肥大细胞在幽门螺杆菌相关性胃炎中的作用

目的探讨肥大细胞（MC）在幽门螺杆菌（Hp）相关性胃炎中的作用。方法选择200例行胃镜检查的慢性胃炎患者,取胃窦黏膜分别行组织病理学HE染色及Hp检查（快速尿素酶、改良Giemsa染色）、改良甲苯胺兰染色,分别计算黏膜及黏膜下的完整和脱颗粒MC数。结果MC计数在Hp阳性和Hp阴性组间无统计学差异（P〉0．05）。但前者黏膜内MC脱颗粒者明显多于后者（P〈0．01）;MC计数在活动性炎症组显著高于非活动性炎症组（P〈0．01）。结论MC可能在Hp相关性胃炎的发生发展中起重要作用。     

肥大细胞脱颗粒在幽门螺杆菌致病中的作用

目的 研究肥大细胞（MC）在幽门螺杆菌（H pylori)发病中的作用。方法 选胃镜检查者87例，其中诊断十二指肠溃疡（DU）33例，浅表性胃炎45例，糜烂性胃炎9例。取胃窦、体部活检分别作组织病理学（HE染色）及H pylori检查（快速尿素酶、培养及Warthin-Starry银染），免疫组织化学染色（ABC法）后分别计算粘膜及粘膜下的完整和脱颗粒MC数。结果 MC计数在H pylori阳性和H pylori阴性组间无明显差别（P＞0．05），但前者粘膜内MC脱颗粒者明显多于后者（分别为43％和23％，P＜0．01）。MC计数与粘膜炎症程度无明显关系，但在活动性炎症时显著高于非活动性炎症组（P＜0．05）。各病变组间MC计数也无显著差异。结论 MC可能在粘膜H pylori相关炎症的发生发展中起着重要作用。     

幽门螺杆菌相关性胃病的细胞增殖和凋亡

目的 观察幽门螺杆菌（Hp)及其CagA基因对细胞增殖和凋亡的影响,进而探讨Hp增加胃癌发生危险性的机制。方法 研究对象为慢性浅表性胃炎（CSG）、慢性萎缩性胃炎（CAG）、慢性萎缩性胃炎伴肠上皮化生（CAGIM）、不典型增生（DYS）、胃癌（GC）患者127例及正常对照组（NS）14例。应用ki-67免疫组化技术评价幽门窦上皮细胞增生,用切口末端标记法（TUNEL）检测胃上皮细胞凋亡,应用聚合酶链反应（PCR）技术检测Hp的CagA基因。结果 Hp阳性患者的增殖指数（LI）和凋亡指数（AI）显著高于Hp阴性者或正常对照（P＜0．05和P＜0．01）。CSGHp阳性的LI和AI明显高于Hp阴性者（P＜0．01）,而其余四种胃病Hp阳性患者（P＜0．05）。Hp阳性或阴性CSG、NS组的AI与LI呈正相关,GC患者的AI与LI呈负相关。LI和AI与胃粘膜炎症程度无明显关系。结论 Hp诱导胃粘膜上皮细胞过度增殖和凋亡主要发生在Hp感染的早期,CagA^ Hp与CagA^－Hp促增殖和凋亡作用的能力明显不同,Hp感染通过引起增殖和凋亡比例的失调,最终促进肿瘤发生。     

CagA—Hp抗体IgG与胃炎的组织学分析

目的：研究幽门螺杆菌（Hp)感染与胃炎的关系,方法：对204例慢性胃炎患者胃粘膜进行观察分析,并测定其中137例Hp阳性患者血清C A-Hp抗体IgG水平,与组织学对照,结果：慢 萎缩性胃炎伴肠上皮化生患者血清CagA抗体IgG明显高于对照组IP＜0．01）,其他类型胃炎患者血清CagA抗体IgG水平无明显增高（P＞0．05）,续集：CagA-Hp可能是导致慢性萎缩性胃炎伴肠上皮化生的因素之一,对这类患者应;密切随访观察。     

