胃癌与非幽门螺杆菌胃内菌群的相关研究进展

胃癌是临床上十分常见的消化道恶性肿瘤，而幽门螺杆菌（Helicobacter pylori, Hp）感染是导致胃癌的最重要原因。随着四联疗法的广泛应用，Hp相关胃癌的发病率也显著下降。除Hp外的胃内菌群参与了对胃正常生理功能的调控，有研究证据显示胃内菌群失衡参与了胃炎及胃癌的致病过程。此外，对于根除Hp后发生胃癌的患者，胃内菌群失衡也在其中发挥重要作用，相关机制已得到初步研究。基于此，该文综述了胃内菌群失衡与胃癌的相关研究进展，以求进一步了解胃癌的致病机制，并为寻求更为安全有效的防治方法提供参考。     

内镜下评估慢性胃炎患者胃黏膜形态预测幽门螺杆菌感染

正感染与胃癌和胃淋巴瘤的发生密切相关[1],根除H.pylori不但可以改善胃炎及预防感染引起的相关疾病,还可以延缓癌前病变或胃癌的发生和发展[2]。随着早期胃癌筛查的普及,临床医生已经逐渐意识到胃部黏膜背景及H.pylori感染状态的评估在早期病变诊断中的重要作用。实际工作中大部分患者就诊后先行胃镜检查,内镜操作医生对其H.pylori的感染状态很难做出正确判断。目前H.pylori的检测方法无论是侵入性或非侵入性,均存在一定的局限性,而且不能实现实时的胃黏膜形态评估,对于胃癌高危因素的患者,不利于个体化的     

环氧化酶2在胃癌、癌前病变中的表达及其与幽门螺杆菌感染的关系

幽门螺杆菌（Helicobacter pylori,Hp）感染与胃癌、胃黏膜相关淋巴样组织淋巴瘤的发生密切相关,1994年世界卫生组织国际癌症研究机构（IARC）将其列为人类Ⅰ类致癌原,Hp致胃癌机制仍未明了,而环氧化酶2（COX-2）是一种凋亡相关蛋白,通过抑制胃癌细胞的凋亡参与了胃癌的发生发展。我们通过检测COX-2蛋白在胃癌发生过程中的表达变化,探讨COX-2与Hp感染致癌的可能机制。     

幽门螺杆菌感染和慢性胃炎的关系

幽门螺杆菌(H.pylori)是一种微需氧、螺旋状弯曲的革兰氏阴性杆菌,易于在胃内定植,是慢性胃炎的重要病因。细胞毒素相关蛋白A、空泡毒素和硫氧还原蛋白等多种毒力因子在H.pylori的致病过程中发挥重要作用。在炎症早期可有粘膜固有层内中性粒细胞的显著聚集,而后绝大多数患者会进展为慢性胃炎,以淋巴细胞浸润为主。在白光内镜下,H.pylori感染可有弥漫性发红、胃窦结节和胃皱襞增厚等表现;在精查内镜下,集合静脉的缺失、胃小凹的扩大及上皮下毛细血管网显示不清是H.pylori感染相关诊断指标。对于H.pylori阳性的萎缩性胃炎患者,强烈建议早期择优选择H.pylori治疗抗菌素方案进行根除,以预防胃癌的发生。     

幽门螺杆菌感染幽门螺杆菌和胃癌

自从1983年Warren和Marshall首先培养出幽门螺杆菌(H.pylori)[ 1],并把其与消化性溃疡和慢性胃炎的发病相关以来,H.pylori感染是消化性溃疡和慢性活动性胃炎的主要病因早已成为共识.近年来的研究资料提示,H.pylori与胃癌之间有比较密切的关系,胃内有H.pylori感染可能是发生胃癌的一个危险因素.本文从两个方面探讨H.pylori在胃癌发生中的作用.     

