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目的了解NSAIDs与Hellicobecterpylori感染在胃黏膜病变中的作用。方法患者190例,①病例选择:连续服用NSAIDs治疗2周～12周190例。男性121例,女性69例。平均年龄55岁。②均经胃镜检查和病理组织学检查。对糜烂性胃炎的胃镜诊断和病理诊断胃黏膜炎症分级。③进行H.pylori感染的检测。分为H.pylori感染组与H.pylori阴性组。分析两组的病理组织学改变的特点,了解是否有显著性差异。结果①胃镜检查,轻度糜烂106例(55.8%,106/190)。中重度糜烂84例(44.2%,84/190)。糜烂性胃炎的轻重程度与服药的剂量时间无明显的相关性。②H.pylori感染组46例(24.2%)。H.pylori阴性组144例(75.8%)。③两组病人胃镜诊断的糜烂性胃炎程度无显著性差异(P>0.05)。④病理情况:H.pylori感染组黏膜中重度胃炎明显多于H.pylori阴性组(P<0.01)。⑤病理改变中有淋巴组织增生56例。其中H.pylori感染组有淋巴组织增生22例(47.8%),H.pylori阴性组34例(23.6%)。134例未见淋巴组织增生,其中H.pylori感染组24例(52.2%),H.pylori阴性组110例(76.4%)。两组相比,有显著性差异(P<0.01)。结论服用NSAIDs2周以上对胃黏膜有不同程度的损伤。服用NSAIDs同时合并H.pylori感染的患者的胃黏膜损伤的严重程度远远高于非感染组。NSAIDs与H.pylori感染是导致胃黏膜损伤的独立危险因子,它们对胃黏膜的损伤作用是叠加的。NSAIDs相关性胃病合并H.pylori感染,根除H.pylori治疗是必要的。
Objective To investigate the role of NSAIDs and Hellicobecterpylori infection in gastric mucosal lesions. Methods 190 patients, ① case selection: continuous administration of NSAIDs for 2 weeks to 12 weeks in 190 cases. There were 121 males and 69 females. The average age is 55 years old. ② by gastroscopy and histopathological examination. Diagnosis of erosive gastritis and pathological diagnosis of gastric mucosal inflammation grading. ③ H.pylori infection detection. Divided into H.pylori infection group and H.pylori negative group. Analysis of the two groups of histopathological changes in the characteristics of understanding whether there is a significant difference. Results ① gastroscopy, mild erosion in 106 cases (55.8%, 106/190). Moderate to severe erosion in 84 cases (44.2%, 84/190). The severity of erosive gastritis and medication dose time no significant correlation. ② H.pylori infection in 46 cases (24.2%). In H.pylori negative group, 144 cases (75.8%). ③ There was no significant difference between the two groups in the diagnosis of erosive gastritis by gastroscope (P> 0.05). ④ pathological conditions: H.pylori infection mucosal moderate-severe gastritis was significantly more than the H.pylori negative group (P <0.01). ⑤ pathological changes in 56 cases of lymphoid hyperplasia. In H.pylori infection group, there were 22 cases (47.8%) of lymphoid hyperplasia and 34 cases (23.6%) of H.pylori negative group. There were no lymphoid hyperplasia in 134 cases, among which H.pylori infection was found in 24 cases (52.2%) and in H.pylori negative group (110 cases, 76.4%). There was a significant difference between the two groups (P <0.01). Conclusions Taking NSAIDs for more than two weeks has different degrees of damage to gastric mucosa. Gastric mucosal injury was more severe in patients with NSAIDs and H. pylori infection than in non-infected patients. NSAIDs and H.pylori infection are the independent risk factors of gastric mucosal injury. Their damage to gastric mucosa is superposition. Gastric NSAIDs associated with H.pylori infection, eradication of H.pylori treatment is necessary.