庄河16村镇胃癌高危人群幽门螺杆菌感染状况普查

目的幽门螺杆菌（Helicobacterpylori，Hp）感染与胃癌的发生关系密切．我们剖析胃癌高发区Hp感染状况及其与胃疾病及胃癌的相关性，旨在为Hp感染及胃癌的综合防治提供依据．方法胃癌高发区16村镇胃癌高危人群3033人，经血清胃蛋白酶原检测及X线初筛出1779例，接受了胃粘膜活检精查．其切片作HE及亚甲兰（MB）染色，观察病理组织学改变及Hp感染情况，同时利用PCR检测Hp．结果Hp总检出率为60．8％．其中男高于女；30岁～59岁组最高（62．4％）；山区（64．4％）高于沿海区（56．7％）；胃窦（36．2％）高于胃角（32．6％）及胃体（31．2％）；以上P＜0．01．胃癌Hp检出率为43．8％；各型胃疾病Hp检出率由高至低，前四位依次为胃粘膜糜烂（90．6％）、胃溃疡（87．0％）、中重度浅表性胃炎（79．8％）及萎缩性胃炎（75．3％），上述各组Hp检出率与轻度浅表性胃炎Hp检出率（6．8％）相比，P＜0．01．与未检出Hp的组织学基本正常胃粘膜0％相比，异型增生（80．0％）及肠上皮化生（77．7％）的Hp检出率皆明显升高，P＜0．01．结论庄河居民Hp感染与胃粘膜糜烂、胃溃疡、中重度浅表性胃炎、萎缩性胃炎等呈明显正相关．庄河不仅胃癌高发且Hp感染亦是高流行．文内尚对有关结果只行了初步探讨，呼吁在我国胃癌高发     

幽门螺杆菌与胃癌的关系

目的为了探索幽门螺杆菌（Hp）与胃癌及其病理类型的关系．方法对住院的经内镜及病理证实的23例胃癌，21例慢性浅表性胃炎及26例十二指肠溃疡患者进行冒窦粘膜Hp检测（采用快速尿素酶试验）及血清Hp-IgG抗体测定（采用ELISA法）．结果Hp在慢性浅表性胃炎、十二指肠溃疡、中晚期胃癌的检出率分别为52．4％，88．5％及78．3％．Hp在十二指肠溃疡及慢性浅表性胃炎的感染率具有明显差异（P＜0．01），而Hp在中晚期胃癌及慢性浅表性胃炎的感染率无差异（P＞0．05）．胃腺癌的Hp检出率高于印戒细胞癌的Hp检出率（P＜0．05）．结论①Hp与中晚期胃癌无明显相关性．②胃腺癌患者的Hp检出率较胃印戒细胞癌者的高．     

肥大细胞在胃感觉过敏患者胃黏膜中的改变

目的：了解国人功能性消化不良（FD）患者是否存在胃机械感觉过敏，对胃感觉过敏患者胃黏膜肥大细胞数量及脱颗粒情况进行研究，探讨肥大细胞在胃感觉过敏中的作用。方法：运用电子恒压器测定40例FD患者和15例正常人的胃感觉阈值。根据感知阈值将23例FD患者分为两组：感觉正常组（FD－N）和感觉过敏组（FD－H）。免疫组化方法染色肥大细胞，计数肥大细胞数；图像分析了解肥大细胞在扩张刺激前后平均吸光度值（A）的变化；电镜观察大细胞超微结构改变。结果：FD患者对胃机械扩张刺激的感知阈值，不适阀值，疼痛阈值均较正常人显著下降（P＜0．01，P＜0．01，P＜0．05），感觉过敏感患者近端胃黏膜肥大细胞数量明显多于FD－N组和对照组（P＜0．05）。刺激前后感觉过敏患者肥大细胞平均A值减少百分数较FD－N组和对照组明显增多（P＜0．05），电镜观察到肥大细胞与神经末梢关系密切，肥大细胞释放的颗粒有向神经末梢靠扰趋势。结论：部分FD患者存在胃机械感觉过敏；胃感觉过敏与胃黏膜肥大细胞数量增多，脱颗粒增加有关。     

