Lewis blood genotypes of peptic ulcer and gastric cancer patients in Taiwan

AIM: The Lewis b (Leb) antigen has been implicated as a possible binding site for attachment of Helicobacter pylori (H pylori) to gastric mucosa. However, studies both supporting and denying this association have been reported in the literature. Differences in secretor (Se) genotype have been suggested as a possible reason for previous discrepancies. Therefore, we investigated the relationship between Le and Se genotypes and H pylori infection rates in people with peptic ulcer or gastric cancer. METHODS: Peripheral blood samples were obtained from 347 patients with endoscopic evidence of peptic ulcer disease (235 cases of duodenal ulcer, 62 of gastric ulcer, and 50 of combined duodenal ulcer/ gastric ulcer) and 51 patients with gastric cancer on endoscopy. Peripheral blood specimens from 101 unrelated normal volunteers were used as controls. Lewis phenotype was determined using an antibody method, whereas Le and Se genotypes were determined by DNA amplification and restriction enzyme analysis. Gastric or duodenal biopsies taken from patients with endoscopic evidence of peptic ulcer or gastric cancer were cultured for H pylori. Isolates were identified as H pylori by morphology and production of urease and catalase. The H pylori infection status was also evaluated by rapid urease test (CLO test), and urea breath test (13C-UBT). Results of studies were analyzed by chi-square test (taken as significant). RESULTS: H pylori was isolated from 83.7% (303/347) of patients with peptic ulcer disease. Statistical analysis did not show any significant difference in Lewis phenotype or genotype between patients with and without H pylori infection. No significant association was found between Lewis genotype and peptic ulcer or gastric cancer. CONCLUSION: Lewis blood genotype or phenotype may not play a role in the pathogenesis of H pylori infection. However, bacterial strain differences and the presence of more than one attachment mechanism may limit the value of epidemiological studies in elucidating this matter.     

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.     

治疗的依从性、年龄、性别对胃溃疡患者使用三联7天疗法根除幽门螺杆菌治疗的影响

目的研究胃溃疡患者使用三联7天疗法治疗幽门螺杆菌（Helicobacter pylori,H.pylori）感染的根除率,评估患者依从性、年龄、性别对于此类人群根除H.pylori治疗的影响。方法将经胃镜检查确诊为新发胃溃疡,并经活组织病理学检查明确有H.py-lori感染的1 075例患者纳入研究范围,所有入选患者均接受三联（洛赛克或耐信20 mg/次、2次/天,联合克拉霉素500 mg/次、2次/天,与阿莫西林1 000 mg/次、2次/天）7天疗法行根除H.pylori治疗,之后予以耐信或洛赛克20 mg/次、1次/天、治疗49天。所有入选患者系统治疗完成后6-8周复查胃镜。结果40-59岁与60岁以上人群的胃溃疡患者对治疗的依从性差异无显著性,而40岁以下人群对治疗的依从性较差（P〈0.05）。〈40岁、40-59岁和≥60岁胃溃疡患者的H.pylori根除率分别为61.0%、72.7%和81.9%。〈40岁与40-59岁和≥60岁患者的H.pylori根除率差异有统计学意义（P〈0.05）。不同性别胃溃疡患者的H.pylori根除率差异无显著性（P〉0.05）。结论使用三联7天疗法治疗胃溃疡患者的H.pylori感染,H.pylori的根除率较低,患者对治疗的依从性、年龄是影响胃溃疡患者H.pylori根除率的重要因素,而性别对此无影响。     

