幽门螺杆菌感染慢性胃炎患者红细胞膜补体受体1型分子的表达及其临床价值

[目的]观察幽门螺杆菌（Hp）感染慢性胃炎患者红细胞膜补体受体1型（CR1）分子表达特点以及治疗对其表达的影响，并探讨其临床价值。[方法]Hp阳性（＋）慢性胃炎58例，给予抗Hp三联和胃动力药（得乐冲剂、普瑞博思、阿莫西林和甲硝唑）治疗2周。治疗前及治疗结束后分别进行胃镜及Hp检测，并采用免疫酶联（ELISA）法定量测定CR1分子的数量。[结果]Hp（＋）组治疗后有2例胃黏膜无炎症，较治疗前轻度例数显著增高，中、重度例数显著降低（P〈0．01）。Hp（＋）组治疗前外周血红细胞CR1分子数量显著低于正常对照组（P〈0．01），治疗后显著升高（P〈0．01）。[结论]Hp感染慢性胃炎患者抗Hp三联和胃动力药联用，不仅能显著改善黏膜炎症表现，还能增加红细胞CR1分子活性，提高红细胞免疫功能。     

Hp感染对胃粘膜增殖、DNA含量及癌基因表达的影响

幽门螺杆菌(Helicobacter pylori,Hp)感染是慢性胃炎、消化性溃疡、胃癌的主要病因[1-5].Hp感染胃粘膜后,既能破坏胃粘膜屏障功能[6],同时也可刺激胃粘膜细胞增殖[7-13],结果可能导致DNA异常和癌变[14,15].目前Correa所提出的Hp感染、慢性胃炎、萎缩、肠上皮化生、异型增生、肠型胃癌发展模式及其影响因素的假说受到普遍重视.在Hp根除治疗后这些癌 前病变是否能逆转仍有争论[16,17 ].为此,我们对Hp阳性患者抗Hp治疗前后胃粘膜组织学特点、细胞增殖活性、DNA含量、bcl-2,p53,C-myc基因表达进行了对比研究.     

多组分重组减毒沙门疫苗菌对幽门螺杆菌感染的免疫保护作用

目的　利用人类幽门螺杆菌 (Helicobacterpylori,Hp)感染的小鼠模型研究多组分重组减毒沙门疫苗菌对幽门螺杆菌感染的免疫保护作用。方法　将二级C5 7BL/ 6小鼠随机分成 6组 ,通过灌胃方法分别给予生理盐水 (A组 )、PBS(B组 )、减毒鼠伤寒沙门菌SL32 6 1(C组 )、重组减毒鼠伤寒沙门菌pTrc99A -ureB +pGSTag -katA(D组 )、重组减毒鼠伤寒沙门菌pTrc99A -ureB +pTrc99A -HPaA(F组 )及重组减毒鼠伤寒沙门菌 pTrc99A -ureB +pGSTag -katA +pTrc99A -HPaA(F组 )。免疫后 4周 ,予Hp进行攻击 (A组不攻击 )。攻击菌量 10 7CFU/只 ,灌胃 2次 ,每日 1。再 4周后处死动物 ,取胃组织分别行尿素酶试验、改良Giemsa染色及定量细菌培养 ,观察Hp定植情况。行HE染色观察胃粘膜组织炎症情况。取脾组织行淋巴细胞增殖试验。结果　A组小鼠Hp定植密度为 0 ,B组为 9 4 9× 10 6CFU/ g胃组织 ,C组为 1 4 2× 10 6CFU/ g胃组织 ,D组、E组和F组小鼠分别为 2 92× 10 5CFU/g、5 5 1× 10 5CFU/g和 2 16× 10 5CFU/g胃组织 ,C组、D组、E组和F组与A组和B组相比定植密度均明显降低 (P <0 0 5 )。免疫组与对照组胃粘膜均无明显炎症反应。免疫组脾淋巴细胞增殖试验阳性。结论　口服多组分重组减毒沙门疫苗菌对小鼠Hp感染具有一定免     

幽门螺杆菌感染BALB/c小鼠模型的研究

目的　建立稳定的Hp感染BALB/c小鼠模型 ,用于Hp致病、免疫和防治的研究。 方法　选用临床分离株 ,应用外科手术法向小鼠胃内直接接种Hp菌液 0 2ml(10 9CFU/ml) ;接种后不同时间取小鼠胃粘膜组织进行细菌学和病理学检查。结果　接种后 2～ 8周 ,小鼠胃内均可分离到Hp ,Hp分离阳性率为 95 %。病理学检查显示鼠胃粘膜明显炎症。感染鼠用阿莫西林治疗后 ,鼠胃组织Hp培养均转阴性。结论　使用Hp鼠胃接种法 ,能建立稳定的Hp感染BALB/c小鼠模型     