幽门螺杆菌感染与白细胞介素-8、粒细胞集落刺激因子含量的关系

目的：探讨幽门螺杆菌（Hp)与胃黏膜白细胞介素（IL）－8和粒细胞集落刺激因子（G－CSF）相关胃炎间的关系。方法：应用酶联免疫吸附试验法测定60例接受胃镜检查患者胃窦黏膜组织培养上清中IL－8、G－CSF的含量，比较Hp感染与非感染患者其含量的差异。其中慢性浅表性胃炎14例，胃溃疡13例，十二指肠溃疡13例，胃黏膜正常者20例。结果：60例受检者中Hp感染40例，其胃黏膜IL－8及G－CSF含量明显高于14非Hp感染者（P＜0．01）。慢性浅表胃炎、胃溃疡Hp阳性者IL－8）及G－CSF明显高于正常组织Hp阳性者（P＜0．01）。慢性浅表性胃炎中，Hp阳性组的IL－8及G－CSF含量高于Hp阴性组（P＜0．05）。结论：Hp感染可以诱导胃黏膜炎症细胞合成和释放IL－8及G－CSF，IL－8及G－CSF可能在Hp相关性胃十二指肠疾病的发病过程中发挥关键作用，是引起炎症反应以及进一步病理损害的重要途径。     

肠易激综合征患者结肠黏膜P物质、血管活性肠肽和肥大细胞的变化

背景：肠易激综合征（IBS）的发病机制尚不明确。目的：探讨IBS患者结肠黏膜P物质（SP）、血管活性肠肽（VIP）、肥大细胞（MC）的变化及其在IBS中的可能作用。方法：20例腹泻型IBS患者、22例便秘型IBS患者和18名正常对照者纳入本研究．取回盲部、乙状结肠黏膜行SP、VIP免疫组化染色和MC计数。结果：IBS患者回盲部、乙状结肠黏膜SP、VIP免疫阳性神经纤维较正常对照组增多、增粗，阳性增强（P〈0．05）。IBS患者乙状结肠黏膜SP、VIP免疫阳性神经纤维与回盲部相比无显著差异。IBS患者回盲部黏膜MC计数较正常对照组显著增高（P〈0．01），乙状结肠黏膜MC计数与正常对照组相比无显著差异。IBS患者乙状结肠黏膜MC计数与正常对照组相比，显著低于回盲部（P〈0．01）。结论：SP、VIP和MC在IBS的发病中起有一定作用。     

非糜烂性胃食管反流病食管黏膜肥大细胞的改变

目的探讨在非糜烂性胃食管反流病（non erosive reflux disease，NERD）患者中食管黏膜肥大细胞的改变。方法选择14例NERD患者（NERD组）与10例正常健康志愿者（对照组），取食管黏膜组织，行免疫组化法染色观察并计数肥大细胞，电镜下观察肥大细胞超微结构。结果NERD组患者食管黏膜肥大细胞数量显著高于对照组（P〈0．01）；黏膜脱颗粒肥大细胞比率显著高于对照组（P〈0．01）；电镜观察到NERD组患者肥大细胞内高尔基体、线粒体及内质网较多，有特异性分泌颗粒，存在较多脱颗粒后留下的空泡。结论NERD患者食管黏膜肥大细胞数增多，功能活跃，可能在NERD的发病机制中具有一定作用。     

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.     

Comparison of He/icobacter py/ori 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. Hematoxylineosin 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.     

胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin6的表达及其与幽门螺杆菌感染的关系

目的探讨胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin 6(Prx6)表达水平变化及其与幽门螺杆菌(H.pylori)感染的关系。方法根据组织形态学将104例临床内镜检查活检标本分为慢性浅表性胃炎(33例)、慢性萎缩性胃炎(25例)、肠上皮化生(32例)及异型增生(14例)4组。用免疫组织化学方法检测组织标本中Prx6的表达水平。用快速尿素酶试验及Warthin-Starry银染检测H.pylori感染。结果 Prx6在慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、异型增生组的阳性表达率分别为39.4%(13/33)、80.0%(20/25)、93.8%(30/32)、92.9%(13/14),过表达率分别为15.2%(5/33)、44.0%(11/25)、81.3%(26/32)、85.7%(12/14)。慢性浅表性胃炎、慢性萎缩性胃炎组H.pylori阳性者Prx6阳性表达率显著高于H.pylori阴性者(P<0.05),肠上皮化生组Prx6的表达在H.pylori阳性者和阴性者无显著差异(P>0.05)。结论在胃黏膜病变演化过程中,Prx6的表达随着胃黏膜病变的进展而增加,H.pylori在胃黏膜病变演化的早期阶段促进了Prx6的表达。     

Mucosal tumour necrosis factor alpha and interleukin-6 in patients with Helicobacter pylori associated gastritis.

The production of tumour necrosis factor alpha (TNF alpha) and interleukin-6 by human antral mucosa during short term culture in vitro has been measured by enzyme linked immunosorbent assay. TNF alpha and interleukin-6 concentrations in culture supernatants were significantly greater (p less than 0.001) in patients infected with Helicobacter pylori, all of whom had chronic gastritis, than in patients who were H pylori negative with histologically normal gastric mucosa. Among H pylori colonised patients, TNF alpha concentrations were significantly higher in those with active gastritis and neutrophil infiltration into the epithelium than in those with inactive gastritis. In contrast, interleukin-6 concentrations were raised in both active and inactive gastritis. This study shows that H pylori gastritis is associated with increased gastric mucosal production of TNF alpha and interleukin-6 and that the nature of the mucosal cytokine response varies with the immunohistology of the disease. Inflammatory cytokines generated locally within the gastric mucosa could be relevant to the gastric physiology of H pylori infection.     

幽门螺杆菌阳性胃炎患者胃粘膜-氧化氮合酶活力变化的意义

目的探讨幽门螺杆菌(Hp)感染时胃粘膜内一氧化氮合酶(NOS)活性和一氧化氮(NO)含量与细胞凋亡改变的意义.方法选择慢性活动性胃炎病人27例,其中Hp阳性者15例,Hp阴性者12例正常对照组10例.应用生物化学方法和切口末端标记法(Tunel)检测胃粘膜组织中一氧化氮产物N0-2水平、NOS活性及细胞凋亡指数.结果Hp感染时,胃粘膜NOS活性、NO-2水平及细胞凋亡指数明显升高,较Hp阴性组差异显著(P＜0.01),胃炎积分数与胃粘膜组织中NOS活性和NO-2水平呈明显正相关(r=0.66和0.84,P＜0.01).当根除Hp后,胃粘膜组织NOS活性,NO-2水平及细胞凋亡指数则显著降低,细胞凋亡指数与NOS活性和N0-2水平呈明显正相关(r=0.68和0.79,P＜0.01).结论Hp感染时可引起胃粘膜组织NOS活化,NO过量产生,细胞凋亡增加,这从又一方面说明Hp感染在胃腺癌发病机制中作用.     

Gastric mucosal secretion of interleukin-10: relations to histopathology, Helicobacter pylori status, and tumour necrosis factor-alpha secretion.

