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。     

胃粘膜肥大细胞及其脱颗粒与Hp致病关系的探讨

目的：探讨胃粘膜肥大细胞（MC）及其脱颗粒与幽门螺杆菌（Hp）致病性的关系。方法：采用改良甲苯胺蓝染色法检测120例患者胃粘膜中MC计数及脱颗粒细胞所占比例。结果：1．Hp阳性患者胃粘膜MC计数及脱颗粒比显著高于Hp阴性患者（P＜0．01）;2．不同Hp感染胃病患者之间胃粘膜MC计数及脱颗粒比也有差异,消化性溃疡（PU）和慢性浅表性胃炎（CSG）患者胃粘膜MC计数及脱颗粒比显著高于慢性萎缩性胃炎（CAG）患者（P＜0．01）。结论：胃粘膜肥大细胞及其脱颗粒参与了Hp致病而导致胃粘膜受损。     

胆汁反流和幽门螺杆菌感染在远端胃切除术后残胃炎发生中的作用

胆汁反流和幽门螺杆菌（H．pylori）感染是远端胃切除术后残胃炎发生的致病因素，但其确切的作用机制尚未明了。目的：明确胆汁反流和H．pylori感染与远端胃切除术后残胃黏膜炎症的相关性。方法：调查281例胃远端切除术后1年以上接受内镜随访的患者，除外胃镜检查发现恶性肿瘤者。内镜下观察残胃炎严重程度；根据炎症和活动性等指标评估残胃黏膜组织学严重程度。观察胆汁反流和H．priori感染对残胃炎内镜下表现和组织学炎症的影响。结果：81．1％的患者具有1级和1级以上程度的内镜下残胃炎，其H．pylori感染率和胆汁反流发生率均显著高于内镜下无明显炎症的患者（分别为20．6％对1．9％，P〈0．01和88．6％对24．5％，P〈0．0001）。有明显胆汁反流的各级残胃炎患者，胃黏膜慢性炎症和活动性程度与无明显胆汁反流的患者相比无显著性差异（P均〉0．05）；但伴有H．pylori感染的各级残胃炎患者，炎症和活动性分数均显著高于H．pylori阴性患者（P均〈0．05）。结论：远端胃切除术后胆汁反流发生率高，而H．pylori感染率降低。胆汁反流加重残胃炎内镜下炎症，而H．pylori感染与残胃炎内镜下和组织学炎症均相关。     

幽门螺杆菌阴性消化性溃疡的病例对照研究

背景：幽门螺杆菌（H．pylori）感染是消化性溃疡（PU）的重要病因，但H．pyZori阴性溃疡在PU中仍占有一定比例。目的：分析总结H．pyfori阴性PU的临床特点。方法：回顾性分析2004年1月-2007年3月北京大学第三医院住院PU患者的病例资料。从H．pylori阳性患者中以l：l的比例为H．pylori阴性组随机选取性别相同、年龄相近的对照，分析比较两组临床特点。结果：共纳入480例PU患者，男女比例为3．62：1；HpyZori阴性120例，阳性360例，阴性患者中位年龄显著高于阳性患者（P〈0．001）。病例对照研究显示，Hpylori阴性组首发症状存在腹痛者显著少于对照组，有恶心、呕吐症状以及有PU史和非甾体抗炎药（NSAIDs）服用史者显著多于对照组（P〈0．05）。H．pyZori阴性组胃溃疡显著多于对照组，十二指肠溃疡显著少于对照组（P〈0．05）；内镜下慢性非萎缩性胃炎显著少于对照组，息肉显著多于对照组（P〈0．05）：组织学上胃黏膜炎症、炎症程度和活动性显著轻于对照组，淋巴组织增生和肠化生显著少于对照组（P〈0．05）。结论：H．pyfo矗阴性PU占本组PU总数的25．O％，患者年龄相对较大，临床多表现为无痛性溃疡，多有PU史和NSAIDs服用史。溃疡多发生于胃部，黏膜炎症程度较轻，活动性炎症少见。     