根除幽门螺杆菌对胃溃疡愈合质量及复发的影响研究

目的探讨幽门螺杆菌（Helicobacter pylori，Up）对胃溃疡愈合质量及复发的影响。方法120例坳阳性活动期胃溃疡患者，口服泮托拉唑、阿莫西林、甲硝唑一周后，继续口服泮托美拉唑5周。治疗结束后复查胃镜取病理组织学检查并检测Hp根除情况，对比却根除组与却根除失败组内镜下溃疡愈合形态差异和愈合质量（包括内镜下再生黏膜成熟度和再生黏膜组织学成熟度）。所有患者随诊1年以上了解溃疡复发情况。结果治疗后92例胃溃疡患者月p检测阴性，坳根除率为80．43％；却根除组与跏根除失败组在内镜下愈合率方面的差异无显著性意义（P〉0．05），但两组在再生黏膜成熟度和再生黏膜组织学成熟度方面的差异有显著性意义（P〈0．01）。坳根除组1年溃疡复发率为4．35％，却根除失败组为21．43％，两组差异有显著性意义（P〈0．05）。结论根除Hp可提高胃溃疡的愈合质量，减少溃疡病复发。     

慢性肝病胃粘膜乙型肝炎病毒表达及幽门螺杆菌感染

目的 探讨乙型肝炎病毒（HBV）的泛嗜性及与幽门螺杆菌（Hp）感染的关系。方法选择慢性乙型肝炎（慢肝）28例、乙型肝炎后肝硬化（肝硬化）44例,共72例作为观察组,无肝病的胃病患者30例作为对照组。受检者常规胃镜检查,取胃窦幽门周围3cm以内活体组织3块,除普通病理检查外,分别做乙型肝炎病毒表面抗原（HBsAg）、乙型肝炎病毒核心抗原（HBcAg）检测及快速尿素酶、品红染色和免疫组化法检测Hp。结果 慢肝组有不同程度的胃粘膜慢性炎症者达92.9％（26/28）、肝硬化组达95.5％（42/44）,其中慢肝组以单纯慢性炎症为多,而肝硬化组以伴萎缩和肠化者为多。72例慢性肝病者中有51例胃粘膜HBV阳性,其中HBsAg、HBcAg双阳性16例;肝硬化组HBV抗原表达高于慢肝组,而HBsAg、HBcAg双阳性者低于慢肝组（P均<0.05）。在慢肝和肝硬化组有炎症的胃粘膜中Hp阳性率分别为76.9％（20/26）、69.0％（29/42）,与对照组相比无显著差别。慢性肝病Hp阳性、阴性者胃粘膜HBV抗原表达率分别为69.8％（37/53）、73.7％（14/19）,亦无统计学差异（P>0.05）。结论 （1）HBV在慢肝及肝硬化患者胃粘膜表达明显,应重视其在胃粘膜病变中的作用,加强防护措施。（2）在胃粘膜中HBV与Hp表达未见相关关系。     

消化性溃疡与ABO血型、Lewis表型分布及幽门螺杆菌感染的相关性研究

目的探讨消化性溃疡（PU）与ABO血型、Lewis表型的分布及幽门螺杆菌（H．pylori）感染的关系。方法70例消化性溃疡患者为研究组,96例健康志愿者为对照组,比较ABO血型、Lewis表型分布和H．pylori感染的差异。结果PU组O型血者占52．9％,明显高于O型血在正常人群中的分布（31．3％,P〈0．05）;在非O型血患者中Lewis表型为Le（a＋b＋）者占51．5％,明显高于Le（a＋b＋）表型在对照组非O型血中的频率（9．1％,P〈0．001）。PU组不同ABO血型者H．pylori感染率比较无统计学差异（P〉0．05）;PU组Le（a-b＋）表型者H．pylori感染率为67．6％,明显高于其他Lewis表型（P〈0．05）。结论ABO血型中O型血者易患消化性溃疡,且非O型血Lewis表型为Le（a＋b＋）者也是消化性溃疡的高危人群。ABO血型间H．pylofi感染比较无显著性差异,Le（a-b＋）表型可能是H．pylori感染的一个危险因素。     

Endoscopic characteristics and Helicobacter pylori infection in NSAID-associated gastric ulcer

