原发性胃恶性淋巴瘤与幽门螺杆菌感染的相关性初探

为了探讨原发性胃恶性淋巴瘤(RGML)与幽门螺杆菌(Hp)感染的相关性，本收集39例PGML以及22例巴性胃炎、32例Hp无关疾病的胃粘膜行对照研究。结果：PGML组Hp检出率87．18％，显高于对照的63.64、53.13%（P<0．005)。粘膜相关淋巴样组织(MALT)来源的淋巴留占92.31％，Hp检出率达86．11％，瘤周慢性活动性胃炎及淋巴滤泡检出率分别为84.62、56．41％，且炎症活动程度与Hp分布密度相关。组织学研究提示胃B细胞MALT淋巴瘤与Hp感染相关。     

不同胃粘膜组织中幽门螺杆菌感染与端粒酶的关系

目的：探讨胃癌胃粘膜演变过程中各个不同阶段粘膜组织端粒酶表达规律及幽门螺杆菌（HP）感染的关系。方法：采用端粒酶TPCR－ELISA法检测19例慢性浅表性胃炎（CSG）、15例胃粘膜肠上皮化生（ICM）、15例胃粘膜轻度异型增生、14例胃粘膜重度异型增生、29例胃腺癌组织端粒酶活性，并对其中HP阳性与阴性病变组织的端粒酶阳性率进行对比研究。结果：端粒酶阳性率由CSG→ICM→胃粘膜轻度异型增生→重度异型增生→胃癌逐渐增高，分别为0、40．0％、40．0％、78．6％、79．3％、胃粘膜轻度异型增生66．7％、重度异型增生64．3％、胃癌44．8％。ICM及轻度异型增生组与CSG组比较差异显著(x^2＝5．85，P＜0．05）。各病变组织中HP阳性与阴性组间端粒酶阳性表达率无明显差异。结论：端粒酶激活是胃癌发生的早期事件。HP现行感染与端粒酶阳性表达无明显关系。     

原发性胃恶性淋巴瘤与幽门螺杆菌感染的相关性初探

为了探讨原发性胃恶性淋巴瘤（ＰＧＭＬ）与幽门螺杆菌（Ｈｐ）感染的相关性，收集３９例ＰＧＭＬ与２２例淋巴性胃炎、３２例Ｈｐ无关疾病的胃粘膜作病例对照研究；Ｈｐ感染的确定采用改良的Ｇｉｅｍｓａ染色；ＰＧＭＬ的分类结合组织学和免疫组化染色。结果：ＰＧＭＬ组Ｈｐ检出率为８７．１８％，显著高于对照的６３．６４％及５３．１３％（Ｐ＜０．００５）。粘膜相关淋巴样组织（ＭＡＬＴ）来源的淋巴瘤占９２．３１％，Ｈｐ检出率达８６．１１％，瘤周慢性活动性胃炎及淋巴滤泡检出率分别为８４．６２％及５６．４１％。组织学检测的初步结论为：胃Ｂ细胞ＭＡＬＴ淋巴瘤与Ｈｐ感染相关。     

幽门螺旋菌感染治愈后原发性胃粘膜相关性淋巴样组织淋巴瘤的消退

正常胃粘膜没有淋巴组织,有粘膜相关性淋巴组织的病人大多数都有慢性幽门螺旋菌(HP)感染。有证据显示HP胃炎与胃粘膜相关性淋巴组织型(MALT)淋巴瘤有关。本研究旨在了解根除HP感染对MALT淋巴瘤的影响。 33例同时有原发性低度恶性MALT淋巴瘤的HP胃炎病人进入本研究,口服为期14天的HP根除疗法:奥美拉唑40mg每日三次和羟氨苄青霉素750mg每日三次。 治疗前后均行胃镜检查,在胃窦及胃体部取活检,以便对胃炎进行分类和分级及寻找HP。在肿瘤或可疑处取6～10块标本作组织学检查,其中4个标本进行分子遗传学分析,还     

