胃蛋白酶原Ⅰ、Ⅱ水平与幽门螺杆菌感染相关性胃病的关系

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目的探讨胃蛋白酶原(PG)Ⅰ、Ⅱ水平与幽门螺杆菌(Hp)感染相关性胃病的关系。方法选取2014年6月至2015年6月遂宁市中心医院消化内科收治的胃癌患者40例(胃癌组)、萎缩性胃炎45例(萎缩性胃炎组),慢性胃炎45例(慢性胃炎组)和同时期就诊健康人群40例(正常对照组),应用时间分辨荧光免疫法测定血清PGⅠ、PGⅡ水平,应用快速尿激酶法测定各组Hp感染情况,分析PGⅠ、PGⅡ水平与Hp感染的关系。结果慢性胃炎组、萎缩性胃炎组及胃癌组Hp阳性率显著高于对照组[62.22%(28/45)、66.67%(30/45)、70.00%(28/40)比17.50%(7/40),P<0.05],而胃癌组、慢性胃炎组及萎缩性胃炎组Hp阳性率比较差异无统计学意义(P>0.05)。慢性胃炎组、萎缩性胃炎组及胃癌组血清PGⅠ[(91.17±12.85)、(86.68±11.02)、(82.49±9.96)μg/L比(99.36±15.36)μg/L]、PGⅠ/PGⅡ[(5.92±1.78)、(5.67±0.85)、(5.38±0.78)μg/L比(14.48±2.63)μg/L]水平显著低于对照组(P<0.05)。对照组、慢性胃炎组、萎缩性胃炎组及胃癌组Hp(+)者血清PGⅠ、PGⅠ/PGⅡ水平显著低于Hp(-)者(P<0.05),而各组Hp(+)者血清PGⅡ水平与Hp(-)比较差异无统计学意义(P>0.05)。胃癌组Hp(+)者血清PGⅠ、PGⅠ/PGⅡ水平低于慢性胃炎组、萎缩性胃炎及对照组(P<0.05)。萎缩性胃炎Hp(+)者血清PGⅠ、PGⅠ/PGⅡ水平低于慢性胃炎组及对照组(P<0.05),慢性胃炎Hp(+)者血清PGⅠ、PGⅠ/PGⅡ水平低于对照组(P<0.05),两两比较差异有统计学意义(P<0.05)。结论 Hp感染与PG水平有密切的关系,血清PG水平可作为Hp阳性胃病患者癌前病变患者筛查指标,有助于早期胃癌诊断。 Objective To investigate the relationship between the levels of pepsinogen (PG) Ⅰ and Ⅱ and the related gastric diseases associated with Helicobacter pylori (Hp) infection. Methods Forty gastric cancer patients (gastric cancer group), 45 atrophic gastritis (atrophic gastritis group), 45 chronic gastritis (chronic gastritis) group and 40 patients with chronic gastritis were enrolled from June 2014 to June 2015 in Suining Central Hospital. In the same period, 40 healthy subjects (normal control group) were enrolled. Serum PGⅠ and PGⅡ levels were measured by time-resolved fluorescence immunoassay. Hp infection was detected by rapid urokinase assay. The relationship between PGⅠ and PGⅡ levels and Hp infection was analyzed. Results The positive rate of Hp in chronic gastritis group, atrophic gastritis group and gastric cancer group was significantly higher than that in control group [62.22% (28/45), 66.67% (30/45), 70.00% (28/40), 17.50% 40), P <0.05]. There was no significant difference in the positive rate of Hp between gastric cancer group, chronic gastritis group and atrophic gastritis group (P> 0.05). The levels of PGⅠ in the group of chronic gastritis, atrophic gastritis and gastric cancer were 91.1 ± 12.85, 86.68 ± 11.02 and 82.39 ± 9.96 μg / L, respectively, 5.92 ± 1.78), (5.67 ± 0.85) and (5.38 ± 0.78) μg / L (14.48 ± 2.63) μg / L, respectively, compared with the control group (P <0.05). The levels of PGⅠ and PGⅠ / PGⅡ in Hp (+) patients in chronic gastritis group, chronic gastritis group, atrophic gastritis group and gastric cancer group were significantly lower than those in Hp (-) group (P <0.05) There was no significant difference between Hp (-) and Hp (-) (P> 0.05). The levels of serum PGⅠ and PGⅠ / PGⅡ in Hp (+) gastric cancer group were lower than those in chronic gastritis group, atrophic gastritis group and control group (P <0.05). The serum levels of PGⅠ and PGⅠ / PGⅡ in patients with atrophic gastritis were lower than those in patients with chronic gastritis and controls (P <0.05). The levels of serum PGⅠ and PGⅠ / PGⅡ in patients with chronic gastritis were lower than those in controls (P < 0.05). There was significant difference between every two groups (P <0.05). Conclusion Hp infection is closely related to the level of PG. Serum PG level can be used as a screening index for precancerous lesions in patients with Hp positive gastric diseases, which is helpful for the diagnosis of early gastric cancer.
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