Background and Aim: Helicobacter pylori infection and non‐steroidal anti‐inflammatory drugs (NSAIDs) are deeply involved in the etiology of gastric ulcers. The aim of our study was to clarify the endoscopic characteristics and H. pylori infection status of NSAID‐associated gastric ulcers. Methods: The study group comprised 50 patients (23 men, 27 women; mean age 66.5 years) with NSAID‐associated gastric ulcers and 100 sex‐ and age‐matched patients with gastric ulcer associated with other factors (control group). Ulcer morphology, size and number of lesions, onset site and incidence of hemorrhagic ulcers were investigated endoscopically in both groups. H. pylori infection was diagnosed by serology, histology and ¹³C‐urea breath test. Results: Multiple lesions (68% vs 20%, P < 0.001), occurrence in the antrum (56% vs 6%, P < 0.001), and hemorrhagic ulcer (34% vs 4%, P < 0.001) were significantly more prevalent in patients with NSAID‐associated gastric ulcers than in patients with non‐NSAID‐associated gastric ulcer. The H. pylori infection rate was significantly lower in NSAID‐associated gastric ulcer patients than in non‐NSAID‐associated gastric ulcer patients (48% vs 96%, P < 0.001). In the NSAID‐associated gastric ulcer group, the prevalence of H. pylori infection was significantly lower in patients with ulcers in the antrum than in those with ulcers in the angulus or corpus (25% vs 77.3%, P < 0.001). Conclusions: In contrast to non‐NSAID‐associated gastric ulcers, NSAID‐associated gastric ulcers frequently occur in the antrum with bleeding. The rate of H. pylori infection in NSAID‐associated gastric ulcers is significantly lower than that in non‐NSAID‐associated gastric ulcers.     

消化性溃疡患者Hp感染与粘膜血流量

目的研究幽门螺杆菌（Ｈｐ）感染与消化性溃疡（ＰＵ）胃肠粘膜血流量（ＧＤＭＢＦ）的关系．福建省立医院消化内科福建省福州市３５０００１方法采用多普勒激光血流仪测定内镜检查患者的非病灶区贲门、胃体、胃窦部及溃疡或胃炎病灶区的ＧＤＭＢＦ．结果非病灶区ＧＤＭＢＦ以贲门部最高，胃体部次之，胃窦部较低，分别为１．６８±０５５Ｖ，１７０±０４２Ｖ和１３５±０３７Ｖ，均明显高于ＰＵ病灶区０８９±０３３Ｖ（Ｐ＜００１）；伴有Ｈｐ感染的ＰＵ患者病灶区及其它非病灶区ＧＤＭＢＦ均显著低于不伴Ｈｐ感染者．结论Ｈｐ感染可造成胃肠粘膜血流量降低，可能是溃疡病灶难愈或复发的原因之一．     

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.     

胶体果胶铋联合泮托拉唑三联治疗H.pylori阳性胃溃疡的疗效分析

目的观察胶体果胶铋联合泮托拉唑三联对H.pylori阳性胃溃疡的溃疡愈合质量的影响以及根除H.pylori的疗效。方法将经胃镜检查及14C呼气试验确诊的90例H.pylori阳性胃溃疡患者随机分为两组:对照组45例,口服泮托拉唑40 mg bid+左氧氟沙星200 mg bid+阿莫西林1 000 mg bid,连续口服10 d后,停服阿莫西林及左氧氟沙星,继续口服泮托拉唑40 mg qd维持3周;试验组45例,在对照组的基础上加用胶体果胶铋干混悬剂150 mg qid。停药4周后复查14C呼气试验,观察H.pylori根除情况;疗程结束后,胃镜复查评估溃疡愈合情况。结果试验组和对照组H.pylori根除率分别为88.89%、71.11%,两组相比,差异有统计学意义(P0.05);溃疡愈合率分别为86.67%、68.89%,两组相比,差异有统计学意义(P0.05)。试验组溃疡愈合S2期获得率57.78%,显著高于对照组的33.33%(P0.05)。结论胶体果胶铋联合泮托拉唑三联治疗H.pylori阳性胃溃疡是一种高效、简便、安全的临床方案,胶体果胶铋在抗H.pylori、提高溃疡愈合质量上起着重要作用。     

十二指肠胃化生与幽门螺杆菌感染

本文调查了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％,显著高于对照组的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。     

