根除幽门螺杆菌对胃黏膜病变的影响

幽门螺杆菌（H.pylori）被认为是导致胃黏膜病变的重要因子，根除H.pylori能使胃黏膜病变改善。目的：观察根除H.pylori对胃黏膜病变的影响。方法：予100例经胃镜和组织病理学检查确诊为萎缩性胃炎伴H．pylori感染患者抗H.pylori治疗，1年后复查胃镜和组织病理学，评定组织学变化。结果：所有患者均有不同程度的活动性炎症和慢性炎症。抗H.pylori治疗后，86例被根除。与根除前相比，根除后慢性炎症、活动性炎症、腺体萎缩程度评分均明显下降（P〈0．01），肠化生评分无显著改善。结论：根除H.pylori对胃黏膜病变具有临床治疗意义。     

根除幽门螺杆菌对胃黏膜炎症变化的人群随访研究

目的 观察胃癌高发区中幽门螺杆菌(Hp)阳性者根除Hp5年后胃黏膜组织的炎症变化,以探讨。Hp感染与胃黏膜组织炎症及胃癌的关系。方法 对胃癌高发区山东省烟台市成年人群随机抽样1006例,做内镜、快速尿素酶试验及胃窦、胃体部黏膜组织学检查,将Hp阳性者随机分为治疗组(奥美拉唑20mg、克拉霉素500mg、阿莫西林1000mg)及对照组,2组入选者分别于1年后、5年后进行内镜复检,本研究是将5年后复查胃镜及相同部位胃黏膜组织病理检查与5年前结果进行比较并做χ^2检验。结果 552例Hp阳性者随机分为治疗组及对照组各276例,5年后Hp持续阴性者161例,持续阳性者198例。2组结果统计显示：(1)入选前2组胃窦部炎症及活动度发生率与体部相比差异无显著性,P值分别为0．105及0．084,但萎缩及肠化生发生率明显高于体部,P值均为0．000;(2)根除Hp 5年后胃窦、胃体部炎症及活动度均明显减轻,P值均为0．000;(3)根除Hp5年后胃窦部肠化生减轻或未进展,而Hp持续阳性组肠化生发生率明显增加,P=0．032;(4)根除Hp 5年后窦、体部萎缩改善差异无显著性,两组比较P值分别为0．223及0．402。结论 根除Hp可使胃慢性炎症及活动度明显减轻,窦部肠化生得到显著控制,溃疡病发病明显减少;持续Hp感染可使萎缩及肠化生呈进行性加重。     

幽门螺杆菌及其根除治疗与胃癌前病变

幽门螺杆菌 (H .pylori)感染与胃癌前病变的发生及演变过程密切相关 ,而其根除治疗在胃癌前病变干预和治疗中的作用倍受争议。该文综述了胃癌前病变中H .pylori的感染状况 ;H .pylori致萎缩、肠化的机制 ;H .pylori对胃癌前病变细胞增殖与凋亡的影响。进一步总结了根除治疗所取得的成果 ,展望了今后研究发展的方向和前景。     

根除幽门螺杆菌对胃黏膜萎缩并肠上皮化生以及COX-2、C- met表达的影响

目的研究幽门螺杆菌(helicobacter pylori,Hp)根除前后胃黏膜萎缩和肠上皮化生的变化以及环氧合酶-2(cyclooxygenase-2,COX-2)和肝细胞生长因子受体(C-met)的表达。方法 13例患者均为胃镜加病理确诊有萎缩并肠化生合并HP感染,且成功根除HP感染者。用免疫组化方法半定量检测HP除前后萎缩性胃炎并肠上皮化生COX-2蛋白和C-met蛋白的表达。结果根除前和根除后1个月萎缩程度积分分别为1.3±0.3,1.2±0.7,根除后1个月与根除前比较无显著差异(P>0.05)。萎缩并肠化生胃黏膜C-met平均阳性细胞率从根除前53.2±12.4％下降至根除后48.8±7.7％,比较有显著差异(P=0.034)。胃黏膜COX-2平均阳性细胞率从根除前36.5±14.0％下降至根除后23.3±7.9％,有显著差异(P=0.023)。COX-2表达与C-met表达有一定的相关性(r=0.310,P<0.05)。结论 HP根除短期内不能逆转胃黏膜萎缩,但可使慢性萎缩性胃炎胃黏膜中COX-2和C-met癌基因表达下降。COX-2表达与C-met表达相关。     

