胃癌中幽门螺旋杆菌感染与HIF-1α表达情况对比研究

目的通过观察胃癌患者幽门螺旋杆菌的感染情况及HIF-1α的表达情况,探讨胃癌中幽门螺旋杆菌与HIF-1α的相关性。方法本研究是对临床已经确诊的60例胃癌患者进行碳呼气试验进行幽门螺旋杆菌检测(阴性及阳性各30例),同时将患者手术后胃癌组织采用免疫组织化学的方法检测HIF-1α表达情况,用统计学对结果进行分析。结果幽门螺旋杆菌阳性的患者胃癌组织中HIF-1α呈高表达状态,阳性率为86.67%(26/30),有显著性差异(P0.05)具有统计学意义。幽门螺旋杆菌阴性的患者胃癌组织中HIF-1α呈低表达状态,阳性率为26.67%(8/30),其有显著性差异(P0.05)具有统计学意义。结论胃癌中幽门螺旋杆菌感染可以诱导HIF-1α的表达,从而控制幽门螺旋杆菌可以达到胃癌预防及治疗的目的。     

螺旋杆菌与胆管癌的关系

幽门螺旋杆菌(HP)已被世界卫生组织列为胃癌的第一致癌原,全世界近半数人群有感染史。近年来的研究表明,螺旋杆菌感染与多种其他部位的肿瘤有关。从螺旋杆菌的分类及流行病学、螺旋杆菌与肝胆肿瘤的关系和螺旋杆菌诱导肿瘤发生的机制3个方面介绍螺旋杆菌感染与肝内外胆管肿瘤的研究现状,为进一步探索肿瘤的病因及诊断治疗提供参考,以期待能改善与提高螺杆菌引起胆管癌的诊治与预后。     

胃癌癌前病变癌变机制及其逆转的研究进展

胃癌癌前病变与胃癌的发生关系,日益受到重视,近几年来特别强调幽门螺杆菌为引起慢性萎缩性胃炎与胃癌的重要危险因子.因此,许多学者进一步深入研究幽门螺杆菌感染对发生胃癌的危险性,胃癌癌前病变发生癌变的机制以及如何使其逆转,是预防和降低胃癌发病的重要课题.     

幽门螺旋杆菌可能是胃癌的一个原因

据《柳叶刀》杂志报道,幽门螺旋杆菌感染是萎缩性胃炎和肠组织变形的重要危险因素,这强烈提示该菌是胃癌的一个原因。     

幽门螺旋杆菌感染与急性冠状动脉综合征

目的观察幽门螺旋杆菌感染与急性冠状动脉综合征的关系以及急性冠状动脉综合征患者血浆C反应蛋白水平与幽门螺旋杆菌感染的关系,探讨幽门螺旋杆菌感染在急性冠状动脉综合征发病中的作用.     

幽门螺旋杆菌感染与心血管疾病关系研究进展

幽门螺旋杆菌是常见的一种胃肠道感染的细菌。随着近年研究的深入,幽门螺旋杆菌感染还参与了心血管系统、内分泌系统、神经系统、血液系统、免疫系统等消化系统外疾病的发生与发展。现对幽门螺旋杆菌感染与心血管疾病关系的研究进展进行综述。     

HP感染与ITP的相关性分析

目的分析幽门螺旋杆菌感染(HP)与免疫性血小板减少症(ITP)之间存在的关系。方法将2013年2月—2015年2月收治的168例ITP患者作为研究的对象(观察组),另取同期来我院接受检查的168例健康体检者作为纳入对照(对照组),对两组感染幽门螺旋杆菌的发生率进行对比评价。结果观察组168例ITP患者中,感染幽门螺旋杆菌70例,感染率为41.67%;对照组健康体检者中,感染幽门螺旋杆菌(HP)32例,感染率为19.05%。在幽门螺旋杆菌感染率方面,观察组与对照组相比明显要高(P0.05)。结论幽门螺旋杆菌感染易导致免疫性血小板减少性紫癜发生;针对ITP患者,在明确感染幽门螺旋杆菌的情况下,需积极采取抗幽门螺旋杆菌感染治疗,进而确保患者获得优化治疗。     