幽门螺杆菌感染与上胃肠道疾病

1982年Marshall和Mareen首次从慢性活动性胃炎患者的胃粘膜中分离出为幽门螺杆菌(Hp)。本文概括了Hp与上胃肠道疾病的关系，并评估其感染的治疗。现已确认Hp与4种上胃肠道疾病密切相关：(1)慢性胃炎；(2)消化性溃疡病；(3)胃癌；(4)胃粘膜相关淋巴样组织(MALT)淋巴瘤。Hp是慢性胃炎的主要病因，与消化性溃疡病的发生密切相关，Hp感染增加了胃腺癌发生的危险性，而且也涉及到胃MALT淋巴瘤发生的致病机理。Hp感染的治疗是以PPI、铋制剂以及RBC为基础的三联疗法，当三联疗法失败时则推荐四联疗法。四联疗法是传统的三联疗法(铋剂为基础的三联疗法)十PPI组成。     

荆花胃康胶丸、布拉氏酵母菌散联合四联疗法治疗Hp阳性慢性胃炎的临床疗效

目的:探讨四联疗法联合布拉氏酵母菌散、荆花胃康胶丸治疗Hp阳性慢性胃炎的临床效果.方法:选取2020年4月-9月就诊的Hp阳性慢性胃炎患者180例,依随机数字表法分为2组,每组各90例.对照组行四联疗法(奥美拉唑+阿莫西林+呋喃唑酮+枸橼酸铋钾)治疗2周;观察组在四联疗法的基础上服用布拉氏酵母菌散、荆花胃康胶丸,疗程2...     

荆花胃康胶丸联合PPI三联疗法治疗Hp相关性慢性胃炎52例临床观察

[目的]观察荆花胃康胶丸联合PPI三联疗法对幽门螺杆菌(Hp)相关性慢性胃炎的治疗效果。[方法]将104例患者随机分为治疗组和对照组,治疗组给予兰索拉唑30mg bid+阿莫西林1 000mg bid+克拉霉素500mg bid+荆花胃康胶丸160mg tid,治疗10d后,再单独服用荆花胃康胶丸2周;对照组给予兰索拉唑30mg bid+阿莫西林1 000mg bid+克拉霉素500mg bid+枸橼酸铋钾220mg bid,治疗10d。比较2组治疗后的症状改善情况,以及停药28d后Hp的根除效果。[结果]在Hp根除方面,2组的根除率分别为84.4%、88.9%,差异无统计学意义;在症状改善方面,2组较前均有明显改善(P<0.05),其中荆花胃康胶丸组在改善上腹胀、嗳气、上腹痛方面优于含铋剂四联组(P<0.05)。[结论]2组根除Hp效果相当,但荆花胃康胶丸组在改善症状方面的效果更为明显。     

幽门螺杆菌感染患者血清可溶性黏附分子1(sICAM-1)检测研究

目的研究慢性胃病患者幽门螺杆菌(Helicobacter pylori,Hp)感染与血清可溶性黏附分子1(Soluble Intercellular Adhesion molecule-1,sICAM-1)水平关系。方法对205例慢性胃病患者进行了血清sICAM-1水平检测,并同时进行RUT、组织MB染色、Hp抗体和~(14)C-UBT四项方法检测Hp感染。结果胃粘膜Hp阳性组患者血清sICAM-1为889.43±22.52ng/m1,明显高于Hp阴性组患者747.07±30.45ng/ml(P<0.05);胃粘膜Hp感染菌量+、++、+++三组患者sICM-1水平分别为841.68±72.36ng/ml、905.43±37.59ng/ml和1012.54±49.34ng/ml,三组间差异显著(P<0.05);慢性胃炎、消化性溃疡患者血清sICAM-1水平明显高于正常对照组(P<0.05).结论胃粘膜Hp感染患者血清sICAM-1水平明显升高,血清sICAM-1水平可作为判断Hp感染新的感染免疫活动指标。     