根除幽门螺杆菌对胃窦黏膜萎缩和肠上皮化生逆转影响的前瞻性研究

目的 探讨根除幽门螺杆菌(Hp)对逆转胃窦黏膜萎缩和肠上皮化生(肠化生)病理改变的作用.方法 对行胃镜检查的门诊患者,于胃窦处取黏膜活检行病理学检查,并确定Hp感染状态.将Hp感染的慢性胃炎伴胃窦黏膜萎缩或(和)肠化生患者作为入选对象并分为两组,一组行Hp根除治疗,为Hp根除组(48例);另一组未行抗Hp治疗,为对照组(38例).分别在1年和5年后对两组患者进行胃镜随访,并在同一部位取材,根据2次病理结果的不同分为逆转和未逆转两种情况.结果 胃窦黏膜萎缩逆转率在Hp根除组显著高于对照组(37.1%比12.0%).5年后Hp根除组的胃窦黏膜萎缩逆转率显著高于1年后,45岁以下者显著高于45岁以上者.而在对照组中,胃窦黏膜萎缩逆转和随访的时间及年龄无明显关系.在2次随访中,肠化生逆转率在Hp根除组和对照组间差异均无统计学意义(P>0.05).结论 根除Hp尚不能逆转胃窦黏膜肠化生,但对逆转胃窦黏膜萎缩有作用,这种作用与随访观察时间及患者的年龄有关.因此,对有Hp感染的胃窦黏膜萎缩者应及早行根除Hp治疗.     

幽门螺杆菌及其根除治疗与胃癌前病变

幽门螺杆茵(H．pylori)感染与胃癌前病变的发生及演变过程密切相关，而其根除治疗在胃癌前病变干预和治疗中的作用倍受争议。该文综述了胃癌前病变中H．pylori的感染状况；H．pylori致萎缩、肠化的机制；H．pylori对胃癌前病变细胞增殖与凋亡的影响。进一步总结了根除治疗所取得的成果，展望了今后研究发展的方向和前景。     

幽门螺杆菌感染与胃癌前病变的关系

为探讨幽门螺杆菌（ＨＰ）与胃癌前病变的关系，本文回顾性分析了４５１例因上腹部不适而在本院做胃镜的患者。共检查出ＨＰ阳性２４２例（５３．７％），ＨＰ感染时肠化生及胃粘膜萎缩的发生率分别为１４．９％（３６／２４２）及９．１％（２２／２４２），显著高于无ＨＰ感染的肠化生及萎缩发生率８．１％（１７／２０９）及３．３％（７／２０９）（Ｐ＜０．０５）。ＨＰ感染时发生肠化生及萎缩的平均年龄分别为４６．６±１４．５岁及３９．３±１３．７岁，显著小于无ＨＰ感染时的肠化生及萎缩年龄５６．２±９．２岁及５８．２±８．７岁（Ｐ＜０．０１）。本文结果提示早年感染ＨＰ可使肠化生及萎缩性胃炎发病率升高，故ＨＰ感染可能是胃癌的致病因素之一。     

根除幽门螺杆菌对胃黏膜萎缩和肠化影响的随访研究

幽门螺杆菌（Hp）感染可导致胃黏膜的炎症，长期感染进一步引起萎缩、肠化，是肠型胃癌的主要病因之一，许多学者强烈推荐根除Hp以预防胃癌，但是根除Hp后是否能使癌前病变逆转或终止则是判断预防作用的重要指标。我们对萎缩性胃炎患者根除Hp后进行了3年随访观察，以了解胃黏膜组织学变化情况。     

Helicobacter Pylori and Precancerous Gastric Lesions

Background: To determine the relationship between Helicobacter pylori (H. pylori) infection and the precancerous gastric lesions: atrophic gastritis (AG) and intestinal metaplasia (IM) and dysplasia. Methods: A total of 347 dyspeptic patients, including 141 H. pylori‐positive patients and 206 H. pylori‐negative patients, were studied alongside age‐ and sex‐matched controls. The patients underwent gastroscopy and endoscopic biopsy for detection of H. pylori, and histological examinations. Helicobacter pylori was detected by a urease test (CLO; Delta West; Bentley, Australia), by histology (H&E stain, Giemsa) and by serology (BioSig; BioMeditech, NJ, USA). Atrophic gastritis, IM and dysplasia were detected by histological examination (Giemsa, H&E stain). Results: There is a higher rate of atrophic gastritis in H. pylori‐positive than in H. pylori‐negative patients (46 vs 13.5%, odds ratio (OR) = 5.4; P < 0.01). Gastritis in H. pylori‐positive patients also has a higher rate of activity than in H. pylori‐negative patients. The rate of IM is higher in H. pylori‐positive patients than in H. pylori‐negative patients (35 vs 11%; OR = 4.3; P < 0.01). Metaplasia is more often diffuse in H. pylori‐positive than in H. pylori‐negative patients. Dysplasia is more common in H. pylori‐positive than in H. pylori‐negative patients (12 and 3.8%; OR = 3.3; P < 0.01). Conclusions: This study supports the suggestion of a relationship between H. pylori infection and precancerous gastric lesions. Wherever H. pylori is present, the precancerous lesions are more common and more severe.     