幽门螺杆菌感染的评价

目前幽门螺旋杆菌(Hp)感染作为慢性胃炎、消化性溃疡的最主要病因已得到医学界的公认。并由此导致上消化道疾病治疗的一次革命。幽门螺杆菌感染与胃癌和胃淋巴瘤的发生也密切相关。1994年世界卫生组织已将其确定为一类致癌因子。自1982年澳大利亚Marshll分离培养出幽门螺杆菌以来,有关这一微生物的基础及     

根除幽门螺杆菌是降低胃癌发病率的必由之路

胃癌目前已成为全球第四常见的恶性肿瘤,在全球恶性肿瘤致死原因中位居第二位。幽门螺杆菌感染是胃癌发生发展的主要危险因素之一。在胃癌的多阶段发病机制中,幽门螺杆菌感染缓慢诱导慢性活动性胃炎的发生,并经过萎缩性胃炎、肠上皮化生、异型增生等癌前阶段,最终发展为胃癌。相关研究证明根除幽门螺杆菌,特别是在早期阶段,能够有效预防胃癌的发生,并且通过根除幽门螺杆菌可阻止一部分胃癌前病变的发展并使其逆转。文章就根除幽门螺杆菌在胃癌预防中的作用进行总结。     

幽门螺杆菌cagA^（＋）株和胃上皮细胞增殖和凋亡的研究

幽门螺杆菌(Hp)感染是慢性胃炎的主要病因,是消化性溃疡的主要发病因素,并与胃癌的发生密切有关,但其作用机制尚不完全清楚。近年研究发现Hp感染可引起胃粘膜上皮细胞过度增殖和凋亡,并认为这可能是Hp感染导致胃癌发生的机制之一(1)。     

Role of Helicobacter pylori in stomach cancer after partial gastrectomy for benign ulcer disease.

OBJECTIVE: To determine the prevalence of Helicobacter pylori infection in patients having undergone gastrectomy for non-neoplastic disease who later developed gastric stump cancer. MATERIAL AND METHODS: Retrospective study of all patients with partial gastrectomy for non-malignant peptic disease who were submitted to an endoscopic exploration between 1995 and 2001. A comparison was made of major clinical and histological characteristics, and the presence of Helicobacter pylori among patients with and without gastric cancer in the stomach remnant. RESULTS: A total of 73 patients were studied in this period. Fifteen patients (20.5%) had remnant-stump gastric cancer. All but one were adenocarcinomas (71% intestinal and 29% diffuse, respectively). The average time between diagnosis of gastric cancer and previous gastrectomy was 32 (14-48) years. There was a higher detection rate of Helicobacter pylori in patients with cancer in the gastric remnant (100 vs. 81.5%, respectively, p < 0.07). No relationship was seen between type of gastric reconstruction (Billroth I or II) and rate of Helicobacter pylori detection. CONCLUSIONS: Helicobacter pylori infection is frequent in patients with previous gastrectomy for non-neoplastic disease. The results of the study suggest that Helicobacter pylori infection may play a role in gastric stump cancer.     

胃癌患者中反流性食管炎与幽门螺杆菌感染的相关性分析

目的探讨胃癌患者中反流性食管炎与幽门螺杆菌感染的相关性。 方法选取2015年8月至2017年1月,在新疆维吾尔自治区人民医院就诊的胃癌合并反流性食管炎患者45例与同期在本院就诊的胃癌患者45例,比较两组患者幽门螺杆菌的感染率,并对幽门螺杆菌感染与反流性食管炎进行相关性分析。 结果胃癌合并反流性食管炎组和胃癌患者幽门螺杆菌感染率的发生率分别是22.22%和88.89%,差异有统计学意义（χ²=15.568,P＜0.05）。胃癌合并反流性食管炎组的幽门螺杆菌感染率低于胃癌患者。 结论胃癌患者中幽门螺杆菌感染可能对反流性食管炎发病有一定的保护作用。     