幽门螺杆菌感染对胃粘膜超微结构的影响

目的研究幽门螺杆菌（Ｈｐ）感染及其根除前后胃粘膜超微结构的变化．方法Ｈｐ感染患者１０例经三联疗法２８ｄ．Ｈｐ阴转７例于停药１月后及治疗前内镜下取胃窦粘膜，经切片染色后分别行透射电镜及扫描电镜观察．结果透射电镜显示，Ｈｐ聚集处上皮细胞微绒毛变短、减少或消失，细胞呈毛刺状或外突形成分枝状，细胞膜内侧粘液颗粒聚集，细胞破裂，释放粘液颗粒．扫描电镜下Ｈｐ横卧于微绒毛表面或垂直镶嵌在微绒毛里．应用三联疗法（德诺１２０ｍｇ＋四环素０２５ｇ＋呋喃唑酮１０ｍｇ，４次／ｄ）治疗２８ｄ，停药１月后７例Ｈｐ根除．电镜显示Ｈｐ消失，粘膜细胞变性逆转，上皮细胞及微绒毛结构恢复正常．结论Ｈｐ引起的胃粘膜超微结构损害在根除Ｈｐ后有改善及恢复     

Association of peptic ulcer with increased expression of Lewis antigens but not cagA, iceA, and vacA in Helicobacter pylori isolates in an Asian population

BACKGROUND: Studies in Western populations suggest that cagA, iceA, and vacA gene status in Helicobacter pylori isolates is associated with increased virulence and peptic ulcer disease. AIM: To investigate the relationship between peptic ulcer and expression of Lewis (Le) antigens as well as cagA, iceA, and vacA in H pylori isolates in Singapore. METHODS: Expression of Le antigens in H pylori isolates obtained from patients with dyspepsia was measured by enzyme linked immunosorbent assay. The cagA, iceA, and vacA status was determined by polymerase chain reaction. RESULTS: Of 108 H pylori isolates, 103 (95.4%) expressed Le(x) and/or Le(y), while Le(a) and Le(b) were expressed in 23 (21.3%) and 47 (43.5%) isolates, respectively. Expression of two or more Le antigens (Le(x), Le(y), Le(a), or Le(b)) was significantly higher in H pylori isolated from ulcer patients than in non-ulcer patients (89.6% v 73.2%, p=0.035). There were no significant differences in the prevalence of cagA or iceA1 in H pylori isolates from peptic ulcer and non-ulcer patients (86.6% v 90.2% for cagA; 70.1% v 68.3% for iceA1), and no association of peptic ulcer with any specific vacA genotype. CONCLUSIONS: The present study indicates that peptic ulcer disease is associated with increased expression of Lewis antigens but not cagA, iceA, or vacA genotype in H pylori isolates in our population. This suggests that cagA, iceA, and vacA are not universal virulence markers, and that host-pathogen interactions are important in determining clinical outcome.     

幽门螺杆菌感染与胃粘膜增殖细胞核抗原表达的关系

目的探讨幽门螺杆菌（Ｈｐ）感染对胃粘膜细胞增殖活性的影响．方法采用免疫组化法，观察３４例Ｈｐ阳性的慢性胃病患者（男１９例，女１５例）胃窦粘膜增殖细胞核抗原标记指数（ＰＣＮＡＬＩ），同时以１２例Ｈｐ阴性的慢性胃病患者作对照，并对Ｈｐ阳性患者进行抗Ｈｐ治疗，４周后复查ＰＣＮＡＬＩ．结果Ｈｐ感染胃窦粘膜ＰＣＮＡＬＩ较无Ｈｐ感染显著增高（２９０２±１０２３比１４３１±６８７，Ｐ＜００１）；Ｈｐ根除（ｎ＝２４）后胃窦粘膜ＰＣＮＡＬＩ由２８１１±１１５降至１７６８±９６５（Ｐ＜００１），而Ｈｐ未根除（ｎ＝１０）时则无显著降低（２９１７±８１４→２４４２±７４４，Ｐ＞００５）．Ｈｐ感染时胃粘膜ＰＣＮＡＬＩ与炎症程度正相关（Ｐ＜００５），但与Ｈｐ菌量无相关（Ｐ＞００５）．结论Ｈｐ感染可增加胃粘膜细胞增殖活性，从而增加胃癌发生的危险性，根除Ｈｐ后可纠正这一变化，对预防胃癌发生可能有重要意义．     