幽门螺杆菌感染与胃癌前病变

幽门螺杆菌（H．pylori）感染致胃癌前病变是其致癌过程中的重要步骤。H．pytori感染可引起胃黏膜上皮细胞增殖与凋亡失衡及其调控基因异常、诱导氧化应激、上调诱导型一氧化氮合酶（iNOS）、环氧合酶（COX）-2、过氧化物酶体增生物激活受体（PPAR）-γ、端粒酶相关基因等的表达，最终导致胃癌前病变和胃癌。根除H．pylori可阻断胃癌前病变的进展，使胃黏膜上皮细胞的分子生物学行为和生化异常得到部分恢复，从而降低胃黏膜癌变的危险性。     

胃粘膜癌前病变中幽门螺杆菌与c-met原癌基因蛋白表达关系的研究

为研究Hp感染后胃粘膜细胞中c-met原癌基因蛋白表达的情况,了解Hp在胃癌发生过程中的作用,对110例经病理证实为慢性胃炎的病人用免疫组化方法检测了胃粘膜细胞中e-met原癌基因蛋白表达情况。结果表明,在浅表性胃炎、萎缩性胃炎、肠化生及异型增生中,e-met原癌基因蛋白的表达率分别为22.2％、44.1％、67.5％和61.9％。过表达率分别为5.5％、26.4％、37.8％和38.1％。Hp感染后c-met原癌基因蛋白表达率较末感染者高,分别为63％及32％,在萎缩,肠化生及异型增生等癌前病变中Hp感染者与未感染者表达率分别为58.9％及29.7％(P<0.005)。本研究结果显示,随着病变的进展,c-met原癌基因的表达随之增加,从而说明Hp感染对c-met原癌基因蛋白表达有一定的影响,Hp启动了胃癌发展的早期阶段,也可能推进胃癌的发展过程。     

胃内三羟胆酸与萎缩性胃炎及胃癌癌前病变关系的研究

通过对86例原发性胆汁返流性胃炎空腹1h胃液三羟胆酸含量、游离酸测定，研究三羟胆酸与萎缩性胃炎（CAG）、胃癌癌前病变的关系。结果表明：CAG组三羟胆酸含量明显高于浅表性胃炎组（CSG）及对照组，尤以CAG伴结肠型肠化、不典型增生者含量最高，而游离酸值最低。胃粘膜活检见大量中性粒细胞浸润，以CAG组明显（55．2％）。提示胆汁酸浓度与胃粘膜炎症程度、性质密切相关，胆汁返流致胃酸过少继发细菌感染，是促使CAG、胃癌前病变发生的重要因素之一。胃游离酸检测与胃腺体受损程度不平行，但测定空腹胃游离酸对判断病情轻重及预后有临床实用价值。     

沙土鼠感染幽门螺杆菌后胃粘膜病理学改变的研究

目的和方法:应用HP标准菌株ATCC43504,增菌培养后接种于6周龄沙土鼠胃内。分别于2周、12周后杀死实验鼠。鼠胃经过福尔马林固定,石蜡切片,进行HP组化染色、AB/PAS染色及Brdu.PCNA免疫组化染色。结果:接种HP2周后,胃粘膜上皮细胞间有中性粒细胞、淋巴细胞浸润,上皮细胞及腺窝内可见大量HP存在,AB/PAS染色处见肥大细胞增多。Brdu.PCNA呈阳性表达,明显高于对照组。接种HP12周后,胃窦部出现溃疡(2/3),胃粘膜上皮细胞可见核分裂相及淋巴滤泡。结论:①接种HP2周后的沙土鼠胃粘膜呈急性炎症改变,HP定植于胃窦粘膜呈慢性炎症改变。提示沙土鼠是研究HP感染性胃病有价值的动物模型;②HP感染性胃粘膜Brdu.PCNA呈阳性高表达,表明HP感染过程中,伴有细胞部增值性变化。     