胃粘膜肠上皮化生CST—π的表达及其与H.pylori相关性研究

目的：探讨GST－π在胃癌发生过程中表达，及在肠化阶段在GST－π为代表的人体对致癌物解毒系统与H.pylori致毒作用间的相互作用。方法：利用S－P法对219例胃粘膜活检标本进行GST－π单克隆抗体的检测；利用HID－AbpH2.5-PAS粘蛋白组化学技术对171例肠化粘膜进行分型；利用HE及H.pylori-DNA PCR及ELISA方法对正常胃粘膜和肠化粘膜进行H.pylori的检测。对80例H.pylori阳性患进行H.pyrori根除治疗三个月后进行H.pylori、GST－π的检测。结果：正常胃粘膜未见GST－π的表达，肠化粘膜GST－π阳性率为69．5％，胃癌GST－π阳性率为44．4％，高于正常胃粘膜（P＜0．01），低于肠化粘膜（P＜0．05）。H.pylori阴性组SGT－π阳性率高于H.pylori阳性组（P＜0．05）。H.pylori根除治疗后，根除组GST－π表达高于未根除组（P＜0．05）。结论：正常胃粘膜→肠化粘膜→胃癌组织GST－π表达由无→高→低，GST－π弱阳性或阴性的Ⅲ型肠化与胃癌关系密切；肠化粘膜中GST－π弱阳性或阴性表达如合并H.pylori感染，胃癌发生的危险性增加，提示在肠化阶段H.pylori的致毒作用与机体对致癌物的解毒作用彼此相互拮抗。     

根除幽门螺杆菌对胃黏膜病变的影响

幽门螺杆菌（H.pylori）被认为是导致胃黏膜病变的重要因子，根除H.pylori能使胃黏膜病变改善。目的：观察根除H.pylori对胃黏膜病变的影响。方法：予100例经胃镜和组织病理学检查确诊为萎缩性胃炎伴H．pylori感染患者抗H.pylori治疗，1年后复查胃镜和组织病理学，评定组织学变化。结果：所有患者均有不同程度的活动性炎症和慢性炎症。抗H.pylori治疗后，86例被根除。与根除前相比，根除后慢性炎症、活动性炎症、腺体萎缩程度评分均明显下降（P〈0．01），肠化生评分无显著改善。结论：根除H.pylori对胃黏膜病变具有临床治疗意义。     

抗胆汁反流治疗对胃内幽门螺杆菌感染的影响

体外研究发现胆汁可抑制幽门螺杆菌（H.pylori)的生长，但人体内胆汁反流对H.pylori的作用尚不清楚。目的：探讨抗胆汁反流治疗对胃内H.pylori感染的影响。方法：50例经胃镜检查确诊有胆汁反流的慢性胃炎患者纳入本研究。取胃窦黏膜活检标本行组织病理学检查和快速尿素酶试验（RUT），用改良Giemsa染色、RUT或血清H.pylori-IgG检测H.pylori感染情况。患者接受铝碳酸镁治疗（1000mg.tid,4周），治疗结束后复查胃镜和H.pylori感染情况。结果：治疗前患者的H.pylori感染率为66．0％，H.pylori感染者在I、Ⅱ、Ⅲ级胆汁反流性胃炎中的分布无显著差异。治疗后共有48例患者接受胃镜复查，结果显示胃内胆汗反流程度较治疗前明显减轻，H.pylori感染率为64．6％，与治疗前相比无显著差异。合并H.pylori感染者的胃黏膜炎症细胞浸润较非H.pylori感染者为重，且肠化发生率（39．4％）与非H.pylori感染者（11．8％）相比有显著差异（P＜0．05）。结论：合并H.pylori感染胆汁反流患者的胃炎和肠化均较单纯胆汁反流者为重。抗胆汁反流治疗可有效缓解胆汁反流性胃炎，但未能改善胃黏膜的H.pylori感染情况。     

