the resolution of this wall thickening upon eradication of H. pylori and resolution of gastritis.
胃大皱襞可能由累及胃壁部分或全部的感染性、炎症性、肿瘤性、血管性及浸润性疾病引起。胃黏膜幽门螺杆菌感染与以中性粒细胞、嗜酸性粒细胞、巨噬细胞及淋巴细胞浸润黏膜和黏膜下层为特征的活动性胃炎相关。本研究的目的是:1)研究在计算机断层扫描、上消化道造影或内镜检查中发现胃大皱襞的患者,通过内镜检查及活检和内镜超声来确定幽门螺杆菌感染的患病率以及胃壁增厚的部位;2)对抗菌治疗后的幽门螺杆菌感染患者进行超声内镜复查,以确定胃壁增厚的消退是否伴随幽门螺杆菌的根除及组织学胃炎的改善。
对32例胃皱襞增厚的患者进行研究。18例患者有幽门螺杆菌感染,接受阿莫西林1g,每日2次及奥美拉唑40mg,每日2次,共14天的治疗。抗菌治疗1个月后,对患者进行超声内镜复查,并取胃组织活检。
32例患者中有18例有幽门螺杆菌感染及胃炎。在感染幽门螺杆菌的胃炎患者中,超声内镜显示胃壁内三层(黏膜-腔界面、深层黏膜、黏膜下层)弥漫增厚,胃壁第四层和第五层未增厚。抗菌治疗及胃炎消退后,超声内镜显示这种增厚现象随之消退,1-3层恢复正常。
幽门螺杆菌胃炎是胃壁增厚的常见原因。超声内镜可对胃大皱襞和幽门螺杆菌感染患者的胃壁增厚进行定位,并记录幽门螺杆菌根除及胃炎消退后胃壁增厚的消退情况。