慢性胃炎伴良性结节状改变与幽门螺杆菌及淋巴滤泡的关系

目的研究慢性胃炎伴良性结节状改变与幽门螺杆菌（Hp）及胃黏膜淋巴滤泡的关系。方法从2004年7月1日-2005年6月30日行内镜检查患者中，筛选出胃窦黏膜有良性结节样改变者为研究对象，在患者胃窦黏膜处喷洒靛胭脂作色素内镜观察，确定有结节状形态改变，并在有明显结节处取活检组织3块，其中1块立刻作Hp快速试验，判定有无Hp感染；另外2块送病理检查，观察胃黏膜淋巴滤泡形成和淋巴细胞浸润情况，并采用亚甲蓝-硼酸染色法进一步明确诊断Hp感染情况。结果将胃黏膜良性结节状改变的慢性胃炎患者分为三组：结节性胃炎组、萎缩性胃炎组和疣状胃炎组，患者平均年龄分别为（31．OO±11．62）岁、（58．61±12．14）岁和（51．29±12．99）岁，其中结节性胃炎组患者发病年龄最小（P〈0．01）；Hp感染率分别为92．86％、82．56％和69．89％，其中结节性胃炎组的感染率明显高于其他两组（P〈0．01）；有淋巴组织增生所见依次为94．90％、27．9％、18．28％，其中结节性胃炎患者淋巴组织增生明显高于其他胃炎患者（P〈0．01）。伴有结节样改变的萎缩性胃炎患者中萎缩和肠化生百分率分别为100％和59．3％，远高于疣状胃炎组的7．53％、8．60％和结节状胃炎组的4．03％、0．00％。结论在三种常见的胃黏膜良性结节状改变的胃炎中，结节性胃炎与Hp感染及胃黏膜淋巴滤泡形成之间存在密切相关性。可以把Hp感染及淋巴组织滤泡形成和淋巴细胞浸润作为诊断结节性胃炎的病理诊断依据。     

淋巴细胞性胃炎

淋巴细胞性胃炎是一种特殊类型的胃炎,其组织学特点为胃表面及小凹上皮细胞内大量的淋巴细胞浸润.内镜下表现为胃粘膜皱襞增大增粗、结节状改变和糜烂。病变部位以胃体为主,或涉及全胃,内镜下常诊为痘疮(疹)样胃炎.临床表现为上腹痛、恶心和体重下降及厌食。病因不明,可能与免疫反应有关。应用常规治疗胃病药物无效,而应用免疫抑制剂和激素可取得较好效果.     

慢性糜烂性胃炎合并幽门螺杆菌感染的临床及病理学分析

目的分析慢性糜烂性胃炎(CEG)合并幽门螺杆菌(HP)感染的临床及病理学特点。方法选取胃镜下明确诊断为CEG的200例患者作为研究对象,回顾性分析其HP感染情况,按是否合并HP感染,分为HP感染阳性[HP(+)]组和HP感染阴性[HP(-)]组,观察两组个体差异、镜下及病理学特点。结果 HP(+)组年龄、低密度脂蛋白胆固醇炎症活动性、胃小凹及腺体增生、异型增生和肠上皮化生比例均显著高于HP(-)组(均P0.05)。结论 HP感染可通过增加胃黏膜的不典型增生率和肠化生的发生率从而增加CEG的癌变率。     

胃镜下的隆起糜烂性胃炎与幽门螺杆菌及病理之间的关系探讨

隆起糜烂性胃炎是按慢性胃炎的悉尼分类,胃镜检查得出的诊断,其病理和幽门螺杆菌(Hp)间的关系目前难以确定。我院对2002年间胃镜检查所见的151例隆起糜烂性胃炎进行了一分钟尿素酶试验、病理组织学的Hp检查,探讨二者间关系如下。     

胃粘膜淋巴滤泡的发生与幽门螺杆菌感染

目的：了解胃粘膜淋巴滤泡的发生与ＨＰ感染的关系、胃炎活动程度对其发生的影响以及它在ＨＰ相关性胃十二指肠疾病中的存在状况。方法：本文对６５５例慢性胃、消化性溃疡的患者进行胃镜检查，取粘膜组织作幽门螺杆菌（ＨＰ）检测和组织病理观察。结果 在ＨＰ天津的患者中胃粘膜淋巴滤泡的检出率为６０．１％，而无ＨＰ感染者仅为１７．１％；ＨＰ感染者中，胃窦部粘膜淋巴滤泡的发生率（５１．１％）明显高于胃体部粘膜（１９．３     

