幽门螺杆菌及胃粘膜肠上皮化生与ＣＤ４４Ｖ６表达的关系

目的　探讨幽门螺杆菌(Hp)感染及慢性萎缩性胃窦炎伴肠上皮化生与CD     

幽门螺杆菌感染与胃粘膜萎缩及肠上皮化生

对连续就诊的２２０例慢性胃炎患者进行幽门螺杆菌（ＨＰ）检测和胃粘膜活检病理学检查。结果显示ＨＰ阳性率为５８．７％，ＨＰ阳性患者胃粘膜腺体萎缩和肠上皮化生（肠化生）的发生率及严重程度均显著高于ＨＰ阴性患者；肠化生分型表明Ⅱ型和Ⅲ型肠化生更多见于ＨＰ阳性患者；流式细胞术分析表明ＨＰ阳性患者胃粘膜细胞的Ｓ期比率和增殖指数均显著高于ＨＰ阴性患者。提示ＨＰ感染可能通过刺激胃粘膜细胞的增殖加速、更新加快，从而加速了胃粘膜腺体萎缩和肠化生的形成与发展，继而增加了患胃癌的危险性。     

幽门螺杆菌相关性胃炎中肠上皮化生和非典型增生的发生率

幽门螺杆菌相关性胃炎中肠上皮化生和非典型增生的发生率张文刘秀清近年来对幽门螺杆菌（Ｈｐ）的研究已证明Ｈｐ的存在不仅与胃窦炎、而且与胃和十二指肠溃疡也高度相关。在对晚期胃癌术后标本进行观察，结果也表明Ｈｐ和胃恶性肿瘤之间具有相关性，证明Ｈｐ是发生胃腺癌...     

Ⅰ型幽门螺杆菌感染与胃黏膜萎缩和肠上皮化生关系的探讨

随着近 10余年来对幽门螺杆菌 (Ｈｐ)研究的深入 ,Ｈｐ感染导致胃炎与胃癌的观点被广泛接受 ,国际肿瘤研究署(ＩＡＲＣ)已将Ｈｐ列为Ａ类致癌原。研究发现Ｈｐ可分两种类型 ,其中Ⅰ型Ｈｐ菌株感染与胃炎、溃疡病、胃癌的发生有密切关系。我们通过检测Ｈｐ阳性的慢性萎缩性胃炎伴肠化生患者血中Ｈｐ细胞毒素相关蛋白Ａ免疫球蛋白Ｇ(ＣａｇＡＨｐ ＩｇＧ) ,与Ｈｐ感染的慢性非萎缩性胃炎 (无胃黏膜萎缩和肠化生 )相比较 ,探讨Ⅰ型Ｈｐ与慢性萎缩性胃炎胃黏膜萎缩和肠化生程度之间的关系 ,为临床治疗提供一些依据。材料和方法一、临床资料12 0…     

幽门螺杆菌长期感染与胃黏膜炎症和肠上皮化生的关系

目的探讨幽门螺杆菌(Hp)长期感染及根除与胃黏膜炎症和肠上皮化生(IM)的关系。方法随访71例5年前和78例10年前Hp感染者,分析对比其前后Hp感染情况、胃黏膜炎症和IM的变化。结果5年前Hp阳性71例中,现在52例(73.2％)Hp仍呈阳性,19例(26.8％)转阴;10年前Hp阳性的78例中,现在59例(75.6％)Hp仍呈阳性,19例(24.4％)转阴。Hp长期阳性者5年前和现在及10年前和现在慢性炎症严重程度积分分别为1.635±0.376与1.808±0.301(P>0.05)和1.661±0.398与2.232±0.335(P<0.01);IM的发生率分别为17.3％(9/52)与26.9％(14/52)(P>0.05)和11.9％(7/59)与39.0％(23/59)(P<0.01);IM严重程度积分分别为1.444±0.527与1.667±0.442(P>0.05)和1.571±0.534与2.286±0.488(P<0.05)。Hp转阴者5年前和现在及10年前和现在慢性炎症严重程度积分分别为1.684±0.369与1.369±0.426(P<0.05)和1.647±0.389与1.182±0.396(P<0.01);IM的发生率为31.6％(6/19)和52.6％(10/19);IN严重程度积分分别为1.333±0.516与1.167±0.775(P>0.05)和1.600±0.516与1.100±0.316(P<0.05)。结论Hp感染持续时间越长,胃黏膜炎症越严重,IM程度亦越严重且发生率高;根除Hp不仅能减轻胃黏膜的炎症程度和IM程度,而且能防止IM的发生。     