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。     

消化性溃疡与幽门螺杆菌L型感染相关性研究

目的　探讨消化性溃疡 (PU)与幽门螺杆菌 L型 (HP- L )感染的关系。方法　取 386例 PU患者胃窦、胃体及十二指肠粘膜组织 ,常规切片后以革兰氏染色和免疫组化染色镜检 HP- L 型细菌 ,并计算检出率。结果　 HP- L 型检出率为 5 3.37% ,其中革兰氏染色和免疫组化染色检出率分别为 5 6 .73%、5 4 .2 9% ,差异无显著性(P>0 .0 5 ) ;胃溃疡、十二指肠溃疡 HP- L 型检出率分别为 5 8.33%、5 5 .5 0 % ,差异无显著性 (P>0 .0 5 ) ;男女患者HP- L 检出率前者 (6 1.18% )明显高于后者 (38.17% ) (P<0 .0 1) ;30岁以下、30岁～、4 0岁～、5 0岁～患者 HP- L检出率依次为 32 .0 5 %、4 1.94 %、5 9.18%、71.79% ,差异显著 (P<0 .0 1)。结论　 PU患者 Hp- L型感染率较高 ,且男性高于女性 ,HP- L型检出率随年龄增长而增高。 PU患者 HP- L型变异可能是导致溃疡迁延不愈、反复发作的重要原因之一     

胃黏膜幽门螺杆菌感染病理组织学专家共识

胃黏膜幽门螺杆菌（Helicobacter pylori, HP）感染是引发胃部疾病的主要危险因素之一,HP也被世界卫生组织等列为明确致癌物。目前临床常用的非侵入性法检测HP具有一定的限制性,如无法明确HP定植位置,也可能因其处于休眠期而漏诊或误诊。相较而言,病理学方法检测HP结果更为精准,可了解组织病变情况,并指导后续治疗与预后判断。组织学检测HP方法众多,不同地区、不同医院的病理医师在检测方法的选择上尚存在较大差异。因此,中华医学会消化内镜学分会病理学组根据我国实际情况制定此共识,旨在规范胃组织标本HP感染的病理诊断,为临床医师提供有关胃黏膜HP感染病理组织学的诊断治疗建议,以提高对疾病的认识和提升疾病治疗效果。     

Helicobacter pylori infection delays the healing of acetic acid-induced gastric ulcer in Japanese monkeys

To clarify the relationship between Helicobacter pylori and the healing of gastric ulcers, we investigated the healing of acetic acid-induced gastric ulcers in the antral mucosa of Japanese monkeys (n=5) infected with H. pylori and in control monkeys without H. pylori infection (n=6). Using H. pylori-infected Japanese monkeys as an experimental model, gastric ulcers were induced endoscopically with acetic acid. Healing of ulcers and factors that influenced healing were studied. Continuous colonization with H. pylori was confirmed in the infected group throughout the observation period; no H. pylori were isolated from the gastric mucosa of the control group. White scarring was not observed in any infected monkeys 4 weeks after ulcer formation, but was observed in one (20%) of five monkeys at 6 weeks and in all five monkeys eight weeks after ulcer formation. In the control group, white scarring was observed in one (16.7%) of six monkeys at 4 weeks and in six monkeys at 6 (P< 0.01 vs infected group) and 8 weeks. The ammonia concentration of the gastric secretions and the grade of inflammation were significantly increased in the H. pylori-infected group compared with the control group (P< 0.01 and P< 0.001, respectively). The volume of intracellular PAS-positive substance was decreased (P< 0.025–0.01) at the ulcer margin in the infected group compared with the ulcer margin in the control group. The proliferation of gastric epithelial cells was markedly accelerated at the ulcer margin in the infected group compared with the ulcer margin in control group (P< 0.025–0.01). Our results strongly suggest that H. pylori infection delays the healing of gastric ulcers.