十二指肠胃化生与幽门螺杆菌感染

本调查了155例十二指肠溃疡旁粘膜的组织病理学变化，并与对照组相比较。结果显示：溃疡旁组织炎症、胃化生和Hp检出率分别为69．7％、75．5%和24．5%，显高于对照组的18．8%、10．4％和4．2％(P＜0．01)．Hp在胃化生组织中的检出率为32．8％，81例不伴胃化生的粘膜中均未检出Hp(P＜0．01)，透射电镜观察胃化生有其特征性改变。提示胃化生可能是溃疡形成的基础，Hp在化生区定植并非是产生溃疡的唯一直接因素，还可能通过其他复杂环节间接起作用。     

胃上皮化生、幽门螺杆菌与十二指肠溃疡关系的探讨

目的：研究胃上皮化生、幽门螺杆菌（HP）与十二指肠溃疡之间的关系。方法：应用特殊染色方法对60例十二指肠溃疡球部活检标本进行形态学观察及HP检测，并以50例正常十二指肠粘膜作对照。结果：胃上皮化生率球溃组（81．7％）高于对照组（26％）（P＜0．005）；球部HP检出率球溃组（50％）高于对照组（14％）（P＜0．005）；球部HP94．6％（35／37）生长在胃上皮化生区，5．4％（2／37）生长在无化生区（P＜0．050），轻度，中度，重度胃上皮化生区HP检出率分别为21．4％，64．3％，70．0％，中－重度胃上皮化生区HP检出率高于轻度化生区（P＜0．05）。结论：胃上皮化生与HP相继作用，形成十二指肠溃疡。     

十二指肠胃上皮化生,胃酸与幽门螺杆菌相互关系研究的进展

传统观点认为,十二指肠溃疡(ＤＵ)的发生与胃酸的过度分泌有关,抑酸治疗能治愈溃疡,但复发率高。当今的研究表明,幽门螺杆菌(Ｈｐ)是ＤＵ的重要致病因素,根除Ｈｐ治疗可促进溃疡愈合,使复发率大大降低。十二指肠球部胃上皮化生(ＤＧＭ)是ＤＵ常见的病理变化,是Ｈｐ能够感染十二指肠的前提。因而推测,胃酸、Ｈｐ与ＤＧＭ之间存在密切的关系,在十二指肠溃疡的发生发展中起着重要作用。一、ＤＧＭ与胃酸许多实验及临床研究表明,ＤＧＭ与高酸分泌有关,酸度越高,ＤＧＭ程度越重。早在1964年,Ｊａｍｅｓ[1]报道在十二指肠酸度高时易于发生ＤＧＭ,…     

胃上皮化生、幽门螺杆菌感染和十二指肠溃疡的关系

近年来大量研究资料表明幽门螺杆菌(Hp)是引起消化性溃疡的重要致病因素,十二指肠溃疡(DU)患者Hp的感染率为90％。正常情况下Hp主要定植于胃型上皮,也有DU患者十二指肠可见胃上皮化生,可供Hp定植引起溃疡形成。我们对79例DU患者的十二指肠胃上皮化生、Hp感染与DU发病及愈合的关系进行分析,并与胃溃疡(GU)、功能性消化不良(FD)患者资料进行对照,分析如下。     

十二指肠胃化生与幽门螺杆菌相关性慢性胃炎

为从组织形态学角度评价幽门螺杆菌(HP)对胃酸分泌的影响,以231例胃体、胃窦及十二指肠粘膜活检病例为研究对象,探讨十二指肠胃化生(GM)与HP相关性慢性胃炎的感染部位、炎症活动度及萎缩之间的关系.结果表明HP在胃窦感染为主时十二指肠GM的发生增加;在冒体感染为主时则相反.十二指肠GM的程度与胃窦炎的活动度成正相关,与胃体炎活动度成负相关;胃窦粘膜萎缩时HP感染可减少十二指肠GM的发生.本文结果提示:HP在胃窦感染时能促进胃酸的分泌,而在胃体感染或胃窦粘膜萎缩时则可抑制胃酸分泌.     

十二指肠球部胃化生与胃酸和Hp感染关系的研究

十二指肠球部粘膜胃化生（DGM）在十二指肠溃疡（DU）的发生和治疗中有重要意义，但DGM与胃泌酸量和幽门螺杆菌（Hp）感染的关系，B前看法不一［1，2］。我们对有、无DGM二组DU患者的基础胃酸量（BAO）、最大胃酸量（MAO）、24小时胃内pH及Hp感染作了检测，探讨DGM与胃酸和Hp感染的相关性。材料和方法一、病例选择1997年1月至1997年7月我院收治DU患者94例，年龄为20～72岁，平均36．8岁，其中男78例，女16例。94例患者经内镜和病理检查确诊DU，其中DGM58例，无DGM36例。除外心、肝、肾等疾病患者。二、检查方法（一）胃镜及…     

