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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,P0.05),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。
Objective To investigate the effect of Helicobacter pylori (Hp) infection on gastric G and D cells in patients with ulcer. Methods Seventy-one patients with active duodenal ulcer (DU) were divided into group A (Hp eradication group), 51 cases (37 males and 14 females), aged 35 years and 13 years old, successfully eradicated Hp. Group B (Hp continuous positive group) 12 cases, 9 males and 3 females, aged 35 ± 10 years, did not eradicate Hp; C group (Hp negative group) 14 cases, 9 males and 5 females, aged 38 years ± 12 years old, D group was Hp-positive functional dyspepsia (FD) in 25 cases, 15 males and 10 females, aged 38 ± 13 years of successful eradication of Hp, before treatment and 1mo after the end of the end of the review of endoscopic , To understand the healing of ulcers and Hp infection, and to take antral mucosa to check the number of G and D cells (ABC immunohistochemistry), gastrin and somatostatin (SST) gene expression (α- 32) p-dATP incorporates RT-PCR). Results After treatment, the ulcer lesions of all the DU groups healed, and there was no significant difference in the number of G cells in each group (P> 0.05). The number of D cells in Hp positive group (a / mm2, A group 9.3 ± 2.4, B group 11.9 ± 5.3, D group 12.9 ± 5.9) were lower than those in Hp negative group (19.2 ± 5.6 / mm ~ 2, P <0.05) in group C, and the number of D cells increased after Hp eradication (group A 18.5 ± 5.6, group D 20.3 ± 7.1 / mm ~ 2, P <0.01), the number of D cells in group B not eroded Hp was still low (10.6 ± 6.4 / mm ~ 2) .A, D The number of D cells, G / D cells (A / Bq, 424 ± 152 in group A, 435 ± 114 in group B, and 368 ± 184 in group C) were higher than those in group FD (216 ± 95 A / Bq in group D, P <0.01). There was no significant difference in Hp positive DU group (A, B group) and Hp negative DU group (C> 0.05). After treatment, regardless of whether Hp was eradicated, (P <0.05). Gas gene expression in group D was lower than that in group E (113 ± 73 A / Bq) after eradication of Hp <0.05). The level of SST gene in FD group was higher than that in the ulcer group (group B, 180 ± 65 A / Bq), and Hp-negative ulcer group (group C 120 ± 48 A / Bq) (A / Bq, 65 ± 22 in group A, 77 ± 23 in group B, P <0.05). After treatment, the expression of SST in each group was increased (P <0.01) SST gene expression was still low (324 ± 144 in group A, 147 ± 47 in group B, 541 ± 197 in group C, and 369 ± 144 A / Bq in group D, P <0,05). Conclusion Hp infection did not affect the number of gastric G cells, but decreased the number of D cells, decreased the expression of SST gene and increased the expression of Gas gene. In ulcer lesions, the expression of SST gene was inhibited and the excessive release of gastrin was stimulated.