荆花胃康胶丸联合三联疗法治疗老年幽门螺杆菌感染慢性胃炎的疗效

目的了解荆花胃康胶丸联合三联疗法治疗老年幽门螺杆菌(Hp)感染慢性胃炎的临床效果。方法选取2010年2月至2013年1月160例老年慢性胃炎患者,采用随机数字表分为对照组和荆花胃康胶丸治疗组,每组80例;对照组采用兰索拉唑、阿莫西林与克拉霉素联合治疗,荆花胃康胶丸治疗组在对照组的治疗基础上加用荆花胃康胶丸,治疗4 w后观察两组患者Hp的根除率、临床症状缓解情况及不良反应的发生情况。结果对照组患者中59例(73.8%)Hp得到根除,67例(83.8%)慢性胃炎症状得到缓解,7例患者在治疗期间发生不良反应;荆花胃康胶丸治疗组77例(96.3%)Hp得到根除,71例(88.8%)慢性胃炎症状得到缓解,3例患者治疗期间出现不良反应,荆花胃康胶丸治疗组的Hp根除率与临床症状缓解率高于对照组(P<0.05),不良反应发生率低于对照组(P<0.05)。结论荆花胃康胶丸联合三联疗法能够提高Hp根除率和降低不良反应发生率,对老年Hp感染慢性胃炎的临床效果显著。     

和胃止痛颗粒联合耳穴压豆治疗180例Hp感染慢性萎缩性胃炎的疗效观察

[目的]观察和胃止痛颗粒联合耳穴压豆治疗Hp感染慢性萎缩性胃炎的临床疗效。[方法]收集就诊的180例Hp感染的慢性萎缩性胃炎患者,分为治疗组和对照组,每组90例,疗程均为4周。治疗组采用标准铋四联+和胃止痛颗粒口服,配合耳穴压豆治疗;对照组单纯给予杀菌治疗,4周后观察临床疗效。[结果]治疗组Hp根除率(93.33%)高于对照组(71.11%),差异有统计学意义(P<0.01);治疗组总有效率为95.56%,明显高于对照组的83.33%(P<0.01)。治疗后2组患者中医症状积分均较治疗前下降,治疗组症状积分低于对照组(P<0.01);2组患者胃蛋白酶原(PG)Ⅰ、PGⅠ/PGⅡ、血清胃泌素(G-17)水平均较治疗前升高,PGⅡ水平较治疗前下降(P<0.01),且治疗组PGⅠ、PGⅠ/PGⅡ、G-17水平均高于对照组(P<0.01);胃镜下胃黏膜的形态改善,在黏膜色泽、黏膜皱襞、黏膜颗粒状改变等方面,观察组优于对照组。[结论]和胃止痛颗粒联合耳穴压豆治疗Hp感染的慢性萎缩性胃炎有较好疗效,可以明显提高血清中PGⅠ、PGⅠ/PGⅡ、G-17的水平,进而改善胃黏膜功能,提高Hp根除率。     

幽门螺杆菌破坏胃粘膜屏障的研究

为了解幽门螺杆菌（Ｈｐ）对胃粘膜屏障的损伤作用，对５０例Ｈｐ感染的胃炎及５０例非Ｈｐ感染胃炎者测定其胃窦粘膜的磷脂和氮基已糖值，并与病理改变相比较。结果示Ｈｐ感染组胃窦粘膜的磷脂平均值低于非Ｈｐ感染组（Ｐ＜０．０５）。Ｈｐ感染组的胃窦粘膜氨基己糖值明显低于非Ｈｐ感染组（Ｐ＜０．００５）。而Ｈｐ感染组的活动性胃炎明显高于非感染组。结果表明，Ｈｐ可通过破坏胃粘膜屏障而导致胃粘膜炎症性改变。     

幽门螺杆菌相关性胃病的细胞增殖和凋亡

目的 观察幽门螺杆菌（Hp)及其CagA基因对细胞增殖和凋亡的影响,进而探讨Hp增加胃癌发生危险性的机制。方法 研究对象为慢性浅表性胃炎（CSG）、慢性萎缩性胃炎（CAG）、慢性萎缩性胃炎伴肠上皮化生（CAGIM）、不典型增生（DYS）、胃癌（GC）患者127例及正常对照组（NS）14例。应用ki-67免疫组化技术评价幽门窦上皮细胞增生,用切口末端标记法（TUNEL）检测胃上皮细胞凋亡,应用聚合酶链反应（PCR）技术检测Hp的CagA基因。结果 Hp阳性患者的增殖指数（LI）和凋亡指数（AI）显著高于Hp阴性者或正常对照（P＜0．05和P＜0．01）。CSGHp阳性的LI和AI明显高于Hp阴性者（P＜0．01）,而其余四种胃病Hp阳性患者（P＜0．05）。Hp阳性或阴性CSG、NS组的AI与LI呈正相关,GC患者的AI与LI呈负相关。LI和AI与胃粘膜炎症程度无明显关系。结论 Hp诱导胃粘膜上皮细胞过度增殖和凋亡主要发生在Hp感染的早期,CagA^ Hp与CagA^－Hp促增殖和凋亡作用的能力明显不同,Hp感染通过引起增殖和凋亡比例的失调,最终促进肿瘤发生。     