胃黏膜炎症和肠上皮化生与幽门螺杆菌长期感染分析

目的 探讨幽门螺杆菌(Hp)长期感染及根除与胃黏膜炎症和肠上皮化生(IM)的关系.方法 随访142例4年前和156例7年前Hp感染者,分析对比其前后Hp感染情况、胃黏膜炎症和IM的变化.结果 4年前Hp阳性142例中,现在104例(73.2%)Hp仍呈阳性,38例(26.8%)转阴.7年前Hp阳性的156例中,现在118例(75.6%)Hp仍呈阳性,38例(24.4%)转阴.Hp长期阳性者4年前和现在及7年前和现在的慢性炎症严重程度积分分别为1.635±0.376与1.808±0.301(P＞0.05)和1.661±0.398与2.232±0.335(P＜0.01);IM发生率分别为17.3%(18/104)与26.9%(28/104)(P＞0.05)和11.9%(14/118)与39.0%(46/118)(P＜0.01);IM严重程度积分分别为1.444±0.527与1.667±0.442(P＞0.05)和1.571±0.534与2.286±0.488(P＜0.05).Hp转阴者4年前和现在及7年前和现在的慢性炎症严重程度积分分别为1.684±0.369与1.367±0.426(P＜0.05)和1.647±0.389与1.182±0.396(P＜0.01);IM的发生率为31.6%(12/38)和52.6%(20/38);IM严重程度积分分别为1.333±0.516与1.167±0.775(P＞0.05)和1.600±0.516与1.100±0.316(P＜0.05).结论 Hp感染持续时间越长,胃黏膜炎症越严重,可能IM程度亦越严重,且发生率高;根除Hp不仅能减轻胃黏膜的炎症程度和IM程度,也可能防止IM的发生.     

老年人胃黏膜肠上皮化生与幽门螺杆菌感染相关性分析

目的 了解老年慢性胃炎患者肠上皮化生与幽门螺杆菌感染之间的相关关系.方法 2008年1月至2009年12月在本院接受胃镜检查的60岁及以上的慢性胃炎患者499例,根据病理结果分为肠化生组186例和非肠化生组313例,分别观察每组胃黏膜的幽门螺杆菌(Hp)感染、中性粒细胞浸润、腺体萎缩、淋巴滤泡等病理表现.结果 肠化生组...     

胃黏膜炎症和肠上皮化生与幽门螺杆菌关系的远期观察

[目的]远期追踪幽门螺杆菌(Hp)相关胃炎及Hp阴性的胃炎胃黏膜炎症和肠上皮化生(IM)在病程演变中的关系.[方法]经胃镜检查确诊的Hp阳性胃炎86例(A组),Hp阴性的胃炎92例(B组),对照观察两组5年前后的逆转变化,胃黏膜炎症和IM的程度积分.[结果]5年后A组86例中Hp阳性者61例(70.9%)、转阴者25例(29.1%);5年后两组Hp阳性者、5年前后的炎症程度积分差异无统计学意义;B组Hp阴性者、A组Hp阳性者5年前后比较差异无统计学意义;5年后B组中Hp仍阴性者与A组Hp仍阳性者,其胃黏膜炎症和IM积分比较差异有统计学意义(P＜0.01).[结论]Hp在胃黏膜内存在的时间越长,其炎症和IM的程度越重,发生率也增加,而Hp阴性的胃炎和Hp阳性胃炎转阴后其炎症和IM的程度及发生率均有下降.     

幽门螺杆菌长期感染对胃粘膜的影响

目的为了研究Hp长期感染对胃粘膜病变转归的影响.方法随防了63例10年前Hp感染患者,并分析对比10年前后Hp感染情况、胃镜和病理组织学变化.结果①63例患者中16例(25.4%)Hp转阴,47例(74.6%)Hp持续阳性.②Hp持续阳性者10年前后消化性溃疡(PU)的发生率分别为14例(29.78%)和25例(53.19%)(P＜0.05),Hp转阴者10年前后消化性溃疡(PU)的发生率分别为11例(68.8%)和2例(12.5%)(P＜0.05).③Hp持续阳性者10年前后慢性炎症严重程度积分分别为1.77±0.43和2.13±0.34(P＜0.01),肠上皮化生(IM)严重程度积分分别为1.13±0.35和1.63±0.52(P＜0.05);Hp转阴者10年前后慢性炎症严重程度积分分别为1.81±0.40和1.31±0.48(P＜0.01),肠上皮化生(IM)严重程度积分分别为1.6±0.55和1.4±0.59(P＞0.05);Hp持续阳性者10年前后胃粘膜糜烂的发生分别为8例(17.02%)和18例(38.29%)(P＜0.05),IM的发生分别为8例(17.02%)和21例(44.68%)(P＜0.01);Hp转阴者10年前后IM的发生均为5例(31.25%),胃粘膜糜烂10年后完全消失.结论Hp持续感染可增加消化性溃疡的发生机率,加剧胃粘膜的炎症程度,并促进肠化的形成和发展,根除Hp不仅能减轻胃粘膜的炎症程度,而且能阻止肠化的发生和发展.     