淋巴细胞性胃炎的内镜和病理特点及随访分析

目的 :探讨淋巴细胞性胃炎 (LCG)的内镜、病理特点 ,以及根除幽门螺杆菌 (Hp)后对其的影响。方法 :分析 50例LCG的电子胃镜表现和病理所见 ,应用分级法评价淋巴细胞的浸润程度 ,应用PPI三联疗法根除Hp。结果 :LCG多见于中年男性 ,Hp感染率为84%。内镜特点 :90 %以上的病变位于胃窦和胃体的下段 ,特征性表现为多发性或弥漫性隆起样糜烂或脐样糜烂 ,共占 70 % ,可并发十二指肠球部病变 ,占 40 %。病理特点 :全部组织均有淋巴细胞浸润 ,淋巴滤泡形成占 58%。Hp根除后 ,41 .7%患者的胃镜表现胃黏膜大致正常 ;33 .3 %患者表现为黏膜稍充血水肿和花斑样改变 (P <0 .0 5) ;2 5%患者的糜烂灶明显减少 ,主要为散在的平坦性糜烂 (P <0 .0 5) ,而隆起样糜烂消失 ,淋巴滤泡完全消失 ;66.7%患者无淋巴细胞浸润 ,33 .3 %患者为 1级改变。根除Hp后 ,淋巴细胞分级为 0 .33± 0 .49级 (P <0 .0 0 1 )。结论 :LCG有一定的内镜和病理特点。根除Hp后 ,可明显减少淋巴细胞的浸润 ,且可治愈LCG。     

淋巴滤泡形成与幽门螺杆菌致病——313例青年志愿者病理研究报告

作调查了313例青年志愿胃内HP感染状态与胃粘膜淋巴滤泡形成的关系，通过内铙普查，细菌和病理学诊断发现螺杆菌感染率为58．5%(183／313)，淋巴滤泡形成率为28.4%(52／183)，通过研究HP的感染量与淋巴滤泡大小证实了二的正相关关系，并发现淋巴滤泡形成与内镜诊断无关，结合国外的报道提出了淋巴滤泡形成可能是HP感染致胃MALT发生过程中的一个重要步骤。     

原发性胆汁反流性胃炎胃黏膜ghrelin的表达

目的:探讨原发性胆汁反流性胃炎患者胃黏膜ghrelin的表达变化.方法:选取我院2007-06/2007-11就诊的原发性十二指肠胃返流患者96例,分为低反流组和高反流组,同时选取胃镜检查大致正常,没有胆汁反流者30例为对照组.免疫组化法检测胃黏膜ghrelin的表达.结果:ghrelin在浅表性胃炎组、肠上皮化生组、不典型增生组和萎缩性胃炎组中的表达均低于正常对照组(653.822±99.303,98.913±14.079,65.875±13.844,52.290±11.463VS 9 884.420±1 26.362,均P＜0.05).浅表性胃炎组、萎缩性胃炎组和肠上皮化生组中的Hpylori阳性组的ghrelin表达与H pylori阴性组比较均有显著性差异(599.320±87.300 VS 721.950±67.836,47.157±9.582 VS 55.283±11.580,92.700±10.372 VS 107.600±17.560,均P＜0.05).结论:胆汁反流是造成胃黏膜损伤的危险因素,随着胆汁反流程度加重,胃黏膜萎缩程度加重,ghrelin表达减少.     

幽门螺杆菌性胃炎的动物模型

许多研究者认为,幽门螺杆菌(Helicobacter Py-lori,HP)是胃炎和消化性溃疡的一个致病因子,目前对HP 感染的认识有了很快的发展。但是,正如人类的许多疾病一样,如果能建立一个供实验用的HP 感染动物模型,将会使人们对HP相关性胃炎的认识有一个飞跃。为未来研究着想,应优先考虑在常规饲养动物中选择优良的动物作为感染的模型,这样一个动物模型的建立可以帮助完善Koch’s 原则,明确致病机理和治疗方法。     

幽门螺杆菌感染胃粘膜抗体产生细胞的研究

利用免疫组织化学方法对幽门螺杆菌(HP)感染胃粘膜内IgA,IgG和IgM产生细胞进行了研究.结果表明,HP感染引起了胃粘膜内局部抗体产生细胞的增加.其中以IgG和IgM产生细胞增加更着.提示:HP感染时局部体液免疫反应增强,进一步为HP是引起慢性活动性胃炎的病原提供了依据.     