幽门螺杆菌感染对胃黏膜病理变化的影响

背景：幽门螺杆菌(H．pylori)感染已被公认为慢性胃炎和消化性溃疡的重要危险因素，根除H．pylori能加速消化性溃疡的愈合，但其对胃黏膜病理变化的影响尚有待进一步探索。目的：了解根除H．pylori对慢性胃炎胃黏膜病理变化和癌前状态的影响。方法：采用多中心随机对照临床试验和回顾性队列研究，样本选自胃癌高发区：上海郊区的金山区和奉贤区。共纳入360例经内镜检查证实有H．pylori感染的慢性胃炎伴或不伴十二指肠溃疡患者，随机分为两组。治疗组用三联疗法(质子泵抑制剂或Hz受体阻滞剂加两种抗生素)治疗，对照组单纯慢性胃炎患者予西沙必利、十二指肠溃疡患者予西米替丁治疗。在第1年和第4年末随访胃镜，根据H．pylori是否根除将患者分为两组：H．pylori阳性组和H．pylori阴性组。所有胃黏膜活检标本由两位病理科医师统一复读。结果：至第4年末，有120例患者完成全部随访，其中H．pylori持续根除组54例，阳转组5例；H．pylori持续未根除组45例，阴转组16例。持续根除组第1年随访时，活动性炎症比例减少(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例减少(P＜O．05)。持续未根除组第1年随访时，慢性炎症程度增加(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例增加(P＜O．05)，萎缩程度较第1年随访时增加(P＜O．05)。结论：根除H．pylori可以减轻慢性胃炎的炎症程度，防止肠化的发生和发展。     

NSAIDs在幽门螺杆菌相关性胃黏膜病变中的作用

目的 了解NSAIDs与Hellicobecter pylori感染在胃黏膜病变中的作用。方法 患者190例，①病例选择：连续服用NSAIDs治疗2周-12周190例。男性121例，女性69例。平均年龄55岁。②均经胃镜检查和病理组织学检查。对糜烂性胃炎的胃镜诊断和病理诊断胃黏膜炎症分级。③进行H．pylori感染的检测。分为H．pylori感染组与H．prlori阴性组。分析两组的病理组织学改变的特点，了解是否有显著性差异。结果 ①胃镜检查，轻度糜烂106例（55．8％，106／190）。中．重度糜烂84例（44．2％，84／190）。糜烂性胃炎的轻重程度与服药的剂量时间无明显的相关性。②H．pylori感染组46例（24．2％）。H．prlori阴性组144例（75．8％）。③两组病人胃镜诊断的糜烂性胃炎程度无显著性差异（P〉0．05）。④病理情况：H．prlori感染组黏膜中．重度胃炎明显多于H．prlori阴性组（P〈0．01）。⑤病理改变中有淋巴组织增生56例。其中H．prlori感染组有淋巴组织增生22例（47．8％），H．prlori阴性组34例（23．6％）。134例未见淋巴组织增生，其中H．pylori感染组24例（52．2％），H．pylori阴性组110例（76．4％）。两组相比，有显著性差异（P〈0．01）。结论 服用NSAIDs2周以上对胃黏膜有不同程度的损伤。服用NSMDs同时合并H．pylori感染的患者的胃黏膜损伤的严重程度远远高于非感染组。NSAIDs与H．pylori感染是导致胃黏膜损伤的独立危险因子，它们对胃黏膜的损伤作用是叠加的。NSAIDs相关性胃病合并H．pylori感染，根除H．prlori治疗是必要的。     

幽门螺杆菌相关性胃部疾病的病理变迁

目的：探讨幽门螺杆菌（Hp)清除与否与胃黏膜病理转归的关系。方法：191Hp感染的胃炎或溃疡病患者分别随机给予抗Hp或非抗Hp治疗,1年后复查胃镜,病理分型根据悉系统。结果191例患者中,慢性炎症1年后的炎症程度较1年前减轻（P＜0．05）。其中萎缩和肠化生的程度也较前减轻（P＜0．05）,但活性动性炎症和蔼前后比较差异无显著性（P＜0．05）。根据1年后胃镜复查有无Hp清除分为两个队列,Hp清除列有107例,Hp未肖除列有84例,Hp清除列较未清除列1年后慢性炎症程度轻（P＜0．05）活动性炎症者少（P＜0．05）。对不疾病和不同的治疗分层后发现,Hp清除者的胃黏膜炎症程度总是较Hp未清除者轻（P＜0．05）。结论本研究提示,Hp感染与胃黏膜活动性炎症关系较为密切。Hp清除有利于胃黏膜炎症程度的减轻。     