端粒酶在胃癌及癌前病变组织中的表达及其意义

目的：通过检测胃癌及癌前病变组织端粒酶的活性,探讨在这些病变演化中端粒酶活性表达的规律及其意义。方法：采用端粒酶TRAP－ELISA法定量检测33例胃癌、8例胃粘膜重度异型增生、5例轻度异型增生、 胃粘膜肠上皮化生、19例慢性浅表性胃炎组织端粒酶活性。结果：由慢性浅表性胃炎→胃粘膜肠上皮化生→轻度异型增生→重度异型增生→胃癌,端粒酶阳性率逐渐增高,分别为0％、42．9％、40．0％、75．0％、84．0％。端粒酶阳性率在胃癌及重度异型增生组明显高于其它各组（P＜0．005）。慢性浅表性胃炎与肠上皮化生及轻度异型增生组比较也有显著差异（P＜0．025）,而胃癌与重度异型增生组比较差异无显著性。结论：端粒酶在胃癌的发生中可能具有重要意义。追踪端粒酶阳性的胃癌前病变患者有利于早期发现胃癌。     

胃黏膜相关淋巴组织淋巴瘤BCL10核表达与其对幽门螺杆菌根除治疗无反应相关

背景：经幽门螺杆菌（H．pylori）根除治疗，约75％的早期胃黏膜相关淋巴组织（MALT）淋巴瘤患者可获得完全缓解。肿瘤细胞有BCL10核表达和t（11；18）（q21；q21）可能提示胃MALT淋巴瘤对根除治疗无反应。目的：探讨单纯H．pylori根除治疗对国人早期胃MALT淋巴瘤的疗效，以及肿瘤细胞BCL10核表达和t（11；18）（q21；q21）对治疗方案选择的提示作用。方法：收集19例早期胃MALT淋巴瘤患者，以免疫组化方法检测BCL10核表达，以间期荧光原位杂交方法检测t（11：18）（q21；q21）。所有患者均首选H．pylori根除治疗，并行内镜活检病理随访。结果：本组19例早期胃MALT淋巴瘤患者中10例（52．6％）经单纯H．pylori根除治疗获得完全缓解。10例完全缓解者中2例（20，0％）肿瘤细胞BCL10核表达阳性，9例对根除治疗无反应者中7例（77．8％）阳性，阳性率显著高于完全缓解者（P〈0．05）。14例患者行t（11；18）（q21；q21）检测，8例完全缓解者均未检出该易位，6例对根除治疗无反应者中3例（50．0％）检出该易位．两组检出率差异无统计学意义（P〉0．05）。结论：单纯H．pylori根除治疗可使本组52．6％的早期胃MALT淋巴瘤患者获得完全缓解。胃MALT淋巴瘤肿瘤细胞BCL10核表达与其对根除治疗无反应相关。     

原发性胃恶性淋巴瘤与幽门螺杆菌感染的相关性初探

为了探讨原发性胃恶性淋巴瘤(RGML)与幽门螺杆菌(Hp)感染的相关性,本文收集39例 PGML了以及22例淋巴性胃炎、32例 Hp 无关疾病的胃粘膜行对照研究。结果:PGML 组 Hp 检出率87.18%,显著高于对照的63.64、53.13%(P<0.005)。粘膜相关淋巴样组织(MALT)来源的淋巴瘤占92.31%。Hp 检出率达86.11%,瘤周慢性活动性胃炎及淋巴滤泡检出率分别为84.62、56.41%,且炎症活动程度与 Hp 分布密度相关。组织学研究提示胃 B 细胞 MALT 淋巴瘤与 Hp 感染相关。     