PP2a在胃癌及癌旁组织的表达及与幽门螺杆菌感染的相关性

目的研究蛋白磷酸酶2A(PP2a)在胃癌及癌旁正常组织中的表达及幽门螺杆菌(H.pylori)感染与胃癌组织中PP2a表达的相关性。方法入组40例胃癌患者的癌组织(胃癌组)及癌旁组织(癌旁组),2组采用免疫组织化学法检测PP2a蛋白表达情况,TUNEL法检查细胞凋亡,碳14尿素酶呼吸试验检测40例胃癌患者H.pylori感染情况。结果在胃癌组织中PP2a的阳性表达率为70%,明显低于正常胃黏膜组织中PP2a阳性表达率的90%,二者差异有统计学意义(P<0.05);PP2a蛋白表达与胃癌的分化程度、有无淋巴结转移有关;PP2a表达阴性组的胃癌细胞凋亡指数显著低于PP2a阳性组(P<0.05)。胃癌患者H.pylori感染率为57.5%,H.pylori阳性胃癌组织的PP2a蛋白阳性表达率显著低于H.pylori阴性者(P<0.05)。H.pylori感染与胃癌组织中PP2a的表达呈负相关。结论 PP2a可能参与到胃癌的发生发展过程,而H.pylori感染可能通过降低胃黏膜肿瘤抑制基因PP2a蛋白表达水平引起胃黏膜癌变。     

幽门螺杆菌感染癌前病变呼气试验的临床意义

自Warren和Marshall于1982年在胃炎患者的胃黏膜中发现幽门螺杆菌(Helicobacter Pylori,H.pylori)后,H.Pylori感染现已被公认为是胃炎、胃溃疡、胃黏膜相关组织淋巴瘤和胃癌的重要致病因素.     

幽门螺杆菌与胃癌研究进展

胃癌形成是一个多基因参与多步骤发生的复杂的过程,宿主的遗传背景和环境因素均对胃癌的形成起着不同程度的作用.幽门螺杆菌（Helicobacter pylori,Hp）主要定植于胃内,目前已有证据表明Hp是胃癌的Ⅰ类致病因子,Hp感染与胃癌的发生和进展均显著相关,因此根除Hp作为预防胃癌的重要措施受到广泛关注.问题的关键在于如何掌握根除Hp治疗的适应证.为了更好的防治胃癌,有必要将关于Hp感染诱导胃癌发生的机制以及本领域研究的最新成果进行回顾分析.     

幽门螺杆菌的细胞内感染及机制研究进展

幽门螺杆菌(Helicobacter pylori,H.pylori)是一种主要定植于人胃黏膜的革兰氏阴性菌,与多种胃内外疾病密切相关,曾被认为是一种胞外致病菌,然而,越来越多的研究发现H.pylori可以进入细胞内存活、复制,可能为兼性胞内菌。而且,细胞内感染可能在H.pylori致病及耐药方面起重要作用。本文回顾了H.pylori的细胞内感染及机制研究进展。     

幽门螺杆菌对不同分化程度胃癌细胞环氧合酶-2 mRNA及前列腺素E2的影响

流行病学研究显示,幽门螺杆菌(helicobacter pylori,Hp)感染与胃癌发生相关, 1994年世界卫生组织国际癌症研究机构(IARC)将其列为人类Ⅰ类致癌原,但其确切致癌机制目前尚不清楚.近年来研究表明[1-5],Hp感染可增加环氧合酶-2(cyclooxygenase-2,COX-2)的表达和前列腺素E2(prostaglandin E2, PGE2)的产生,COX-2在胃癌的发生、发展过程中起者重要的作用,可能是导致胃癌的机制之一.在Hp通过COX-2途径致癌中,何种菌体成分起作用尚不清楚.有研究报道[6],在肠型胃癌COX-2表达程度明显高于弥漫型胃癌,说明Hp感染促进COX-2表达的程度与胃癌的起源有关.而Hp促进COX-2表达的程度与胃癌分化程度是否有关,尚需进一步研究.本研究拟通过细胞毒素相关基因A(cytotoxin-associated gene A, cagA)阳性和阴性Hp培养滤液与不同分化程度胃癌细胞系高分化癌(MKN28)、低分化癌(MKN45)、未分化癌(BGC823)共培养后检测COX-2 mRNA和PGE2含量的变化,进一步了解Hp通过COX-2途径致癌中cagA的作用以及Hp上调COX-2 mRNA表达和活性与胃癌的分化程度是否有关.     