Distribution of cagG gene in Helicobacter pylori isolates from Chinese patients with different gastroduodenal diseases and its clinical and pathological significance

AIM: To determine the distribution of cagG gene of Helicobacter pylori(Hpylori) isolates cultured from patients with various digestive diseases and its relationship with gastroduodenal diseases.METHODS: cagG was amplified by polymerase chain reaction in 145 H pylori isolates cultured from patients with chronic gastritis (n=72), duodenal ulcer (n=48), gastric ulcer (n=17), or gastric and duodenal ulcer (n=8), and the relationship between cagGstatus and the grade of gastric mucosal inflammation was determined.RESULTS: cagG was present in 91.7% of the 145 H pylori isolates, with the rates were 90.3%, 93.8%, 88.2% and 100.0%, respectively, in those from patients with chronic gastritis, duodenal ulcer, gastric ulcer, and gastric and duodenal ulcer. There was no significant difference among the four groups (P＞0.05). The average grade of gastric mucosal inflammation in the antrum and corpus was 1.819±0.325and 1.768±0.312, respectively in cagG positive patients,whereas the average inflammation grade was 1.649±0.297,1.598±0.278 respectively in cagG negative cases (P＞0.05).CONCLUSION: cagG gene of H pylori was quite conservative,and most H pylori strains in Chinese patients were cagG positive.cagG status was not related to clinical outcome or the degree of gastric mucosal inflammation. Therefore, cagG can notbe used as a single marker for discrimination of H pylori strains with respect to a specific digestive disease.     

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-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 gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.     

Changes in the histology and function of gastric mucosa and in Helicobacter pylori colonization during a long-term follow-up period after vagotomy in duodenal ulcer patients

BACKGROUND/AIMS: To investigate changes in the histology and the Helicobacter pylori (H. pylori) prevalence and density of the gastric mucosa, as well as in fasting serum gastrin and serum pepsinogen I, depending on completeness of vagotomy, and in cases of recurrent ulcer, during 14 years after operation in duodenal ulcer patients. METHODOLOGY: 122 vagotomized duodenal ulcer patients were studied twice on average 9 and 14 years after operation. The presence of recurrent ulcer and completeness of vagotomy were assessed simultaneously endoscopically and by endoscopic Congo red test. The histology of the gastric antrum and corpus mucosa was assessed in accordance with the Sydney system. The amount of H. pylori in the specimens was detected by microscopic counting; gastrin and pepsinogen I in serum were determined radioimmunologically. RESULTS: During the 14-year follow-up period, complete vagotomy patients were characterized by a smaller amount of active antrum gastritis and a larger amount of active chronic corpus gastritis involving corpus atrophy in 46% of cases 14 years after operation. Recurrent ulcer patients were characterized by a significantly higher prevalence of high-grade H. pylori colonization and active mucosal inflammation in the antrum as well as by a lower level of active mucosal inflammation and atrophy in the corpus and a higher serum pepsinogen I level compared with complete vagotomy cases. The data of incomplete vagotomy patients without recurrent ulcer became more similar to those recorded for recurrent ulcer patients. CONCLUSIONS: In duodenal ulcer patients, changes in the histology of the gastric antrum and corpus mucosa as well as in H. pylori prevalence and density and in serum pepsinogen I levels are different depending on completeness of vagotomy during 14 years after operation.     

Prevalence of Helicobacter pylori in southern Indian controls and patients with gastroduodenal disease

Abstract The spiral organism Helicobacter pylori has been casually implicated in the genesis of various gastroduodenal diseases. Since these diseases are common in southern India, this study was undertaken to determine the prevalence of H. pylori in the gastric mucosa of asymptomatic adults and patients with various gastroduodenal diseases. H. pylori was detected in the gastric mucosa of 25 of 30 (83.3%) normal volunteers. Prevalence rates in the disease groups were also high, and included 38 of 41 patients with duodenal ulcer (92.6%), 13/16 with gastric ulcer (81.3%), and 85/119 subjects (71.4%) with non-ulcer dyspepsia. Light microscopic examination of the gastric mucosa provided the best method of detecting H. pylori. H. pylori colonization was significantly associated with histological abnormalities, mainly chronic atrophic gastritis (147) and superficial gastritis (11), while only three of 161 H. pylori positive patients had histologically normal antral mucosa. Ultrastructural examination revealed changes in the apical complex of the gastric mucosal cells in response to bacterial adhesion, with mucus depletion and cellular damage. Bacteria were also noted disrupting the tight junctions and entering the intercellular spaces. The high prevalence of H. pylori infection may explain the high incidence of gastritis, duodenal ulceration and gastric carcinoma in this population. However, in this population, the prevalence of infection in asymptomatic individuals was nearly as high as that in duodenal ulcer, underlining the need for further study to identify the differences in host response or bacterial pathogenicity that lead to the development of ulcer in only some individuals.     