Influence of Helicobacter pylori on the gastric mucosal barrier

AIM: To study the influence of Helicobacter pylori (Hp) on the gastric mucosal barrier (GMB) by the measurement of the potential difference (PD). METHODS: Fifty seven chronic gastritis cases were diagnosed endoscopically and confirmed by forceps mucosal biopsy. PD was measured by the Takeuchi method, and Hp was detected by both culture (modified Skirrow method) and press printing method with the Giemsa stain. Patients were divided randomly into three groups (De-Nol, WeiTong-Ling, and Placebo) for a course of 6 wk therapy. RESULTS: PD across the mucosa of antrum was significantly lower in Hp (+) patients than in Hp (-) patients (16.44 ± 2.36 vs 19.58 ± 2.44, P < 0.0001). In Hp (+) patients, PD in the antrum increased markedly (16.88 ± 2.56 vs 20.03 ± 2.21, P < 0.0001) after Hp was cleared up by the De-Nol treatment. CONCLUSION: Our data strongly indicated that Hp infection might cause a gastric mucosal barrier to be impaired markedly while the clearance of Hp by De-Nol recovered the integrity of the gastric mucosal barrier significantly.     

氨水对大白鼠胃粘膜长期作用的影响：胃粘膜屏障功能的变化

本实验使用0.01％及0.02％的氨水,以自由饮水的形式经口长期喂养大白鼠,观察了氨水对胃粘膜血流、胃粘膜电位差及胃粘膜前列腺素E_2的影响。结果表明:由HP分泌的悄素酶所分解产生的氨长期作用于胃粘膜,可以导致大白鼠的胃粘膜血流和前列腺E_2减少,使胃粘膜电信差降低,破坏胃粘膜的防御机能,可能是HP导致慢性胃炎及胃溃疡的一个重要因素。     

AgNOR and rasp21 expression in gastric mucosal lesions caused by Helicobacter pylori infection

AIM: To investigate AgNOR and rasp21 expression levels in gastric mucosal lesions caused by Helicobacter pylori (Hp) infection in order to gain insight into the related biological processes (i.e. tumor-like behavior) and possible underlying mechanism supporting Hp pathogenesis.METHODS: Hp infection was diagnosed in using the standard Campylobacter-like organism test along with Wathin-Starry staining. The expression of AgNOR was detected by the silver colloid staining technique. The expression of rasp21 was detected by monoclonal antibody and immunohistochemical staining using the ABC method. The study included a total of 278 patients with endoscopically- and pathologically-confirmed gastric mucosal lesions, representing chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), intestinal metaplasia, dysplasia, and gastric cancer. Among these, 146 of the patients were Hp-positive and 132 were Hp-negative.RESULTS: The Hp-positive group of patients showed significantly greater AgNOR in the gastric mucosal lesions than the Hp-negative group, with the exception of the CSG sub-group (P < 0.05 or P < 0.01). The positive rate of rasp21 expression in gastric mucosal lesions in the Hp-positive group was also significantly higher than that in the Hp-negative group, with the exception of the CSG and CAG sub-groups (P < 0.05).CONCLUSION: Hp-positive gastric mucosal lesions show biological behaviour of tumors. Hp may act as a promoter to activate the ras gene and to stimulate cell over-proliferation.     

胃癌中幽门螺杆菌感染与原癌基因c—met表达及预后研究

目的　研究幽门螺杆菌(Hp)感染的胃癌(GC)组织中c-met表达及(Hp)感染对胃癌预后的影响。方法　经病理证实,不同病变胃粘膜145例以免疫组化检测c-met基因表达,以W-S法及快速尿素酶试验检测(Hp)感染。结果　在浅表性胃炎(CSG)、萎缩肠化生胃炎(CAG+IM)、异型增生(DYS)、早期GC和进展期GC中,c-met基因表达率分别为25.53%,51.28%,61.54%,66.67%和68.42%,CAG+IM、DYS、GC均显著高于CSG(P＜0.05)。肠型胃癌c-met阳性表达与(Hp)感染密切相关。CAG+IM,DYS和GC组c-met阳性表达(Hp)感染者明显高于阴性组。(Hp)阳性者5年生存期显著短于(Hp)阴性者。结论　(Hp)感染和c-met表达与胃粘膜增殖和恶化有关,前者也与胃癌预后有关。     

