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目的:探究血清胃蛋白酶原、胃泌素及幽门螺杆菌与老年慢性萎缩性胃炎的相关性。方法:选取2017年1月至2018年12月枣庄市薛城区人民医院消化内科收治的188例慢性胃炎老年患者,男101例,女87例,年龄(71.56±6.04)岁,年龄范围为65~89岁,根据病理类型的不同将患者分为萎缩性胃炎组(n n=96)和浅表性胃炎组(n n=92),并选取同期进行体检筛查的100例老年健康志愿者为健康组。采用酶联免疫吸附试验法测定空腹血清胃蛋白酶原Ⅰ(PG-Ⅰ)、胃蛋白酶原Ⅱ(PG-Ⅱ)、胃泌素17水平。采用n 14C-呼气试验测定幽门螺杆菌感染情况。比较三组纳入者的胃蛋白酶原水平[血清PG-Ⅰ、PG-Ⅱ、胃蛋白酶原比值(PGR)]、胃泌素17水平和幽门螺杆菌阳性率,并比较幽门螺杆菌阳性和阴性患者的血清PG-Ⅰ、PGR、胃泌素17水平。n 结果:萎缩性胃炎组和浅表性胃炎组的血清PG-Ⅰ[(46.19±13.28)μg/L、(55.72±14.13)μg/L]和PGR[(2.17±1.52)、(2.62±1.13)]水平均低于健康组[(102.67±15.35)μg/L、(4.56±1.94)],且萎缩性胃炎组低于浅表性胃炎组,差异均有统计学意义(n P<0.05)。萎缩性胃炎组和浅表性胃炎组的血清胃泌素17水平[(9.11±4.32)pmol/L、(18.56±9.71)pmol/L]和幽门螺杆菌阳性率[77.1%(74/96)、45.7%(42/92)]均高于健康组[(2.46±0.73)pmol/L、15.0%(15/100)],且萎缩性胃炎组的血清胃泌素17水平低于浅表性胃炎组、幽门螺杆菌阳性率高于浅表性胃炎组,差异均有统计学意义(n P<0.05)。幽门螺杆菌阳性患者血清PG-Ⅰ[(45.28±11.31)μg/L]、PGR(2.34±1.04)与胃泌素17水平[(9.81±15.48)pmol/L]均低于幽门螺杆菌阴性患者[(56.74±12.25)μg/L、(3.15±1.21)、(10.72±16.33)pmol/L],差异有统计学意义(n P<0.05)。n 结论:血清PG-Ⅰ和胃泌素17水平降低提示患者可能发生慢性萎缩性胃炎,幽门螺杆菌阳性可能与慢性萎缩性胃炎的发生有一定相关性,此类患者应及时进行胃镜检查。“,”Objective:To investigate the correlation between gastrin, serum pepsinogen, helicobacter pylori and chronic atrophic gastritis in the elderly.Methods:A retrospective study was performed on 188 cases of elderly patients with chronic gastritis who were admitted from January 2017 to December 2018.There were 101 males and 87 females, aged(71.56±6.04)years, ranging from 65 to 89 years old.According to different pathological types, patients were divided into the atrophic gastritis group(n n=96)and superficial gastritis group(n n=92), and 100 healthy elderly volunteers who underwent physical examination and screening were selected as the healthy group.Using enzyme-linked immunosorbent assay method determination of fasting serum pepsinogen Ⅰ(PG-Ⅰ), pepsinogen Ⅱ(PG-Ⅱ), stomach gastrin-releasing 17 levels.Helicobacter pylori infection was determined by n 14C- breath test.Comparison of three groups of into the pepsinogen level[serum PG-Ⅰ, PG-Ⅱ, pepsinogen ratio(PGR)], stomach gastrin-releasing 17 levels and helicobacter pylori positive rate, and compare the helicobacter pylori in patients with positive and negative serum PG-Ⅰ, PGR, stomach gastrin-releasing 17 levels.n Results:Serum PG-Ⅰin atrophic gastritis group and superficial gastritis group[(46.19±13.28)μg/L, (55.72±14.13)μg/L]and PGR levels[(2.17±1.52), (2.62±1.13)]were lower than those of the healthy group[(102.67±15.35), (4.56±1.94)], the levels of atrophic gastritis group is lower than those of the superficial gastritis group, and the difference had statistical significance(n P<0.05). Serum gastrin-releasing 17 levels in the atrophic gastritis group and superficial gastritis group[(9.11±4.32)pmol/L, (18.56±9.71)pmol/L]and helicobacter pylori positive rates[77.1%(74/96), 45.7%(42/92)]were higher than those in healthy group[(2.46±0.73)pmol/L and 15.0%(15/100)]. Moreover, the serum gastrin-releasing 17 level of atrophic gastritis group was lower than that of superficial gastritis group, and the positive rate of helicobacter pylori was higher than that of superficial gastritis group(n P<0.05). serum PG-Ⅰ in patients with positive helicobacter pylori[(45.28±11.31)μg/L], PGR(2.34±1.04)and gastrin-releasing 17 levels[(9.81±15.48)pmol/L]were lower than that of patients with negative helicobacter pylori[(56.74±12.25)μg/L, (3.15±1.21), (10.72±16.33)pmol/L], and the difference was statistically significant(n P<0.05).n Conclusion:Serum PG-Ⅰ and stomach gastrin-releasing 17 level to reduce the patient may be chronic atrophic gastritis, positive helicobacter pylori may be associated with the occurrence of chronic atrophic gastritis, and gastroscopy should be performed in time for such patients.