幽门螺杆菌感染与胃粘膜淋巴组织增生

应用６种方法检测２５６例胃粘膜活检标本的幽门螺杆菌（Ｈｐ），总检出率为７０．７０％，其顺序为活动性胃炎＞非活动性胃炎＞正常胃粘膜，慢性萎缩性胃炎＞浅表－萎缩性胃炎＞慢性浅表性胃炎＞正常胃粘膜。胃粘膜淋巴滤泡检出率为４３．３６％，其顺序与Ｈｐ检出率相同。有淋巴滤泡形成者Ｈｐ检出率显著高于无淋巴滤泡形成者（８１．４８％比６５．４９％，Ｐ＜０．００１）；淋巴滤泡形成与腺上皮萎缩和肠上皮化生关系密切。结果提示，Ｈｐ感染诱导的胃粘膜淋巴组织增生及其伴随的免疫反应可能是Ｈｐ相关性胃炎出现胃粘膜腺体萎缩的主要机制。     

幽门螺杆菌基因多态性的地域差异对感染临床结局的影响

已知幽门螺杆菌（H．pylori）是引起人类慢性胃十二指肠疾病的主要致病菌。流行病学资料显示，全球半数以上人群存在H．pylori感染，但大多数感染者胃内并不发生病变．或表现为轻度慢性胃炎，仅小部分感染者发展为萎缩性胃炎、消化性溃疡、胃癌、胃黏膜相关淋巴组织（MALT）淋巴瘤等严重疾病。     

胃粘膜相关淋巴样组织中低度恶性B细胞淋巴瘤细胞对幽门螺旋菌的反应

胃粘膜相关淋巴样组织(MALT)淋巴瘤发生于幽门螺旋菌(HP)感染而形成的MALT,根除HP后瘤体可消退,提示肿瘤的生长直接或间接地依赖HP的刺激。作者将瘤细胞与热杀灭的不同HP菌株共同培养,观察淋巴瘤细胞的增殖和活力。 瘤细胞取于3例胃低度恶性B细胞MALT淋巴     

胃淋巴增生性疾病IgH基因重排的检测及意义

目的 探讨免疫球蛋白重链（ＩｇＨ）基因单克隆性重排的检测对胃ＭＡＬＴ淋巴瘤的诊断及鉴别诊断价值。方法 应用半巢式聚合酶链反应技术检测石蜡包埋的３１例胃ＭＡＬＴ淋巴瘤、２６例淋巴细胞性胃炎及１１例对照标本免疫球蛋白重锭基因重排的克隆性。引物选用互补于ＩｇＨ基因Ｖ区及Ｊ区保守序更的Ｆｒ２,Ｆｒ３。结果 （１）用Ｆｒ３为引物扩增,７４．２％的胃ＭＡＬＴ淋巴瘤获得单克隆性重条带;联合Ｆｒ２扩增,可使其检出     

Lymphocytic gastritis in Helicobacter pylori-positive gastric MALT lymphoma--report of two cases.

Both lymphocytic gastritis and gastric mucosa associated lymphoid tissue (MALT) lymphoma are associated with Helicobacter pylori (H. pylori) infection. However, this association has not been fully elucidated. We report two cases of lymphocytic gastritis in 57-year-old male and 47-year-old female patients which were diagnosed after the H. pylori eradication to treat gastric MALT lymphoma. MALT lymphoma was successfully treated in case 1, but residual MALT lymphoma remained in case 2. During the follow-up endoscopic examinations, several elevated erosions in case 1 and irregular mucosal atrophy in case 2 were newly detected. Biopsy specimens showed marked infiltration of lymphocytes in the surface epithelium (56.6+/-15.9 intraepithelial lymphocytes (IELs)/100 epithelial cells in case 1 and 40.5+/-9.3 IELs/100 epithelial cells in case 2), which were exclusively CD8-positive T lymphocytes. These findings suggest that H. pylori infection may cause a monoclonal proliferation of B lymphocytes, leading to MALT lymphoma as well as polyclonal proliferation of T lymphocytes which subsequently infiltrated into the surface epithelium as a host immune reaction, resulting in lymphocytic gastritis.     

Lymphocytic gastritis and Helicobacter pylori infection in gastric lymphoma.