根除幽门螺杆菌对胃黏膜肠化的影响

目的　幽门螺杆菌 (Hp)感染可导致慢性活动性胃炎进一步发展为慢性萎缩性胃炎、胃黏膜肠化、最终发展成肠型胃癌。通过 5年随访 ,探讨根除Hp是否对胃黏膜肠化逆转、发生及发展有影响。方法　将 1996年快速尿素酶试验及组织学方法检测Hp均为阳性的 398例病人随机分为治疗组和对照组。治疗组 2 0 1例 ,进行根除Hp治疗 ;对照组 197例 ,给予安慰剂 ;服药前及 5年后分别从胃窦部及胃体部取材检测胃炎、胃炎活动性及肠化。结果　 5年后治疗组中 15 1/2 0 1例Hp为阴性 ,对照组中 16 1/197例Hp为阳性 ;治疗组中Hp被根除的病人胃炎活动性的检出率明显减少 ,与对照组持续Hp感染者比较 ,差异有显著性 (P <0 .0 0 0 1) ;对照组中持续Hp感染者 5年后肠化检出率与自身 5年前、治疗组成功根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (P均 <0 .0 0 1) ,治疗组根除Hp的病人 5年前后比较差异无显著性 ;对照组中持续Hp感染者胃窦部 5年后肠化检出率与自身 5年前、治疗组根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (分别为P <0 .0 0 1,P <0 .0 0 1和P<0 .0 1) ,治疗组根除Hp感染的病人 5年前后比较差异无显著性 ;对照组持续Hp感染的病人与治疗组根除Hp感染的病人胃窦部肠化新增及新减情况比较无差异。 结论　 5年     

幽门螺杆菌感染与十二指肠球部黏膜胃上皮化生的关系

目的 研究十二指肠球部黏膜幽门螺杆菌(Hp)感染与黏膜胃上皮化生的关系，探讨其在十二指肠球部炎症和溃疡发生中的作用。方法 2002年十二指肠球部黏膜活检的存档蜡块82例，作H-E、改良Giemsa和AB／PAS染色。内镜诊断为基本正常球部黏膜10例；十二指肠球炎47例(其中充血糜烂型16例；隆起型31例)和球部溃疡25例。结果 (1)内镜诊断基本正常的十二指肠球部黏膜，组织学60％有轻中度的炎症细胞浸润，但无胃上皮化生和Hp定植。(2)胃上皮化生是十二指肠球部黏膜最常见的病理变化(37／82，45％)。(3)Hp只有在胃上皮化生的黏膜中才能找到，检出率为76％(28／37)。十二指肠球部溃疡边缘黏膜胃上皮化生发生率(72％)明显高于球炎黏膜(40％)，差异有显著性(P=0．0078)。(4)虽然十二指肠球部溃疡边缘胃上皮化生黏膜的Hp检出率(89％，16／18)明显高于十二指肠球炎黏膜(63％，12／19)，但是两者差异无显著性(P=0．062)。不论何期溃疡Hp检出率均很高，本研究中溃疡活动期、愈合期和瘢痕期分别为15例、6例和4例，其溃疡边缘胃上皮化生中Hp检出率分别高达9／10、5／6和2／2例。结论 十二指肠球部溃疡周围黏膜高发胃上皮化生，使Hp更易于定植，推测如不根除Hp感染，可成为十二指肠球部溃疡复发的重要原因。     

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.     

乳腺癌细胞敏感株与耐药株CD_(44)V_6的表达及意义

为探讨乳腺癌细胞耐药株侵袭转移能力增强及多药耐药与侵袭转移之间的关系 ,采用免疫细胞化学方法对乳腺癌细胞敏感株 MCF- 7及其耐药株 MCF- 7/ ADR中 CD4 4V6 的表达进行了检测。结果显示 ,与 MCF- 7细胞比较 ,MCF- 7/ ADR细胞的 CD4 4V6 的表达明显增强 ,后者侵袭转移能力明显高于前者。提示耐药株细胞MCF- 7/ ADR侵袭转移能力增强与其 CD4 4V6 表达增强密切相关 ,乳腺癌侵袭转移能力的提高和多药耐药现象同时并存。     

Relationship between β-catenin expression and epithelial cell proliferation in gastric mucosa with intestinal metaplasia