十二指肠球部多发隆起病变与幽门螺杆菌和胃上皮化生的关系

目的探讨内镜下十二指肠球部多发隆起病变与幽门螺杆菌（Hp）感染和胃上皮化生等组织学异常关系.方法连续调查86例经胃镜检查证实十二指肠球部多发隆起病变患者,并以40例球部基本正常患者作为对照.病变组Hp阳性患者接受三联根除治疗（奥美拉唑20mg、克拉霉素250mg、甲硝唑400mg,每天2次）,疗程7 d,停药后随访6个月后复查胃镜;病变组Hp阴性者接受奥美拉唑20 mg,每天1次治疗,疗程4～6个月,停药后2周复查胃镜.比较2次胃镜检查结果,包括胃镜下隆起病变程度及球部黏膜胃上皮化生等组织学异常,分析Hp感染与上述胃镜下表现及组织学异常关系.结果对照组患者组织学仅部分发现轻度慢性炎症,未发现球部Hp感染.病变组患者Hp检出率为58.1%,胃上皮化生检出率为57.0%.Hp阳性与Hp阴性患者胃镜下隆起病变程度差异无统计学意义（P＞0.05）,但胃上皮化生检出率更高,程度更严重（P＜0.05）.76例患者复查胃镜,根除Hp或奥美拉唑治疗对Hp阳性或阴性患者球部多发隆起病变无明显作用,但根除Hp后6个月,53.6%（15/28）患者胃上皮化生消失,61.0%（25/41）患者绒毛萎缩恢复正常,所有患者淋巴滤泡完全消失（26/26）,杯状细胞减少完全恢复（25/25）,同时炎症和活动性显著减轻（P值均＜0.01）.奥美拉唑疗效不显著.结论十二指肠球部多发隆起病变患者半数以上有Hp感染.Hp感染与隆起病变伴随组织学炎症密切相关,而与其内镜下表现及严重程度无关.根除Hp可使炎症显著减轻,胃上皮化生范围缩小或消退.     

幽门螺杆菌相关十二指肠溃疡患者中根除幽门螺杆菌与胃食管反流病的关系

幽门螺杆菌 (Hp)相关十二指肠溃疡患者在根除Hp后胃食管反流病 (GERD)发生率是否有增高 ,目前尚有争议[1] 。根除Hp前患者是否有GERD症状、根除Hp前的GERD是否对根除后的GERD发生影响不甚清楚。我们前瞻性地观察了Hp相关十二指肠溃疡患者伴发的GERD与根除Hp后GERD发生的相关性。对象与方法1.对象 :十二指肠溃疡患者 96例均经内镜证实。Hp阳性的判断标准为组织学染色和快速尿素酶试验均为阳性。GERD的诊断依据患者具有典型的烧心、反酸症状 ,且内镜提示反流性食管炎或应用奥美拉唑 2 0mg ,每日 2次 ,连续 1周症状消失或基本消…     

幽门螺杆菌感染与十二指肠球部黏膜胃上皮化生的关系

目的 研究十二指肠球部黏膜幽门螺杆菌(Hp)感染与黏膜胃上皮化生的关系，探讨其在十二指肠球部炎症和溃疡发生中的作用。方法 2002年十二指肠球部黏膜活检的存档蜡块82例，作H-E、改良Giemsa和AB／PAS染色。内镜诊断为基本正常球部黏膜10例；十二指肠球炎47例(其中充血糜烂型16例；隆起型31例)和球部溃疡25例。结果 (1)内镜诊断基本正常的十二指肠球部黏膜，组织学60％有轻中度的炎症细胞浸润，但无胃上皮化生和Hp定植。(2)胃上皮化生是十二指肠球部黏膜最常见的病理变化(37／82，45％)。(3)Hp只有在胃上皮化生的黏膜中才能找到，检出率为76％(28／37)。十二指肠球部溃疡边缘黏膜胃上皮化生发生率(72％)明显高于球炎黏膜(40％)，差异有显著性(P=0．0078)。(4)虽然十二指肠球部溃疡边缘胃上皮化生黏膜的Hp检出率(89％，16／18)明显高于十二指肠球炎黏膜(63％，12／19)，但是两者差异无显著性(P=0．062)。不论何期溃疡Hp检出率均很高，本研究中溃疡活动期、愈合期和瘢痕期分别为15例、6例和4例，其溃疡边缘胃上皮化生中Hp检出率分别高达9／10、5／6和2／2例。结论 十二指肠球部溃疡周围黏膜高发胃上皮化生，使Hp更易于定植，推测如不根除Hp感染，可成为十二指肠球部溃疡复发的重要原因。     