Disappearance of Gastritis after Eradication of Helicobacter pylori: A Morphometric Study

Background: Patients with intestinal disease are at risk of developing selenium deficiency due to impaired intestinal absorption. The aim of the present study was to evaluate selenium status and to identify predictive factors of selenium depletion in patients with gastrointestinal disease. Methods: The concentration of selenium and the activity of glutathione peroxidase in plasma and erythrocytes were measured by fluorometry and by spectrophotometry. Eighty-six patients with Crohn's disease, 40 patients with ulcerative colitis, and 39 patients with various other gastrointestinal diseases were studied. Twenty-seven patients (16%) received home parenteral nutrition. Stool mass, faecal fat, and vitamin B₁₂ absorption were analysed in 100 patients. Results: The plasma selenium concentration was decreased in 85% of the patients receiving supplementary parenteral nutrition and in 20% of the patients receiving oral nutrition, among them in 26% of the patients with Crohn's disease. Almost all patients with ulcerative colitis had normal selenium levels. A statistically significant correlation was found between plasma selenium and vitamin B₁₂ absorption, stool mass, faecal fat excretion, body mass index, P-albumin, P-zinc, and the length of the remaining small bowel. Stepwise regression analyses showed that the strongest predictors of selenium deficiency were stool mass, vitamin B₁₂ absorption, and the length of the small-bowel resection. _Conclusion: Selenium deficiency is common in patients with severe gastrointestinal disorders. The deficiency is mainly related to malabsorption, and a low selenium level was almost invariably present in patients who needed parenteral supplementation due to gut failure.     

Helicobacter pylori-Associated Gastritis Evolution of Histologic Changes over 10 Years

Background: Helicobacter pylori seems to be the commonest cause of chronic gastritis, but the natural course of H. pylori-associated gastritis is largely obscure. Methods: We present a histologic follow-up of 39 patients with H. pylori-positive gastritis. Gastroscopies with stepwise biopsies were performed in all the patients at an interval of 10 years. Results: Of the patients 87% (34/39) had a persistent infection and showed a significant decrease in the grades of antral gastritis, eosinophilic granulocytes, corpus eosinophilic granulocytes, and foveolar hyperplasia and a significant increase in the grade of corpus neutrophilic granulocytes. The quantities of H. pylori as estimated histologically did not change significantly during the follow-up period inpatients with a persistent infection. In the five other patients (13%) the H. pylori infection had apparently disappeared spontaneously, and this was accompanied by decreases in the amount of inflammatory cells in the gastric mucosa. Conclusions: H. pylori infection in the gastric mucosa is chronic and may be associated with both regressive and progressive histologic changes. Spontaneous healing of H. pylori infection is possible and is associated with partial resolution of the inflammatory changes in the gastric mucosa.     

幽门螺杆菌相关性胃炎与淋巴组织增生关系的研究

目的:研究幽门螺杆菌(Hp)相关性胃炎病理改变与淋巴组织增生关系及Hp根治后淋巴滤泡消失情况。方法:光镜观察124例Hp阳性的慢性胃炎三联药物治疗前后和胃溃疡64例、十二指肠球部溃疡98例、残胃胃炎24例及Hp阴性正常胃粘膜25例的淋巴滤泡发生率和聚集强度。结果:Hp阳性胃病淋巴滤泡发生率为,胃溃疡90.6％,十二指肠球部溃疡84％,慢性胃炎72.5％,残胃胃炎54.2％,而正常胃粘膜为4％。抗菌治疗后,慢性胃炎的淋巴滤泡明显减少。淋巴滤泡发生率与炎症程度和活动性明显相关。结论:胃粘膜淋巴组织消长与Hp感染关系密切。     

疣状胃炎外周血T淋巴细胞亚群检测及其临床意义

目的:检测疣状胃炎患者(n=35)外周血T淋巴细胞亚群CD_3+、CD_4+、CD_8+,并与107例慢性浅表性胃炎中的幽门螺杆菌(Hp)感染的患者(n=16)比较。方法:所有患者均通过胃粘膜活检快速尿素酶试验和~(14)C-尿素呼气试验以确定是否有Hp感染,用流式细胞术方法检测疣状胃炎和Hp感染的浅表性胃炎患者外周血T淋巴细胞亚群CD_3+、CD_4+、CD_8+。结果:疣状胃炎Hp感染率明显高于慢性浅表性胃炎者(P<0.01);与Hp感染的浅表性胃炎比较,疣状胃炎CD_3+、CD_8+降低以及CD_4+/CD_8+比值增加(P<0.01,P<0.05)。疣状胃炎中Hp阳性组与Hp阴性组比较CD_8也明显降低(P<0.05)。结论:疣状胃炎发病可能有免疫因素参与。     