AIM: To investigate β-catenin expression in patients with intestinal metaplasia, and to look for a possible relationship between β-catenin expression and either epithelial proliferation values or Helicobacter pylori ( H pylori) infection.METHODS: Twenty patients with complete type intestinal metaplasia were studied. β-Catenin expression and epithelial cell proliferation in antral mucosa were assessed using an immunohistochemical analysis. Hpylori infectionwas detected by histology and a rapid urease test.RESULTS: Reduced β-catenin expression on the surface of metaplastic cells was detected in 13 (65%) out of 20 patients. Moreover, in eight (40%) patients intranuclear expression of β-catenin was found. When patients were analyzed according to Hpylori infection, the prevalence of both β-catenin reduction at the cell surface and its intranuclear localization did not significantly differ between infected and uninfected patients. Cell proliferation was higher in patients with intranudear β-catenin expression as compared to the remaining patients, although the difference failed to reach the statistical significance (36±8.9 vs 27.2±11.4, P = 0.06). On the contrary, a similar cell proliferation value was observed between patients with reduced expression of β-catenin on cell surface and those with a normal expression (28.1±11.8 vs26.1±8.8, P= 0.7).Hpyloriinfection significantly increased cell proliferation (33.3±10.2% vs 24.6±7.4%, respectively, P= 0.04).CONCLUSION: Both cell surface reduction and intranuclear accumulation of β-catenin were detected in intestinal metaplasia. The intranuclear localization of β-catenin increases cell proliferation. H pylori infection does not seem to play a direct role in β-catenin alterations, whilst it significantly increases cell proliferation.     

根除幽门螺杆菌对胃黏膜及肠化、不典型增生的影响

目的探讨根除幽门螺杆菌（Hp）后慢性胃炎的胃黏膜炎症及肠上皮化生、不典型增生的变化。方法选择172例伴有Hp感豢的慢性活动性胃炎病人分为两组：阴性组（68例）和阳性组（104例），观察阴性组治疗后的变化并与阳性组进行比较，并观察阴性组肠上皮化生和不典型增生在治疗前后的变化。结果阴性组的胃黏膜炎症有28例（41．2％）好转，2例（2．9％）治愈，明显高于阳性组（P〈0.01），其伴有的肠上皮化生有2例（25％）治愈，4例（50％）好转，不典型增生有7例（38．9％）好转，6例（33．3%）治愈。结论Hp感染阴转后慢性胃炎的治疗效果明显优于阳性者，其伴有的肠化和不典型增生亦能好转或治愈。因此，根除Hp是治疗Hp相关性胃炎和防止发生胃癌的重要措施。     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

胃粘膜肠化中幽门螺杆菌感染与PCNA,c-erbB-2的表达

目的研究肠化胃粘膜幽门螺杆菌（Ｈｐ）阳性率与ＰＣＮＡ,ｃｅｒｂＢ２表达率之间关系,以探讨Ｈｐ感染在胃肠化发生、发展中作用．方法经病理检查证实的慢性胃炎伴肠化１１６例,对照组非溃疡性消化不良．应用改良ＷａｒｔｈｉｎＳｔａｒｙ法检测Ｈｐ,免疫酶组化ＳＰ法检测ＰＣＮＡ,ｃｅｒｂＢ２的表达,比较Ｈｐ阳性组和阴性组间ＰＣＮＡ,ｃｅｒｂＢ２的阳性表达率．结果胃粘膜肠化者Ｈｐ感染率增高（５８６％ｖｓ１８８％,χ２＝１０７９,Ｐ＜００１）,肠化胃上皮内少见Ｈｐ粘附,Ｈｐ阳性组ＰＣＮＡ,ｃｅｒｂＢ２表达高于阴性组（４８／６８ｖｓ１２／４８,χ２＝９０５,Ｐ＜００５;３６／７４ｖｓ２／４２,χ２＝１３２８,Ｐ＜００１）．结论Ｈｐ感染促进胃粘膜肠化,并使肠化胃粘膜细胞增殖迅速而启动恶性变,故Ｈｐ感染可能促进胃癌的形成．     

Endoscopic duodenitis, gastric metaplasia and Helicobacter pylori

BACKGROUND AND AIMS: The purpose of this study was to investigate the relationship between gastric metaplasia and Helicobacter pylori in patients with endoscopic duodenitis. METHODS: The subjects were 57 patients with endoscopic duodentitis with or without H. pylori-associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori-positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria. RESULTS: There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori-positive and -negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori-negative group, whereas the incomplete type was frequently observed in the H. pylori-positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation. CONCLUSIONS: The complete type of gastric metaplasia occurred frequently without H. pylori infection, whereas the incomplete type was frequently associated with H. pylori infection.