胃癌和慢性胃炎患者幽门螺杆菌蛋白质组学分析

背景：胃癌的发生是一个多因素多步骤的过程,幽门螺杆菌（H．pylori）感染在此过程中发挥重要作用。目的：建立胃癌和慢性胃炎H．pylori的双向凝胶电泳（2-DE）图谱,识别鉴定差异表达的蛋白质．探讨细菌本身因素在胃癌发病过程中的作用。方法：取H.pylori而阳性的胃癌和慢性胃炎患者胃黏膜组织后分离培养H.pylori,收集菌体并采用BCA法行蛋白定量,以2-DE分离Hpylori蛋白．采用PDQuest软件分析差异表达的蛋白质点．应用电喷雾四极杆飞行时间串联质谱（Q—TOF）进行鉴定,并在Mascot数据库中进行检索。结果：胃癌和慢性胃炎H．pylori总蛋白均获得分辨率高、重复性好的2-DE图谱。共6个蛋白质点在胃癌和慢性胃炎中存在表达差异．其中超氧化物歧化酶、尿素酶仪亚单位、分子伴侣60kDa在胃癌Hpylori菌株中高表达,而巯基过氧化物酶、二磷酸核苷激酶、S．核糖基同型半胱氨酸裂解酶在慢性胃炎H．pylori菌株中高表达。结论：成功建立了分辨率高且重复性好的胃癌和慢性胃炎H．pylori蛋白的2-DE图谱,并鉴定出两种疾病相关菌株中差异表达的蛋白质点．这些蛋白质点可能在胃癌的发生中起重要作用。     

Iron deficiency anemia after subtotal gastrectomy for gastric cancer

BACKGROUND/AIMS: Sideropenic anemia after a gastrectomy is a frequent complication. The aim of the present study was to evaluate the role of different factors, such as sex, age, atrophic chronic gastritis, Helicobacter pylori infection and iron malabsorption, in iron deficiency after surgery for gastric cancer. METHODOLOGY: Thirty-seven patients who underwent subtotal gastrectomy for carcinoma of the stomach were prospectively studied following a specific three-year protocol. Iron deficiency was evaluated by hemochromocytometric analysis and serum iron-ferritin level assays. RESULTS: Of the different variables analyzed, atrophic chronic gastritis was associated with a lower mean serum iron level, in particular two years after surgery (65mg/dL vs. 103 mg/dL in subjects without gastritis, P<0.01); a correlation between Helicobacter pylori infection of the gastric stump and lower mean serum ferritin level was also found (25+/-6.3 mg/dL vs. 53+/-0.4 mg/dL, P<0.05). On the contrary, no association was observed with the other factors that were evaluated. CONCLUSIONS: Among the factors involved in iron deficiency after gastrectomy for cancer of the stomach, atrophic gastritis seems to be the most important, although Helicobacter pylori infection of the gastric stump also seems to play an important role.     

Molecular alterations in gastric cancer: the role of Helicobacter pylori

Helicobacter pylori has been classified as a human carcinogen contributing to the pathogenesis of gastric cancer. Extensive sero-epidemiological studies and recently animal experiments have established a close link between H. pylori infection and the development of gastric cancer. However, the molecular changes induced by H. pylori directly or the concomitant chronic inflammation of the gastric mucosa, and the impact of these changes on the subsequent development of gastric cancer, remain largely unknown. This review will highlight the present knowledge on the molecular pathogenesis of gastric cancer with an emphasis on molecular and genetic alterations which develop due to chronic infection of the gastric mucosa by H. pylori.     

Helicobacter pylori infection and related gastrointestinal diseases

Helicobacter pylori has been implicated in the pathogenesis of a number of digestive tract disorders, such as chronic active gastritis, peptic ulceration, gastric cancer, and mucosa-associated lymphoid tissue lymphoma. Disease outcome is dependent on many factors, including bacterial genotype, host physiology and genetics, and environmental factors such as diet. Researchers continue to explore the complexities of H. pylori infection, seeking to explain why some individuals have asymptomatic infection, whereas others experience clinical disease. The importance of treating H. pylori infection in patients with gastrointestinal problems has been confirmed in recent years, with clinical trials showing that cure of infection can prevent duodenal ulcer and, to a lesser extent, gastric ulcer recurrence; cure early stage mucosa-associated lymphoid tissue lymphoma; and reduce the chances of developing gastric cancer in high-risk individuals.     