Lymphocytic gastritis and primary gastric lymphoma are rare conditions with unknown aetiology. It has recently been suggested that Helicobacter pylori has a role in the pathogenesis of both of them. The occurrence of lymphocytic gastritis and H pylori was studied in a series of patients with primary gastric lymphoma. The cases of primary gastric lymphomas (n = 35) diagnosed in years 1970-1993 were identified. The specimens of 22 cases contained gastric mucosa sufficiently so that the number of intra-epithelial lymphocytes, severity of gastritis, and occurrence of H pylori could be studied. Lymphocytic gastritis was detected in seven of 22 patients (32%), and in most cases both in antral and body mucosa. Atrophy of the body glands was significantly more severe in lymphocytic gastritis patients. H pylori was detected in 13 of all 22 patients (59%); two of seven lymphocytic gastritis patients (29%), and 11 of 15 (73%) of patients without lymphocytic gastritis were H pylori positive. Patients with gastric lymphoma have significantly increased prevalence of lymphocytic gastritis. Rarity of H pylori in these patients might be connected with atrophic changes in body mucosa. Further studies are needed to show the significance of lymphocytic gastritis as a precursor of gastric lymphoma.     

CD4 + Th1-cells Predominate in Low-grade B-Cell Lymphoma of Gastric Mucosa-associated Lymphoid Tissue (MALT type)

Background: Little is known about the function of T cells in the inflammatory infiltrate in Helicobacter pylori -associated gastritis and B-cell lymphoma of mucosa-associated lymphoid tissue (MALT type). Previous studies have proposed a dominant Th1-type response in low-grade MALT lymphoma consistent with the Th1 response observed in H. pylori -associated gastritis. Methods: We performed a novel flow cytometric approach in which CD3 panning for enrichment and activation of small numbers of T cells and intracellular cytokine analysis were combined to selectively characterize the cytokine profile of T cells (IFN- &#110 for Th1) derived from the gastric mucosa of 23 patients with low-grade MALT lymphoma stage IEI 1 (lymphoma infiltration of mucosa/submucosa sparing the muscularis). Endosonography was performed in each case to control the depth of lymphoma infiltration. For comparison, 19 patients with H. pylori -positive gastritis were also analysed. Results: There was a CD4/CD8 ratio of 4 in patients with MALT lymphoma and of 2 in chronic gastritis. The proportion of IFN- &#110 producing cells within the CD4- positive T-cell population in MALT lymphoma was 22%; in chronic gastritis it was 13% while no such difference could be encountered in CD8-positive T cells. Conclusions: The data point towards a dominant intratumoral IFN- &#110 dominated T-cell response associated with early low-grade MALT lymphoma. A polarized IFN- &#110 dominated Th1-type response may either contribute to the inability of the immune system to eradicate H. pylori infection, thereby promoting the activation status of the lymphocytic infiltrate in low-grade MALT lymphoma, or may mirror a concomitant tumor-specific T-cell response accompanying early stages of tumor progression.     

Interobserver variation in the histopathological assessment of malt/malt lymphoma: towards a consensus

BACKGROUND: The classification of mucosa associated lymphoid tissue (MALT) lymphoma is based on characteristic morphologic and immunophenotypic patterns, with distinctive chromosomal aberrations. The critical first step is diagnosis on evaluating H&E-stained sections. We performed an inter-observer study to determine the degree of agreement among pathologists in evaluating gastric lymphocytic infiltrates for MALT lymphoma. METHODS: A set of 41 H&E-stained gastric sections (36 endoscopic biopsies and 5 surgically resected sections) that ranged from simple gastritis to primary gastric lymphoma was reviewed separately and independently by 17 participants including hematopathologists, pathologists with a special interest in gastrointestinal pathology, and general pathologists. The participants were from the United States, Europe, and Japan. Results were entered into a standardized data collection form and the results were analyzed using kappa statistics. Monte Carlo simulation was used to adjust for multiple biases. RESULTS: Overall, interobserver reproducibility in the morphologic evaluation of gastric MALT was suboptimal. The kappa statistic was 0.3 for simple gastritis, low-grade MALT and for high grade MALT lymphoma. Monte Carlo simulation suggested that the degree of disagreement was directly related to the pathologist's experience in evaluating gastric biopsies for MALT lesions. However, after conjointly reviewing all cases, the Houston workshop agreed on findings that would increase the reproducibility of diagnosis, especially for pathologists with limited experience with this disease. These included the availability of macroscopic data, extensive sampling, the presence of lymphoepithelial lesions, immunophenotyping and particularly abnormal mucosa localization of B-cells, in addition to other molecular finding such as monoclonality and translocation t (11;18). The group also agreed on the need for standardizing the terminology currently used to facilitate future comparison between studies. CONCLUSIONS: Though the study shows poor agreement on morphologic MALT lymphoma categorization, the Houston workshop suggested recommendations that should increase the diagnostic accuracy and reproducibility of MALT lymphoma diagnosis. A follow up workshop will be organized to measure the diagnostic reproducibility for MALT lymphoma using the suggested recommendations.     

