目的分析不同病变胃粘膜端粒酶活性表达的差异,及其与Hp 感染的关系,并探讨端粒酶活性表达、Hp 感染和胃粘膜癌变的关系.方法应用 TRAP 测定172例内镜活检标本和45例胃癌手术标本的端粒酶活性,其中内镜活检标本正常胃粘膜10例、慢性浅...目的分析不同病变胃粘膜端粒酶活性表达的差异,及其与Hp 感染的关系,并探讨端粒酶活性表达、Hp 感染和胃粘膜癌变的关系.方法应用 TRAP 测定172例内镜活检标本和45例胃癌手术标本的端粒酶活性,其中内镜活检标本正常胃粘膜10例、慢性浅表性胃炎46例、胃溃疡30例、慢性萎缩性胃炎68例、胃癌18例,手术标本高分化型胃癌8例、低分化型胃癌37例.同时用 EIA 检测 Hp 感染患者血清中 Hp-CagA-IgG,并分析端粒酶活性的表达和 Hp-CagA-IgG 水平的关系.结果在172例内镜活检标本中,正常胃粘膜、慢性浅表性胃炎、慢性萎缩性胃炎伴0度、1度、2度肠化和胃癌组织的端粒酶阳性率分别为0%,0%,0%,25%,38%,89%.45例手术切除的胃癌组织和相应的非癌胃组织也展现了相似的结果.Hp检出情况,正常胃粘膜、浅表性胃炎、慢性萎缩性胃炎伴0度、1度、2度肠化 Hp 阳性率分别为0%,52%,60%,70%,75%.45例手术切除胃癌的非癌胃组织伴0度、1度、2度肠化的 Hp 感染强度分别为10.8±9.6,41.3±31.1,86.4±47.8个/50腺体.慢性浅表性胃炎患者的 Hp-CagA-IgG 抗体显著低于胃癌患者的 Hp-CagA-IgG 抗体水平(P<0.01),22例 Hp 阳性的胃癌患者感染的 Hp 全部为 CagA^+株,其非癌胃粘膜有12例展现了端粒酶活性(55%);相反 Hp 阳性的22例慢性浅表性胃炎患者感染的 Hp 只有8例为 CagA^+株(36%),其胃粘膜均未展现端粒酶活性.结论正常胃粘膜和浅表性胃炎不表达端粒酶活性.萎缩性胃炎随肠化进展端粒酶活性表达增加,胃癌组织中端粒酶活性表达最高,阳性率达88%以上.在胃癌患者的非癌胃粘膜中端粒酶活性的表达与肠化程度、Hp 感染强度呈平行关系,且感染的Hp 多为 CagA^+株;而慢性浅表性胃炎感染的 Hp 多为 CagA株.端粒酶活性检测可以作为胃粘膜癌变的一个早期预测指标,CagA^+的 Hp 感染可能是端粒酶重新激活的一个启动信号.展开更多
AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from nor...AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from normal controls ( n =11), superficial gastritis ( n =32), atrophic gastritis with intestinal metaplasia ( n =83), dysplasia ( n =25) and gastric carcinoma ( n =10) were studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups ( P <0 01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13 14±1 6 and 19 68±2 22 respectively, significantly higher than 6 95±0 78 and 11 34±1 89 in H. pylori negative patients ( P <0 01); but there was no such difference in other groups ( P >0 05). CONCLUSION H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.展开更多
文摘目的分析不同病变胃粘膜端粒酶活性表达的差异,及其与Hp 感染的关系,并探讨端粒酶活性表达、Hp 感染和胃粘膜癌变的关系.方法应用 TRAP 测定172例内镜活检标本和45例胃癌手术标本的端粒酶活性,其中内镜活检标本正常胃粘膜10例、慢性浅表性胃炎46例、胃溃疡30例、慢性萎缩性胃炎68例、胃癌18例,手术标本高分化型胃癌8例、低分化型胃癌37例.同时用 EIA 检测 Hp 感染患者血清中 Hp-CagA-IgG,并分析端粒酶活性的表达和 Hp-CagA-IgG 水平的关系.结果在172例内镜活检标本中,正常胃粘膜、慢性浅表性胃炎、慢性萎缩性胃炎伴0度、1度、2度肠化和胃癌组织的端粒酶阳性率分别为0%,0%,0%,25%,38%,89%.45例手术切除的胃癌组织和相应的非癌胃组织也展现了相似的结果.Hp检出情况,正常胃粘膜、浅表性胃炎、慢性萎缩性胃炎伴0度、1度、2度肠化 Hp 阳性率分别为0%,52%,60%,70%,75%.45例手术切除胃癌的非癌胃组织伴0度、1度、2度肠化的 Hp 感染强度分别为10.8±9.6,41.3±31.1,86.4±47.8个/50腺体.慢性浅表性胃炎患者的 Hp-CagA-IgG 抗体显著低于胃癌患者的 Hp-CagA-IgG 抗体水平(P<0.01),22例 Hp 阳性的胃癌患者感染的 Hp 全部为 CagA^+株,其非癌胃粘膜有12例展现了端粒酶活性(55%);相反 Hp 阳性的22例慢性浅表性胃炎患者感染的 Hp 只有8例为 CagA^+株(36%),其胃粘膜均未展现端粒酶活性.结论正常胃粘膜和浅表性胃炎不表达端粒酶活性.萎缩性胃炎随肠化进展端粒酶活性表达增加,胃癌组织中端粒酶活性表达最高,阳性率达88%以上.在胃癌患者的非癌胃粘膜中端粒酶活性的表达与肠化程度、Hp 感染强度呈平行关系,且感染的Hp 多为 CagA^+株;而慢性浅表性胃炎感染的 Hp 多为 CagA株.端粒酶活性检测可以作为胃粘膜癌变的一个早期预测指标,CagA^+的 Hp 感染可能是端粒酶重新激活的一个启动信号.
文摘AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from normal controls ( n =11), superficial gastritis ( n =32), atrophic gastritis with intestinal metaplasia ( n =83), dysplasia ( n =25) and gastric carcinoma ( n =10) were studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups ( P <0 01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13 14±1 6 and 19 68±2 22 respectively, significantly higher than 6 95±0 78 and 11 34±1 89 in H. pylori negative patients ( P <0 01); but there was no such difference in other groups ( P >0 05). CONCLUSION H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.