幽门螺杆菌感染对功能性消化不良患者胃酸分泌的影响

目的:探讨幽门螺杆菌(Hp)感染对功能性消化不良(FD)患者胃酸和胃泌素分泌的影响。方法:54例符合FD诊断标准的患者中,Hp阳性23例,Hp阴性31例,所有患者都进行空腹血清胃泌素、基础胃酸排出量(BAO)、五肽胃泌素刺激后的最大胃酸排出量(MAO)和高峰胃酸排出量(PAO)的测定。对照组为Hp阳性的十二指肠溃疡病(DU)患者55例。结果:FD患者中,Hp阳性者与Hp阴性者比较,空腹血清胃泌素(103.1±33.7pg/ml vs 113.3±34.1pg/ml)和BAO(5.21±3.86mmol/h vs 4.80±6.08mmol/h)无明显差异(P>0.05);而Hp阳性者的MAO和PAO分别为16.3±9.30mmol/h和23.6±14.2mmol/h,与Hp阴性者(分别为10.1±8.88mmol/h和14.2±11.3mmol/h)比较,差异有显著性(P<0.05)。Hp阳性的FD患者,其BAO、MAO、PAO及空腹血清胃泌素与Hp阳性的十二指肠溃疡病患者(后者分别为10.4±0.81mmol/h、24.2±1.08mmol/h、31.2±13.1mmol/h和148.5±13.1pg/ml)比较,差异有显著性(P<0.05)。结论:Hp阳性的FD患者,其胃粘膜壁细胞对五肽胃泌素刺激的敏感性增加,刺激后胃酸分泌增高,但增高的程度低于Hp阳性的十二指肠溃疡病患者,提示Hp感染在FD患者的胃酸分泌中可能起一定作用。     

幽门螺杆菌感染十二指肠溃疡患者胃排空功能改变的研究

目的：研究十二指肠溃疡患者幽门螺杆菌感染与胃排空功能的关系。方法;根据Ｇｉｅｍｓａ染色与快速尿素酶检测结果７６例经胃镜证实的ＤＵ分为ＨＰ阴性和ＨＰ阳性两组。健康对照组１３例。用＾９９ｍＴｃ标记法对以上３组对象进行液体与固体胃排空检查。     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

Duodenal gastric metaplasia and Helicobacter pylori infection in high and low duodenal ulcer-prevalent areas in India

Background: Previous reports, based on surgery, showed duodenal ulcer (DU) to be more common in the rice‐eating areas of southern India than in the northern wheat‐eating areas. Aims: Does this difference persist? Can it be explained by risk factors other than diet? Methods: A total of 20 053 records from patients undergoing endoscopy for dyspepsia, and 590 endoscopy patients from two northern and two southern centers in India were studied prospectively. Records were scrutinized to determine the relative incidence of DU and non‐ulcer dyspepsia in wheat‐ and rice‐eating areas. Age, sex, length of history, smoking and medication were recorded. Three antral biopsies and one from each duodenal quadrant were taken. A rapid urease test was carried out on one of the antral biopsies; the others were examined for Helicobacter pylori, gastritis, duodenitis and duodenal gastric metaplasia. Results: The difference in diet‐associated prevalence persisted. No differences in smoking, Helicobacter pylori infection or duodenal gastric metaplasia were found between the two regions, but all three were more common in DU than in non‐ulcer dyspeptic patients from both dietary areas. Conclusions: The dietary differences between the regions remain the only factor to account for the differences in DU prevalence. A strong interrelationship between duodenal gastric metaplasia and cigarette smoking is demonstrated.     

内镜对十二指肠溃疡幽门螺杆菌感染的预测

目的 分析内镜下十二指肠溃疡对H.pylori感染的预测价值。并评价对十二指肠溃疡病人予经验性根除H.pylori治疗的合理性。方法 以盲法比较311例病人胃粘膜病变与H.pylori感染的关系,H.pylori感染以胃粘膜Giemsa染色和^14C-尿素呼吸试验确定,选择十二指肠溃疡作为H.pylori感染的预测指标并计算敏感性、特异性、预测值和似然比。结果 311例病人H.pyloi感染162例,H.pylori感染者十二批肠溃疡发生率显著高于H.pylori阴性之者（21.6%vs4.7%)。以十二指肠溃疡预测H.pylori感染其行异性、阳性预测值和阳性似然比分别为95.3%(C191.9-98.7%)、83.3%(C172.0-94.6%)和4.59。结论 内镜下十二指肠小疡对H.pylori感染具有较高的阳性预测价值;建议临床对十二指肠溃疡病人应于内镜诊断后即直接予经验性根除H.pylori治疗。     

幽门螺杆菌与胃癌的关系

本文报道1994年在福建长乐进行的大规模胃癌防治计划,通过胃镜、血液检查及问卷检查,发现30例胃癌及214例消化性溃疡,幽门螺杆菌的感染率在各类人群中为67％至94％不等。在年龄36岁至65岁组中,长乐地区幽门螺杆菌的感染率明显高于香港,无论是幽门螺杆菌的感染者或非感染者,胃窦肠上皮化生发现率在长乐都高于香港,在长乐,胃窦肠上皮化生发现率高于胃体肠上皮化生。长乐及香港的Cag-A阳性菌株与各种胃疾病有明显关系,在无症状组中,Cag-A阳性菌株在长乐占72％,明显高于香港的29％。Cag-A阳性菌株与胃炎、粘膜萎缩、肠上皮化生、不典型增生和胃癌有明显关系。问卷发现多喝茶及多进食蔬菜有保护作用,而抽烟及饮酒人群或进食咸鱼有较多机会形成胃癌。     

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.