Micronutrient antioxidants in gastric mucosa and serum in patients with gastritis and gastric ulcer: does Helicobacter pylori infection affect the mucosal levels?

Free radicals (FRs) play an important role in the pathogenesis of gastroduodenal mucosal inflammation, peptic ulcer disease, and probably even gastric cancer. Various micronutrients protect the gastric mucosa by scavenging FRs. Only limited data is available regarding the concentration of micronutrients in the gastric mucosa in patients with gastritis and peptic ulcer disease. Our aim was to analyze micronutrient antioxidant concentrations in the antral mucosa in patients with gastritis and gastric ulcer and to determine the influence of Helicobacter pylori infection on gastric mucosal antioxidants in patients with gastritis and gastric ulcer. Patients who underwent upper endoscopy for evaluation of dyspepsia were included in the study. Ascorbic acid, alpha-tocopherol, alpha-carotene, beta-carotene, total carotenoids, lutein, cryptoxanthin, and lycopene levels were measured in the sera and antral mucosal biopsies in these patients. The diagnosis of H. pylori was confirmed by histology, urease test (CLO) and serology. Patients with negative endoscopic findings and normal histology and no H. pylori infection served as controls. In patients with gastritis, alpha-tocopherol levels were reduced in serum and mucosa irrespective of H. pylori status, whereas carotenoids and ascorbic acid levels were similar to controls. However, in patients with gastric ulcer, serum and mucosal levels of all micronutrient antioxidants were markedly decreased compared with both controls and patients with gastritis. The degree of depletion of antioxidants was similar in patients with either H. pylori-induced or nonsteroidal antiinflammatory drug (NSAID)-induced ulcers. Patients with gastric ulcer have very low gastric antioxidant concentrations compared to patients with gastritis and normal mucosa. This depletion in antioxidants seems to be a nonspecific response and was not related to H. pylori infection.     

Characteristics of gastritis in patients with Helicobacter pylori-positive reflux esophagitis

BACKGROUND AND AIM: The influence of Helicobacter pylori on gastric acid secretion differs with the status of gastritis. The histological characteristics of gastritis in H. pylori-positive patients with reflux esophagitis have not been fully investigated. We therefore studied the pattern of endoscopic gastric mucosal atrophy and degree of histological gastritis in such patients. METHODS: Subjects comprised 41 H. pylori-positive patients with reflux esophagitis, 41 age- and sex-matched patients with duodenal ulcer, and 41 patients with early gastric cancer. The endoscopic pattern of gastric mucosal atrophy was reviewed, and the degree of histological gastritis in biopsy specimens from the antrum and corpus was assessed in accordance with the updated Sydney system. RESULTS: The grade of endoscopic and histological gastric mucosal atrophy in patients with reflux esophagitis was significantly lower than that in patients with gastric cancer, and the histological scores for antral atrophy and metaplasia in patients with reflux esophagitis tended to be lower than those in patients with duodenal ulcer. In patients with reflux esophagitis and duodenal ulcer, the scores for antral inflammation and activity tended to be higher than those for the corpus. Conversely, the inflammation and activity score in patients with early gastric cancer showed a corpus-predominant gastritis pattern. CONCLUSION: In H. pylori-positive patients with reflux esophagitis, the degree of endoscopic gastric mucosal atrophy is low and histologically there is an antral-predominant gastritis pattern. Therefore, gastric acid secretion in H. pylori-positive patients with reflux esophagitis may be augmented by H. pylori infection.     

