幽门螺杆菌感染对消化性溃疡患者胃G,D细胞的影响

Effect of Helicobacter pylori infection on antral G and D cells in patients with active duodenal ulcer

目的探讨幽门螺杆菌(Hp)感染对溃疡患者胃 G,D 细胞的影响。方法活动性十二指肠溃疡(DU)患者77例根据 Hp 情况分为A组(Hp 根除组)51例,男37例,女14例,年龄35岁±13岁,成功根除 Hp;B 组(Hp 持续阳性组)12例,男9例,女3例,年龄35岁±10岁,未根除 Hp;C 组(Hp 阴性组)14例,男9例,女5例,年龄38岁±12岁,D 组为 Hp 阳性的功能性消化不良(FD)25例,男15例,女10例,年龄38岁±13岁,成功根除Hp,在治疗之前及疗程结束之后1mo 再复查内镜,了解溃疡愈合和 Hp 感染情况,并取胃窦粘膜查 G,D 细胞数量(ABC 法免疫组化)、促胃液素(Gas)和生长抑素(SST)基因表达(α-^(32)p-dATP 掺入 RT-PCR)。结果治疗后各 DU 组溃疡灶均愈合,各组胃窦 G 细胞数量无统计学差异(P>0.05).Hp 阳性组的 D 细胞数量(个/mm2, A 组9.3±2.4,B 组11.9±5.3,D 组12.9±5.9)低于 Hp 阴性患者(c 组19.2±5.6个/mm^2,P<0.05),Hp 根除之后 D细胞数量增多(A 组18.5±5.6,D 组20.3±7.1个/mm^2,P<O.01),未根除 Hp 的 B 组 D 细胞数量依然较低(10.6±6.4个/mm^2).A,D 两组间的 D 细胞数量、G/D 细胞比值均接近,治疗前各 DU 组 Gas 基因表达水平(A/Bq,A 组424±152,B组435±114,C 组368±184)高于 FD 组(D 组216±95 A/Bq,P<0.01),Hp 阳性 DU 组(A,B 组)与 Hp 阴性 DU 组(C 组)的差异无统计学意义(P>0.05),治疗后不论 Hp 是否被根除,各 DU 组(A,B,C 组)Gas 基因表达有下降趋势,但无统计学差异(P>O.05),D 组在 Hp 被根除后 Gas 基因表达水平(113±73 A/Bq)低于根除前(P<0.05),治疗前 FD 组 SST 基因表达水平(D 组180±65 A/Bq)高于各溃疡组,Hp 阴性的溃疡组(C 组120±48A/Bq)高于 Hp 阳性溃疡组(A/Bq,A 组65±22,B 组77±23,P<0.05);治疗后各组 SST 基因表达均增加(P<0.01),但其他组相比 Hp 持续阳性的 B 组 SST 基因表达水平仍然低下(A 组324±144,B 组147±47,C 组541±197,D 组369±144A/Bq,P<0,05)。结论 Hp 感染不影响胃 G 细胞数量,但使 D 细胞数量减少,SST 基因表达下降,Gas 基因表达增多;溃疡灶可抑制 SST 基因表达,刺激促胃液素过度释放。

AIM To investigate the effect of Helicobacter pylori (Hp)infection and ulcer crater on the function of antral G and D cells in patients with active duodenal ulcer(DU). METHODS According to the status of Hp,77 active DU patients were randomly divided into tree groups:group A, 51 patients in which Hp was successfully eradicated (male 37 and female 14,with mean age of 35±13 years),group B,12 patients Hp infection remain after eradication therapy (male 9 and female 3,35±10 years in age);group C,14 Hp-negative patients(male 9 and female 5,aged 38±12 years).Twenty-five Hp-eradicated functional dyspepsia(FD)patients served as controls(male 15 and female 10,aged 38±13 years).Before and one month after treatment gastroendoscopy was performed and antral mucosa specium was taken to detect the number of G and D cells(immunohistochemistry)and the expression levels of gastrin and somatostatin gene(RT-PCT with addition of α-^(32)P-dATP). RESULTS Ulcer crater was healed in all DU patients after treatment.There was no significant difference in G cell number among the four groups.D cell number was significantly lower in Hp-positive group A,(9.3±2.4), group B(11.9±5.3) and group D(12.9±5.9) than in Hp- negative group C(19.2±5.6 cell/mm^2) (P<0.05).After Hp eradication D cell number increased in group A(18.5± 5.6)and group D (20.3±7.1)(P<0.001),however,it remained lower in group B in which Hp was not successfully eradicated (10.6±6.4).D cell number and G/D ratio were similar between group A and D either before or after the treatment.Before the treatment the expression levels of gastrin gene were significantly higher in all DU patients(group A,425±152;group B,435±114; group C,368±184 A/Bq)than in FD patients(group D, 216±95 A/Bq,P<0.01).There was no difference between those in Hp-positive DU group A and B and Hp- negative DU patients(group C,P>0.05).After treatment the Gas levels in all DU patients tended to decrease but did not reach a significance no matter Hp was eradicated or not.They decreased in FD patients(group D)after Hp eradication(113±73A/Bq,P<0.05).Before the treatment the level of somatostatin gene was higher in FD (group D,178±65)than in DU patients,and higher in Hp- negative DU(group C,120±48)than in Hp-positive DU patients(group A,65±22;group B,77±30 A/Bq, P<0.05),and increased significantly(P<0.001)after treatment,however,it remained lower in group B(group A,324±144;group B,147±47;group C,541±197;group D,369±144A/Bq,P<0.05). CONCLUSION Hp infection does not affect antral G cell number,but decreases D cell number.Either Hp or ulcer crater suppresses the expression of somatostatin gene and stimulates gastrin gene.Therefore,Hp infection and crater may affect the function of antral G and D cell.