血清胃蛋白酶原与良、恶性溃疡

目的通过检测血清胃蛋白酶原Ⅰ(PGI)、血清胃蛋白酶原Ⅱ(PGII),探讨胃溃疡及胃癌患者血清PGI、血清PGII及血清PGI/血清PGII的变化规律。方法研究了2005年5月至2006年1月在我院消化内镜中心行胃镜检查者171例,并设正常人对照12例:用免疫放射法(IRMA)测定了其血清PGI及PGII并计算PGI/PGII即PGR。171例胃病患者分组情况:①消化性溃疡组105例;②胃癌组66例。结果①消化性溃疡患者血清PGI及PGII升高(P<0.05)。在溃疡组的分层研究中,血清PGI及PGII升高在活动组更为明显,而在愈合组变化无统计学意义。②胃癌患者血清PGI降低、PGR降低(P<0.01)。在胃癌组的分层研究中:早期胃癌患者PGI及PGR明显降低;进展期胃癌患者PGI及PGR亦降低,两者间无统计学差异(P>0.05)。结论测定血清PGI、PGII水平及PGR值对胃溃疡及胃癌患者的鉴别诊断具有重要的参考意义。     

Near-total gastric necrosis caused by acute gastric dilatation

Gastric dilatation caused by psychogenic polyphagia or bulimia may, under extreme circumstances, progress to total gastric necrosis. We have described a patient in whom acute abdominal symptoms and signs developed while he was receiving psychiatric treatment. Laparotomy showed massive gastric dilatation with near-total infarction. Total gastrectomy with cervical esophagostomy, feeding and decompressing jejunostomies, and wide drainage of the gastric bed were done. After staged reconstruction, recovery was uneventful.     

胃部手术患者经不同侧鼻孔安置胃管的对比研究

目的 探讨不同侧鼻孔置人胃管对术中胃管调整的影响.方法 将200例胃部手术患者随机分为两组.对照组术前经右鼻孔插人胃管,实验组术前经左鼻孔插入胃管,观察两组患者术中发生胃管调整困难的差异.结果 经左鼻孔插入胃管术中发生胃管涮整困难的患者为1例,经右鼻孔插人胃管术中发生胃管调整困难的患者为24例.对经右鼻孔插入胃管术中发生胃管调整(向里插入一部分)困难的患者实施拔除胃管改为经左鼻孔插入后,成功23例.不同侧鼻孔安置胃管术中发生胃管调整困难的百分率差异有统计学意义(X2=24.18,P<0.05).结论 对行胃部手术的患者,术前经左鼻孔留置胃管可有效降低术中胃管调整的困难,减轻患者鼻咽部及食道黏膜的损伤.     

胃手术后并发胃瘫综合征的诊断和治疗

目的 探讨胃手术后胃瘫综合征的诊断及治疗。方法 回顾性分析21例胃手术后胃瘫综合征的临床资料。结果 本组胃瘫综合征发生率3．9％，诊断主要依据患者的临床症状、上消化道造影和胃镜检查，经保守治疗痊愈。结论 综合保守治疗是胃瘫综合征较为理想的治疗方法。     

Endosonography in gastric lymphoma and large gastric folds.