BACKGROUND: Interleukin-10 (IL-10) is an 18 kDa peptide with a range of anti-inflammatory and immunosuppressive properties. AIM: To determine whether this cytokine is involved in gastric mucosal inflammation in Helicobacter pylori infection. METHODS: The production of IL-10 by antral mucosal biopsy specimens during short term in vitro culture was determined by measuring IL-10 content of supernatants by enzyme linked immunosorbent assay (ELISA). H pylori status was determined by serology and histology, with gastritis scored using the Sydney system. Tumour necrosis factor-alpha (TNF-alpha) content of supernatants was also determined in a subgroup of patients. RESULTS: IL-10 secretion was significantly greater in patients with H pylori associated chronic gastritis than in patients who were H pylori negative with normal mucosa/reactive changes, and those with H pylori negative chronic gastritis (p < 0.01 and < 0.05 respectively). There was a significant correlation overall between IL-10 secretion and chronic inflammation score (r = 0.40). Secretion of TNF-alpha, which was significantly higher in H pylori infected patients than uninfected patients with a normal mucosa (p < 0.04), correlated with scores for chronic inflammation and activity (r = 0.39 and 0.38 respectively), but was only weakly correlated with IL-10 secretion (r = 0.22, NS). CONCLUSIONS: Gastric mucosal production of IL-10 and TNF-alpha are increased in chronic gastritis associated with H pylori infection, and mucosal cytokine secretion varies with important histopathological aspects of gastric inflammation. Whereas the secretion of IL-10 in H pylori infection may be protective, limiting tissue damage caused by inflammation, it may also contribute towards failure of the immune response to eliminate the organism.     

广东地区幽门螺杆菌cagA基因与细菌定植及其致病性关系的研究

目的：分析广东地区细胞毒素相关基因（cagA）在幽门螺杆菌（H.pylori)中的分布情况及其与患者性别、年龄的关系；探讨H.pylori cagA在不同胃肠疾病发生中的作用及其与胃粘膜慢性炎症程度及H.pylori定植密度的关系。方法：采用改良Skirrow培养基分离培养得到191株H.pylori，用特定引物对各株细菌的cagA 3′端行聚合酶链反应（PCR）扩增鉴定；对其中83例患者再各取胃窦粘膜2块，经HE及Giemsa染色后观察胃粘膜慢性炎症程度及H.pylori定植密度。结果：广东地区H.pylori cagA阳性者占85.3%(163/191)；H.pylori cagA阳性率与患者的性别、年龄无关；消化性溃疡及胃癌患者的H.pylori cagA阳性率显著高于慢性胃炎患者；cagA阳性H.pylori菌株在胃粘膜表面的定植密度较cagA阴性菌株更高，引起的胃粘膜慢性炎症也更为严重；H.pylori的定植密度与其引起的慢性炎症程度呈正相关。结论：广东地区cagA阳性H.pylori感染者占绝大多数；cagA阳性菌株较cagA阴性菌株具有更强的致病力，可能引起更为严重的胃肠道损害。     

Cell proliferation in Helicobacter pylori associated gastritis and the effect of eradication therapy.

Helicobacter pylori causes chronic (type B) gastritis. The 'intestinal' form of gastric cancer arises against a background of chronic gastritis, and prospective epidemiological studies have shown that H pylori is a major risk factor for this. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging where there is chronic epithelial cell injury associated with H pylori gastritis. In vitro bromodeoxyuridine labelling of endoscopic antral biopsy specimens was used to measure mucosal cell proliferation in H pylori associated gastritis before and after therapy for H pylori triple infection. Cell proliferation was increased in H pylori associated gastritis patients compared with normal controls and patients with H pylori negative chronic gastritis (p = 0.0001; Tukey's Studentised range). There was no difference in antral epithelial cell proliferation between duodenal ulcer and non-ulcer subjects infected with H pylori (p = 0.62; Student's t test). Antral mucosal cell proliferation fell four weeks after completing triple therapy, irrespective of whether or not H pylori had been eradicated (p = 0.0001). At retesting six to 18 months later (mean = 12 months), however, those in whom H pylori had not been successfully eradicated showed increased mucosal proliferation compared with both H pylori negative subjects at a similar follow up interval and all cases (whether H pylori positive or negative) four weeks after completion of triple therapy (p = 0.024). These findings suggest that H pylori infection causes increased gastric cell proliferation and in this way may play a part in gastric carcinogenesis.