Frequency of Helicobacter pylori and Gastritis in Healthy Subjects without Gastrointestinal Symptoms

To investigate the frequency of Helicobacter pylori and gastritis in asymptomatic adults, 30 healthy volunteers underwent upper endoscopy. Biopsy specimens were obtained from the corporeal and antral mucosa of the stomach. The specimens were examined by light microscopy for gastritis and the occurrence of H. pylori. In 12 subjects signs of gastritis were noted at endoscopy, but only in 7 of them was this diagnosis confirmed histologically. No other abnormalities were observed by the endoscopist. Histologic examination was normal in 17 subjects, but in 13 subjects (43%) inflammation was found in the gastric specimens. Ten had inflammation both in the corpus and in the prepyloric specimens, and in six of these subjects H. pylori was discovered. H. pylori was only found in subjects with inflammation in both the corpus and the antrum. Subjects with gastritis were slightly older than subjects with normal gastric mucosa (median age, 47 versus 37 years; not significant). In the group of subjects with gastritis, persons with H. pylori were older than those without (median age, 53.5 versus 36 years; p = 0.05). The results of our study indicate that gastritis is present before colonization with H. pylori occurs. This could imply that H. pylori is not the cause of gastritis but that the presence of gastritis is a prerequisite for colonization of the bacterium in the stomach.     

Serum Gastrin and Mucosal Somatostatin in Helicobacter pylori-Associated Gastritis

Aims: The aims were to study serum gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter pylori infection. Methods: We measured basal serum gastrin concentrations and somatostatin and gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori-positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. Results: Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean ± SEM: 72 ± 7, 46 ± 10, and 42 ± 7ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean ± SEM: 0.80 ± 0.07, 1.03 ± 0.15, and 2.40 ± 0.31 μg/g(protein), respectively). We also found significantly lower antral mucosal gastrin concentrations in subjects with pangastritis and in those with antral gastritis only as compared with controls (mean ± SEM: 62 ± 13, 78 ± 16, and 165 ± 25 μg/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls. Conclusion: These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.     

胃幽门螺杆菌感染与慢性胃炎镜下表现和消化性溃疡关系的探讨

本文报道用快速尿素酶试验法分析的1 717例慢性胃十二指肠疾病的胃幽门螺杆菌(Helicobacter pylori,HP)的感染情况。结果显示皱襞增粗型胃炎、充血/渗出型胃炎、扁平糜烂型胃炎、隆起糜烂型胃炎、胆汁反流型胃炎、出血型胃炎、皱襞萎缩型胃炎的HP感染率分别为70.00％,49.72％,48.86％,47.37％,41.94％,38.1％,34.48％,但无显著性差异。十二指肠溃疡HP感染率高达71.11％,显著高于胃溃疡的60.83％。男性病人HP感染率为47.8％,显著低于女性病人的63.7％。这表明慢性胃炎胃镜下形态学差异与幽门螺杆菌感染率高低无关,十二指肠球部溃疡与HP感染的关系较胃溃疡者更为密切,人群中HP感染存在性别差异。     

慢性浅表性胃炎患者根除幽门螺杆菌后食管酸暴露的变化研究

目的 探讨慢性浅表性胃炎(CSG)患者根除幽门螺杆菌(Hp)后食管酸暴露的变化关系.方法 采用24 h食管PH监测的方法,定量观察Hp阳性CSG患者根除Hp组和对照组3月后食管酸暴露的变化.CSG患者60例,按就诊门诊号随机分为治疗组和对照组.治疗组均采用丽珠唯三联方案,对照组不采用药物治疗.待Hp根除后,对比研究Hp根除组和对照组所测得的24 h食管pH监测参数.结果 Hp根除组和对照组治疗3月后两组24 h食管pH监测主要5项观察指标均无显著性差异,P>0.05.结论 CSG患者根除Hp菌后食管酸暴露无明显改变,Hp可能与GERD发生无关.