HP阳性浅表性胃炎与弥漫型胃癌的关系探讨

利用粘液组化法对２８２例胃癌活检标本进行分类，同时用硼酸美蓝蓝染色法对胃癌癌旁粘膜作组织切片检测ＨＰ。结果：１５０例肠型胃癌中其癌旁粘膜以萎缩性炎症为主，占７９．３３％，ＨＰ检出率为３６．６７％；１１６例弥漫型胃癌中，癌旁以浅表性胃炎为多见（６２．９３％），总ＨＰＢ是性率为５７．７５％，其中７３例癌旁少表性胃炎，６９．８６％见ＨＰ感染。同时发现青年组中弥漫型胃癌的发生率二倍于肠型胃癌。显示弥漫型胃     

端粒酶在胃粘膜活检组织中的表达及其与幽门螺杆菌关系的 …

目的：探讨幽门螺杆菌（ＨＰ）感染与端粒酶表达在胃癌发生发展中的意义。方法：采用ＴＲＡＰ－银染法对１００例胃粘膜活检标本进行端粒酶活性检测。结果：ＨＰ感染率在慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生及胃腺癌中逐渐升高,且ＨＰ阳性胃癌组端粒酶阳性率（９３．８％）明显高于ＨＰ阴性组（５０．０％）（Ｐ〈０．０１）。结论：ＨＰ感染在胃癌变中有非常重要的生物学意义,端粒酶有可能成为胃癌早期诊断的理想标记物。     

CD4+ Th1-cells predominate in low-grade B-cell lymphoma of gastric mucosa-associated lymphoid tissue (MALT type).

BACKGROUND: Little is known about the function of T cells in the inflammatory infiltrate in Helicobacter pylori-associated gastritis and B-cell lymphoma of mucosa-associated lymphoid tissue (MALT type). Previous studies have proposed a dominant Th1-type response in low-grade MALT lymphoma consistent with the Th1 response observed in H. pylori-associated gastritis. METHODS: We performed a novel flow cytometric approach in which CD3 panning for enrichment and activation of small numbers of T cells and intracellular cytokine analysis were combined to selectively characterize the cytokine profile of T cells (IFN-gamma for Th1) derived from the gastric mucosa of 23 patients with low-grade MALT lymphoma stage IEI1 (lymphoma infiltration of mucosa/submucosa sparing the muscularis). Endosonography was performed in each case to control the depth of lymphoma infiltration. For comparison, 19 patients with H. pylori-positive gastritis were also analysed. RESULTS: There was a CD4/CD8 ratio of 4 in patients with MALT lymphoma and of 2 in chronic gastritis. The proportion of IFN-gamma producing cells within the CD4-positive T-cell population in MALT lymphoma was 22%; in chronic gastritis it was 13% while no such difference could be encountered in CD8-positive T cells. CONCLUSIONS: The data point towards a dominant intratumoral IFN-gamma dominated T-cell response associated with early low-grade MALT lymphoma. A polarized IFN-gamma dominated Th1-type response may either contribute to the inability of the immune system to eradicate H. pylori infection, thereby promoting the activation status of the lymphocytic infiltrate in low-grade MALT lymphoma, or may mirror a concomitant tumor-specific T-cell response accompanying early stages of tumor progression.