阻癌胃泰冲剂治疗胃癌癌前病变的胃粘膜形态学及幽门螺杆菌变化

用阻癌胃泰冲剂治疗胃癌癌前病变并比较治疗前后胃粘膜形态学、胃粘膜内幽门螺杆菌（HP）变化。结果用阻癌胃泰冲剂治疗后胃粘膜颗粒样或结节状隆起、充血水肿、糜烂、溃疡、粘膜变薄等变化明显减轻。治疗前后比较有极显著性差异（P＜0．01），治疗组疗效亦明显高于对照组（P＜0．01）。治疗组对HP的感染具有抑制和清除效果，与对照组比较有极显著性差异（P＜0．01）。总有效率达80．23％。     

幽门螺杆菌长期感染对胃粘膜的远期影响——10年随防研究

目的研究Hp长期感染对胃粘膜病变的转归的影响.方法随防了62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16例(25.4%)Hp转阴,47例(74.6%)Hp持续阳性.②Hp持续阴性者10年前后消化性溃疡(PU)的发生率分别为29.78%和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68.8%和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17.02%和38.29%(P＜0.05),IM的发生分别为17.02%和44.68%(P＜0.01);Hp转阴者10年前后IM的发生均为31.25%,胃粘膜糜烂10年后完全消失.结论根除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.     

Acute Gastric Mucosal Lesion in the Aged

Abstract: Over a period of 3 years between August 1985 and July 1988, 110 patients (male/female ratio, 64: 46, age range 22–89 years, mean 48.1 years) were diagnosed endoscopically as having acute gastric mucosal lesion (AGML). These patients were divided into an elderly group (60 years or more, 26 patients) and a younger group (less than 60 years, 84 patients). The chief complaint, the precipitating factors, the location of the lesion, the disease type, the background gastric mucosa and the state of bleeding were compared between the groups. AGMLs in elderly patients were found to have the following characteristic features. The chief complaints included hematemesis and melena, and oral drugs were the precipitating factor in many patients. The lesion often occurred in the body or whole area of the stomach, and was found to be relatively rare in the vestibule. An acute gastric ulcer was the most frequent clinical finding. The background gastric mucosa was rated C-II or more severe in most cases. Overt bleeding was present in many cases, requiring endoscopic hemostasis.     

Effects of Omeprazole and Eradication of Helicobacter pylori on Gastric and Duodenal Mucosal Enzyme Activities and DNA in Duodenal Ulcer Patients

Vetvik K, Schrumpf E, Mowinckel P, Aase S, Andersen K-J. Effects of omeprazole and eradication of Helicobacter pylori on gastric and duodenal mucosal enzyme activities and DNA in duodenal ulcer patients. Scand J Gastroenterol 1994;29:995-1000.

Background: Duodenal and gastric content of mucosal enzymes in duodenal ulcer (DU) patients differs from that of controls. The purpose of this study has been to examine the effect of omeprazole and eradication of Helicobacter pylori on mucosal enzymes in DU patients

Methods: The enzyme activities of seven gastric and duodenal mucosal marker enzymes from the brush border, lysosomes, and mitochondria have been studied. In study I the measurements were made in 29 patients with an active DU before and after 14 days of omeprazole treatment. In study II 22 duodenal ulcer patients were given bismuth subnitrate, oxytetracycline, and metronidazole (triple therapy) for 2 weeks to eradicate H. pylori. Biopsy specimens were taken from the duodenum and the stomach for enzyme measurements and histologic assessment. In study II additional specimens were obtained from the prepyloric region for urease tests and culture of H. pylori.

Results: The ulcer healing rates were more than 90% after both omeprazole and triple therapy. H. pylori was eradicated in 86% after triple therapy. The activities of the brush-border enzymes lactase, neutral-α-glucosidase, alkaline phosphatase, leucyl-β-naphthylami-dase, and γ-glutamyltransferase (γ-GT) increased significantly in the duodenal bulb and the descending duodenum during treatment with omeprazole. No changes in duodenal enzyme activity were detected after triple therapy, whereas a significant fall in γ-GT and acid phosphatase activities was seen in the stomach. The mucosal DNA in the gastric antrum decreased both after treatment with omeprazole and after triple therapy.

Conclusions: A similar decrease in mucosal DNA of the gastric antrum was demonstrated after both omeprazole and triple therapy with bismuth subnitrate, oxytetracycline, and metronidazole. Omeprazole also affects the content of duodenal mucosal enzymes, whereas triple therapy particularly affects the gastric mucosal enzyme activity.