To establish a correct preoperative differential diagnosis between gastric lymphoma and cancer is essential but can be difficult as endoscopic biopsies can sometimes provide a low diagnostic yield. By EUS, infiltrative carcinoma tends to show a vertical growth in the gastric wall, while lymphoma tends to show mainly a horizontal extension. EUS provides an accurate staging of gastric lymphoma, showing the exact level of infiltration and the presence of perigastric lymph nodes, thus the physician can obtain an accurate prognosis for each patient and select the best form of treatment accordingly. The response to chemoradiotherapy can also be investigated very accurately by EUS. Large gastric folds are seen in a great number of benign and malignant conditions. Diagnosis represents a clinical challenge because etiology may be extremely varied and standard biopsies are often inconclusive. Different diseases show different levels of infiltration of the gastric wall, thus a characteristic echo-pattern helps for the differential diagnosis. Endosonography, used always in combination with biopsy, allows to rule out malignancies and to select the most appropriate treatment for each patient (medical or surgical).     

Acrylonitrile-induced gastric mucosal necrosis: role of gastric glutathione

Acrylonitrile [vinyl cyanide (VCN)] induces acute hemorrhagic focal superficial gastric mucosal necrosis or gastric erosions. In this report the authors have studied the mechanism of the VCN-induced gastric erosions. VCN-induced gastric lesions are coupled with a marked decrease of gastric reduced glutathione (GSH) concentration. Pretreatment of rats with various metabolic modulators (cytochrome P-450 monooxygenase and GSH) before VCN demonstrated that there is an inverse and highly significant correlation between gastric GSH concentration and the VCN-induced gastric erosions. Pretreatment of rats with sulfhydryl-containing compounds protected against the VCN-induced gastric necrosis and blocked the VCN-induced gastric GSH depletion. Furthermore, pretreatment of rats with atropine, which blocks muscarinic receptors, protected rats against the VCN-induced gastric erosions. The working hypothesis is that depletion and/or inactivation of critical endogenous sulfhydryl groups causes configurational changes of cholinergic receptors and increases agonist binding affinity, which, among other actions, leads to the causation of gastric mucosal erosions.     

Delayed gastric emptying and gastric autoimmunity in type 1 diabetes

OBJECTIVE: Delayed gastric emptying and/or gastrointestinal symptoms occur in 30-50% of diabetic patients. Known contributing factors are autonomic neuropathy and acute hyperglycemia, but the role of gastric autoimmunity has never been investigated, although 15-20% of type 1 diabetic patients exhibit parietal cell antibodies (PCAs). We studied gastric motility in diabetes in relation to PCA status, autonomic nerve function, HbA(1c), thyroid-stimulating hormone (TSH), Helicobacter pylori (HP), acid production, and gastric histology. RESEARCH DESIGN AND METHODS: Gastric emptying of solids and liquids (measured by (13)C-octanoic acid and (13)C-glycine breath tests, respectively) was tested in euglycemic conditions in 42 type 1 diabetic patients (male/female: 29/13; 15 PCA+; mean age 40 +/- 15 years; mean HbA(1c) 7.8 +/- 0.9%). Gastrointestinal symptoms, autonomic nerve function (Ewing tests), PCA status (indirect immunofluorescence), gastric histology, and acid secretion (pentagastrin) were assessed. RESULTS: Solid gastric emptying was delayed in 40% and liquid emptying in 36% of patients. Gastric motility did not correlate with symptoms. PCA status, gastric morphology, and acid secretion were similar in those with and without gastroparesis. HbA(1c) level (beta = 1.34, P = 0.011) was the only risk factor for delayed solid emptying in a logistic regression model testing HbA(1c), autonomic nerve function, PCA, HP status, age, sex, diabetes duration, and TSH. Half-emptying time for liquids correlated with TSH level (r = 0.83, P < 0.0001) and autonomic neuropathy score (r = -0.79, P = 0.001). CONCLUSIONS: We found that approximately 50% of type 1 diabetic patients studied had delayed gastric emptying that did not correlate with symptoms. Gastric autoimmunity did not contribute to diabetic gastroparesis. Metabolic control was worse in patients with delayed solid emptying.