胃复康Ⅱ方治疗慢性萎缩性胃炎(脾虚气滞型)临床疗效及对血清胃蛋白酶原、胃泌素17表达的影响

Clinical Effect of Weifukang Prescription Ⅱ in Treating Chronic Atrophic Gastritis with Spleen Deficiency and Qi Stagnation Syndrome and Its Effect on the Expression of Serum Pepsinogen and Gastrin-17

【目的】探讨胃复康Ⅱ方治疗慢性萎缩性胃炎(脾虚气滞型)的临床疗效及对血清胃蛋白酶原、胃泌素17表达的影响。【方法】将84例慢性萎缩性胃炎(脾虚气滞型)患者随机分为治疗组46例和对照组38例。对照组给予标准四联杀菌和常规药物对症治疗,治疗组在标准四联杀菌治疗的基础上给予胃复康Ⅱ方口服治疗,疗程为6个月。观察2组患者治疗前后胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)、胃蛋白酶原Ⅰ/胃蛋白酶原Ⅱ(PGR)、胃泌素17(G-17)等血清学指标的变化情况,比较2组患者治疗后的胃镜和病理组织的改善情况及幽门螺杆菌(Hp)根除情况,评价2组患者的临床疗效。【结果】(1)疗效方面:治疗6个月后,治疗组的总有效率为93.5%(43/46),对照组为78.9%(30/38),治疗组的疗效明显优于对照组,差异有统计学意义(P<0.05)。(2)胃镜检查方面:治疗后,治疗组胃镜下黏膜充血水肿、胆汁反流、红白相间、血管网显露的改善率均明显优于对照组,差异均有统计学意义(P<0.05)。(3)病理组织方面:治疗后,治疗组的腺体萎缩、肠上皮化生改善率均明显优于对照组(P<0.05),而在异型增生方面差异无统计学意义(P>0.05)。(4)Hp根除情况方面:治疗后,治疗组的Hp根除率为81.3%(26/32),明显高于对照组的59.1%(13/22),差异有统计学意义(P<0.05)。(5)血清学指标方面:治疗后,2组患者PGⅠ、PGR、G-17值均较治疗前明显升高(P<0.05),且治疗组治疗后PGⅠ、PGR、G-17值均明显高于对照组,差异均有统计学意义(P<0.05);而2组治疗后PGⅡ值均无明显变化,差异无统计学意义(P>0.05)。【结论】胃复康Ⅱ方治疗慢性萎缩性胃炎(脾虚气滞型)患者具有较好疗效,能显著改善患者的胃镜及病理组织表现,有效促进Hp根除、胃黏膜修复和胃酸分泌。

Objective To investigate the clinical effect of Weifukang PrescriptionⅡ for the treatment of chronic atrophic gastritis with spleen deficiency and qi stagnation syndrome and its effect on the expression of serum pepsinogens and gastrin-17(G-17). Methods A total of 84 cases of chronic atrophic gastritis patients with spleen deficiency and qi stagnation syndrome were randomly divided into treatment group(46 cases)and control group(38 cases). The control group was treated with standard tetrad bactericidal treatment and conventional symptomatic medicine treatment orally, and the treatment group was given tetrad bactericidal treatment and Weifukang PrescriptionⅡ orally. The course of treatment for the two groups covered 6 months. Before and after treatment,we detected the levels of serum indicators of pepsinogen Ⅰ(PGⅠ),pepsinogen Ⅱ(PGⅡ),the ratio of PGⅠ to PGⅡ(PGR),and G-17. After treatment,the improvement of the gastric mucosal features under the gastroscope,improvement of pathological changes in the tissue,and Helicobactor pylori(Hp)eradication in the two groups were compared,and the clinical efficacy was also evaluated. Results(1)After treatment for 6 months,the total effective rate in the treatment group was 93.5%(43/46) and that in the control group was 78.9%(30/38),the efficacy of the treatment group was superior to that of the control group and the difference was statistically significant(P<0.05).(2)After treatment for 6 months,the improvement of the congestion and edema of the gastric mucosa,bile regurgitation,red alternating with white mucosa,and vascular network exposure under the gastroscope in the treatment group was superior to that in the control group,and the difference was statistically significant(P<0.05).(3)After treatment,the rate for the improvement of the pathological changes of gastric gland atrophy and intestinal metaplasia in the treatment group was superior to that in the control group, and the difference was statistically significant(P<0.05). However,the difference of gastric epithelial dysplasia between the two groups was insignificant(P>0.05).(4)After treatment,the Hp eradication rate in the treatment group was81.3%(26/32),and was obviously higher than that in the control group(59.1%,13/22),the difference being statistically significant(P<0.05).(5)After treatment,the levels of serum indicators of PGⅠ,PGR and G-17 in the two groups were higher than those before treatment(P<0.05),and the levels of PGⅠ,PGR and G-17 in the treatment group after treatment were higher than those in the control group, the difference being statistically significant(P<0.05). However, the difference of PG Ⅱ level between the two groups after treatment was insignificant(P>0.05). Conclusion Weifukang Prescription Ⅱ exerts certain effect for the treatment of chronic atrophic gastritis with spleen deficiency and qi stagnation syndrome. It can improve the performance of chronic atrophic gastritis under gastroscopy and pathological tissues,and promote the eradication of Hp,gastric mucosa repair,and gastric acid secretion.