慢性胃病及胃癌中幽门螺杆菌感染与血清胃蛋白酶原水平变化的关系

摘要

目的 探讨幽门螺杆菌(H pylori,HP)感染对慢性胃病患者血清胃蛋白酶原(PG)亚群(PG Ⅰ、PGⅡ)水平变化的影响及意义.方法 选取宁夏医科大学总医院消化内科2010年10月-2011年4月就诊的有消化道症状的患者263例(胃癌67例,慢性萎缩性胃炎104例,消化性溃疡92例)及正常对照88例,采用快速尿激酶实验、病理吉姆萨染色和酶联免疫吸附实验(EUSA)进行H.pylori检测及PG Ⅰ、PGⅡ含量测定.结果 消化性溃疡HP感染的阳性率为71.7％,慢性萎缩性胃炎、胃癌和正常对照分别为63.5％、56.7％和55.6％,各组间差异无统计学意义(P＞0.05).与正常对照比较,慢性萎缩性胃炎患者血清PG Ⅰ、PG Ⅰ /PGⅡ下降,PGⅡ上升,消化性溃疡患者PG Ⅰ/PGⅡ下降,PG Ⅰ、PGⅡ上升(P＜0.05或P＜0.0l).胃癌患者PG Ⅰ、PG Ⅰ /PGⅡ较正常对照降低,但PGⅡ升高(P＜0.0l).正常对照、慢性萎缩性胃炎、胃癌患者中Hp+者血清PG Ⅰ、PGⅡ水平与相应HP-者比较差异无统计学意义(P＞0.05).萎缩伴肠化及萎缩伴不典型增生患者血清PG Ⅰ、PGⅡ及PG Ⅰ /PGⅡ比值与单纯萎缩性胃炎比较无明显变化(P＞0.05),但其PG Ⅰ /PGⅡ比值均明显高于胃癌患者(P＜0.01).单纯萎缩性胃炎、萎缩伴肠化、萎缩伴不典型增生患者中,HP+者血清PG Ⅰ、PGⅡ及PG Ⅰ/PGⅡ比值与相应HP-者比较差异无统计学意义(P＞0.05).结论 慢性胃炎和胃癌患者中HP感染与血清PG水平变化关系不大.%Objective To investigate the impact of Helicobacter pylori (H. Pylori) on the level of serum pepsinogen (PG) subgroup (PG I and PG II ) in patients with chronic gastric diseases and gastric cancer. Methods A total of 263 patients with symptoms of digestive tract diseases treated in the gastroenterology department of the Affiliated Hospital of Ningxia Medical University from October 2010 to April 2011 (67 cases of gastric cancer, 104 cases of atrophic gastritis, and 92 cases of peptic ulcer) were enrolled for the study. Eighty-eight healthy people were entered as normal control. The H. Pylori status was determined by rapid urease test, and the level of serum pepsinogen (PG I and PG II ) was measured by enzyme-linked immunosorbent assay (ELISA). Results The positive rate of HP infection for peptic ulcer was the highest (71.7%), whereas that of atrophic gastritis, gastric cancer and normal control was 63.5%, 56.7% and 55.6%, respectively, there was no significant difference between groups (P>0.05). Compared with the normal control, serum PG I level and PG I /PG II ratio were lower in atrophic gastritis patients, whereas that of PG II elevated; PG I/PG II ratio of peptic ulcer patients was lowered, whereas their PG I and PG II elevated (P<0.05 or P<0.0l). PG I and PG I/PG II ratio of gastric cancer patients were lower than those of normal control; however, PG II was higher (P<0.01). In atrophic gastritis patients, gastric cancer patients and normal control, serum PG I and PG II levels showed no significant difference between HP+ and HP- patients (P>0.05). Serum PG I , PG II and PG I/PG II ratio in patients with atrophic gastritis plus intestinal metaplasia, and those plus dysplasia were not significant different from those in patients with atrophic gastritis alone (P>0.05), while the PG I /PG II ratio was higher when compared with that in patients with gastric cancer (P<0.0l). In patients with atrophic gastritis alone, atrophic gastritis plus metaplasia, and atrophic gastritis plus dysplasia, serum level of PG I and PG II, and PG I /PG II ratio showed no significant difference between HP+ patients and HP- patients (P>0.05). Conclusion H. Pylori infection has little relation with changes in serum pepsinogen level in patients with chronic gastric diseases or gastric cancer.