Helicobacter pylori infection following partial gastrectomy for gastric cancer

Gastric remnants are an inevitable consequence of partial gastrectomy following resection for gastric cancer.The presence of gastric stumps is itself a risk factor for redevelopment of gastric cancer.Helicobacter pylori(H.pylori)infection is also a well-known characteristic of gastric carcinogenesis.H.pylori colonization in the remnant stomach therefore draws special interest from clinicians in terms of stomach cancer development and pathogenesis;however,the H.pylori-infected gastric remnant is quite different from the intact organ in several aspects and researchers have expressed conflicting opinions with respect to its role in pathogenesis.For instance,H.pylori infection of the gastric stump produced controversial results in several recent studies.The prevalence of H.pylori infection in the gastric stump has varied among recent reports.Gastritis developing in the remnant stomach presents with a unique pattern of inflammation that is different from the pattern seen in ordinary gastritis of the intact organ.Bilerefluxate also has a significant influence on the colonization of the stomach stump,with several studies reporting mixed results as well.In contrast,the elimination of H.pylori from the gastric stump has shown a dramatic impact on eradication rate.H.pylori elimination is recognized to be important for cancer prevention and considerable agreement of opinion is seen among researchers.To overcome the current discrepancies in the literature regarding the role of H.pylori in the gastric stump,further research is required.     

K-ras mutations in gastric stump carcinomas and in carcinomas from the non-operated stomach.

BACKGROUND/AIMS: Partial gastrectomy is a well-established pre-malignant condition. It is postulated that in the gastric stump an accelerated neoplastic process takes place, similar to that of (intestinal type) adenocarcinoma from the non-operated stomach. K-ras codon 12 mutation is one of the most frequent oncogenic alterations in human solid neoplasms. It is rare in conventional gastric carcinoma and has not been studied in gastric stump carcinoma. The aim of this study was to compare the prevalence of K-ras codon 12 point mutations in gastric stump carcinomas with those in conventional carcinomas from the non-operated stomach. METHODOLOGY: Twenty-four gastric stump carcinomas were compared with 26 conventional gastric carcinomas. Stage, histology, and demographics were comparable in both groups. Mutations in codon 12 of the K-ras gene were examined with a polymerase chain reaction (PCR)-based method and subsequent dot blot hybridization with mutation-specific probes. The results of Helicobacter pylori infection, Epstein-Barr virus infection and p53 immunohistochemistry were partially known from a previous study. RESULTS: In one of the gastric stump carcinomas as well as in one of the conventional gastric carcinomas a K-ras codon 12 point mutation was found. p53 immunohistochemistry results were comparable in both groups. Interestingly, Helicobacter pylori infection rate and Epstein-Barr virus in situ hybridization for EBER1, as previously studied, appeared were significantly different in the two groups. CONCLUSIONS: K-ras codon 12 point mutations are rare in both gastric stump carcinomas and conventional gastric carcinomas. This supports the postulated hypothesis that the pathways of carcinogenesis in both gastric stump carcinoma and conventional gastric carcinoma share common features. However, these groups differ in infection rate of Helicobacter pylori and of Epstein-Barr virus, which suggests that some neoplastic stimuli differ as well.     

Treatment of Helicobacter pylori and prevention of gastric cancer

Gastric cancer is the second commonest fatal malignancy in the world with a high incidence in China. Helicobacter pylori infection is an important factor in the pathogenesis of gastric cancer. Epidemiological studies have shown a strong causal relationship between H. pylori infection and gastric cancer. Animal studies also show that eradication of H. pylori infection, especially at the early stage, is effective in preventing H. pylori-related gastric carcinogenesis. H. pylori eradication leads to regression and prevents the progression of gastric precancerous lesions, but only in a minority of cases. H. pylori eradication appears to be the most promising approach in gastric cancer prevention. The current available data in human studies showed that H. pylori eradication can reduce the risk of developing gastric cancer and this strategy is more useful in patients without atrophic gastritis or intestinal metaplasia. A longer follow-up and additional studies are needed for better understanding this issue.     

缺氧环境下幽门螺杆菌感染与帕金森病的相关性研究

帕金森病(PD)的确切病因及发病机制目前尚未明确。随着对PD的不断深入研究,发现幽门螺杆菌(Hp)感染与PD具有密切的相关性,在缺氧环境中人群胃黏膜长期处于缺氧状态,易导致胃黏膜损伤,增加Hp的感染机会,可能是影响PD胃肠道症状的因素之一,慢性缺氧受损的风险可能导致PD病情的恶化。本文对近年来缺氧环境下Hp与PD之间的相关性研究进行综述。