Increase in apoptosis and decrease in ornithine decarboxylase activity of the gastric mucosa in patients with atrophic gastritis and gastric ulcer after successful eradication of Helicobacter pylori

OBJECTIVE: Recent reports have shown that patients infected with Helicobacter pylori (H. pylori) have a higher risk of gastric cancer. However, the mechanism of this increased risk is still unclear. In the gastric mucosa, the size of a continuously renewed population of cells is determined by the rates of cell production and of cell loss. Ornithine decarboxylase (ODC) activity is elevated in various gastrointestinal cancers and serves as a marker of mucosal proliferative activity. Apoptosis occurs throughout the gut and is associated with cell loss. Both cell proliferation and cell loss have important roles in H. pylori-associated gastric carcinogenesis. Therefore, we investigated the effect of H. pylori eradication on ODC activity and apoptosis in the gastric mucosa of patients with atrophic gastritis and gastric ulcers. METHODS: Biopsy specimens of the gastric antrum were obtained at endoscopy from 17 H. pylori-positive gastric ulcers patients and 15 H. pylori-positive gastritis patients before and 4 wk after eradication therapy with amoxicillin, omeprazole, and a new anti-ulcer agent, ecabet sodium, and from 10 gastric ulcer patients in whom ulcer healed but H. pylori was left untreated. ODC activity and induction of apoptosis were determined immunohistochemically. RESULTS: H. pylori was successfully eradicated with the triple therapy in 12 (80%) of 15 gastritis patients and 13 (76%) of 17 gastric ulcer patients. ODC activity was present in the gastric mucosa in 21 (84%) patients before eradication but in only four (16%) patients after successful eradication (p = 0.0005). The apoptotic index increased significantly (p = 0.0006) from 4.2% +/- 0.4% before treatment to 7.4% +/- 0.5% after successful eradication. CONCLUSIONS: Successful eradication of H. pylori decreases mucosal ODC activity and increases apoptosis in the gastric mucosa. These findings indicate that by decreasing mucosal cell proliferation and increasing epithelial cell loss, H. pylori eradication may help decrease the subsequent risk of gastric cancer.     

Effect of Helicobacter pylori infection on 24 hour intragastric acidity in patients with gastritis and duodenal ulcer.

Helicobacter pylori status, gastric histology, and 24 hour acidity were studied in 35 gastritis patients, 21 duodenal ulcer patients, and 14 subjects with normal gastric mucosa. H pylori was identified in 21 of 35 patients with chronic active gastritis and in 19 of 21 duodenal ulcer patients, but in none of those with normal gastric mucosa. Mean scores of activity of gastritis were similar in H pylori positive gastritis and duodenal ulcer patients, but were significantly lower in H pylori negative gastritis patients (2.1 (0.8) and 2.3 (0.9) v 1.4 (0.7); p < 0.01, respectively). Median 24 hour hydrogen ion activity (interquartile range) was 21 (8.9-38.0) mmol/l in normal subjects and 23 (11.2-49.0) mmol/l, 19 (7.1-33.1) mmol/l, 44 (25.1-63.1) mmol/l, and 36 (31.6-39.8) mmol/l respectively in gastritis and duodenal ulcer patients with and without H pylori infection. During all predefined time periods, intragastric acidity was significantly higher in patients with H pylori positive duodenal ulcers compared with gastritis patients and normal subjects. However, there was no significant difference in intragastric acidity between the H pylori positive and negative gastritis patients. These results suggest that most of the subjects with chronic H pylori infection have normal gastric acidity.     

Distribution of Campylobacter pylori and Gastritis in the Stomach of Patients with and without Duodenal Ulcer

The presence of Campylobacter pylori and histological changes of gastric mucosa were studied in 50 consecutive patients with gastric complaints. C. pylori was isolated from the antrum, body, and fundus of 40 patients with (n = 20) and without (n = 20) duodenal ulcer. The incidence of gastritis was not significantly different in the antrum of C. pylori-positive patients with and without ulcer. Otherwise, oxyntic mucosa of both body and fundus regions exhibited gastritis in 64.1% of the C. pylori-positive non-ulcer patients, whereas those with duodenal ulcer presented oxyntic mucosa that was histologically normal or near normal.