Effect of the treatment of Helicobacter pylori infection on gastric emptying and its influence on the glycaemic control in type 1 diabetes mellitus

Helicobacter pylori (Hp) infection plays a role in gastric emptying (GE) in type 1 diabetic patients and may have implications for glycaemic control. The aim of our study was to investigate this relationship. Gastric emptying was studied in 13 patients with type 1 diabetes and Hp infection. The Hp infection status was assessed by serology and urease breath test (UBT). In addition upper gastrointestinal endoscopy with gastric mucosal biopsy was performed to look for gastritis. A radionuclide-labeled solid meal was used to study GE before and after eradication therapy (amoxicillin, clarithromycin and omeprazole) for Hp infection. All patients were evaluated for autonomic and peripheral neuropathy and were asked for symptoms of gastrointestinal motor dysfunction. Blood glucose levels were determined before the meal and at 30,60,90 and 120 min after the start of the meal. Home blood glucose self-monitoring and HbA(1c) were performed to document glycaemic control during the study. Three months after treatment, five patients were free of Hp infection and were without gastritis (group I: no Hp infection, no gastritis); eight of the patients continued to have gastritis after treatment (group II) and of these eight patients, six had gastritis without Hp infection and two had gastritis plus persistent Hp infection. These last two patients were re-treated with eradication therapy. Patients with gastritis were re-evaluated 6 months after initial treatment; at which time four were now free of gastritis and were added to group I (n=9) while four continual to have gastritis although without Hp infection (group II, n=4). In group I, GE half-time showed an increase (30.6+/-10.3 min vs. 60.2+/-15.4 min; P<0.05) while no change (28.8+/-9.5 vs. 26.9+/-8.7 min; n.s.) was observed in group II. GE half-time was not altered by autonomic and peripheral neuropathy or blood glucose during solid meal test. HbA(1c) did not change significantly after treatment in either groups but the blood glucose levels were more stable in group I compared to group II. A delay in GE was observed with disappearance of gastritis associated to H. pylori infection after eradication treatment in patients with type 1 diabetes. This change in GE could help to stabilise the blood glucose levels in these patients treated with insulin before each meal.     

幽门螺杆菌感染与C-myc基因和P53基因表达与胃癌的相关性研究

目的探讨幽门螺杆菌（Hp）感染情况与C-myc基因及P53基因的表达与胃癌的相关性。方法用w—s染色法观察不同胃病黏膜组织中Hp感染情况，采用免疫组化检测技术检测不同胃病组织的C-myc基因和P53基因表达产物。结果胃癌及癌前病变组Hp感染率明显高于慢性浅表性胃炎组（P〈0．01），C-myc基因和P53基因的表达也显著高于慢性浅表性胃炎组（P〈0．01）。Hp感染阳性组的C-myc基因和P53基因表达明显高于Hp感染阴性组（P〈0．01）。结论Hp感染可能通过激活C-myc基因，同时使P53基因失活从而诱发胃黏膜的癌变。     

氩离子凝固术对疣状胃炎疗效的临床研究

背景:疣状胃炎是一种特殊类型的慢性胃炎,目前尚无特异性治疗方法。目的:探讨氩离子凝固术(APC)治疗疣状胃炎的疗效。方法:选取2010年9月～2012年7月上海市青浦区朱家角人民医院经内镜检查确诊的疣状胃炎患者65例,随机分为治疗组和对照组。幽门螺杆菌(Hp)阳性者先行四联疗法根除Hp。治疗组患者行APC治疗后给予质子泵抑制剂(PPI)和胃黏膜保护剂治疗8周,对照组接受PPI和胃黏膜保护剂治疗8周。比较两组的治疗效果。结果:经APC治疗后,患者临床症状明显改善。治疗组的病灶数目减少程度明显高于对照组(P<0.05)。22例对照组患者药物治疗疗效不明显,转组接受APC治疗后,病灶数目显著降低(P<0.05)。结论:APC可有效治疗疣状胃炎,且安全性良好。     

根除幽门螺杆菌感染对慢性胃炎疗效影响的多中心临床研究

目的 探讨根除幽门螺杆菌(Hp)对慢性胃炎患者临床症状、内镜表现及病理改变的影响.方法 采用多中心、前瞻性、随机化对照研究,观察2009年1月至2010年12月间入组的慢性胃炎患者,分为Hp阳性根除组、Hp阳性不根除组和Hp阴性组,均予以8周的胃黏膜保护剂治疗,对比各组治疗前后临床症状、内镜下表现及病理炎症的变化.结果...