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。     

Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum.

BACKGROUND: The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS: To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS: Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS: Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS: Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION: The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.     

幽门螺杆菌长期感染与胃黏膜炎症和肠上皮化生的关系

目的探讨幽门螺杆菌(Hp)长期感染及根除与胃黏膜炎症和肠上皮化生(IM)的关系。方法随访71例5年前和78例10年前Hp感染者,分析对比其前后Hp感染情况、胃黏膜炎症和IM的变化。结果5年前Hp阳性71例中,现在52例(73.2％)Hp仍呈阳性,19例(26.8％)转阴;10年前Hp阳性的78例中,现在59例(75.6％)Hp仍呈阳性,19例(24.4％)转阴。Hp长期阳性者5年前和现在及10年前和现在慢性炎症严重程度积分分别为1.635±0.376与1.808±0.301(P>0.05)和1.661±0.398与2.232±0.335(P<0.01);IM的发生率分别为17.3％(9/52)与26.9％(14/52)(P>0.05)和11.9％(7/59)与39.0％(23/59)(P<0.01);IM严重程度积分分别为1.444±0.527与1.667±0.442(P>0.05)和1.571±0.534与2.286±0.488(P<0.05)。Hp转阴者5年前和现在及10年前和现在慢性炎症严重程度积分分别为1.684±0.369与1.369±0.426(P<0.05)和1.647±0.389与1.182±0.396(P<0.01);IM的发生率为31.6％(6/19)和52.6％(10/19);IN严重程度积分分别为1.333±0.516与1.167±0.775(P>0.05)和1.600±0.516与1.100±0.316(P<0.05)。结论Hp感染持续时间越长,胃黏膜炎症越严重,IM程度亦越严重且发生率高;根除Hp不仅能减轻胃黏膜的炎症程度和IM程度,而且能防止IM的发生。     

Effect of Helicobacter pylori eradication on gastric metaplasia of the duodenum.

Helicobacter pylori associated duodenal ulcers occur in patches of gastric metaplasia. The pathogenesis of gastric metaplasia is unclear, but it has been produced in experimental animals by acute injury and has been shown to be present to a greater extent of H pylori positive subjects. This study aimed to discover if gastric metaplasia regressed with eradication of H pylori or healing of duodenal ulcers, or both. Thirty two duodenal ulcer patients with H pylori infection confirmed by biopsy urease test and by antral histological examination were studied. Patients were treated with triple therapy (deNol 240 mg twice daily, amoxycillin 500 mg three times daily, and metronidazole 400 mg three times daily) for two weeks after the first endoscopy and were subsequently re-endoscoped. Three duodenal bulb biopsy specimens were obtained per patient at each endoscopy. Biopsy sections were stained with haematoxylin and eosin to determine the severity of duodenitis, and with diastase periodic acid-Schiff/alcian blue to assess the extent of gastric metaplasia. Slides were assessed by two histopathologists unaware of treatment status. H pylori was eradicated in 63% of subjects and all ulcers were healed at follow up. The median extent of gastric metaplasia at the start of treatment and 6-18 months (median 10) after treatment was compared in the two groups. Gastric metaplasia declined in eradicators from 16% to 8% (p < 0.05) while in non-eradicators there was no significant change (25% initially and at follow up). A positive relation between extent of gastric metaplasia and duodenal inflammation score was present before treatment (r(s) = 0.74, p < 0.001) and was unchanged after treatment in the non-eradicator group (r(s) = 0.89, p < 0.001). In the eradicator group, however, the inflammation score had significantly declined (p < 0.02) and the close relation with gastric metaplasia was no longer present. These results suggest that H pylori itself is at least in part responsible for producing gastric metaplasia of the duodenum.     

十二指肠癌及溃疡组织幽门螺杆菌感染对比

目的研究幽门螺杆菌(Helicobacter pylori,Hp)在十二指肠溃疡及十二指肠癌中的表达及意义。方法采用免疫组织化学染色方法检测40例十二指肠溃疡组织(对照组)和32例十二指肠癌组织(观察组)中Hp表达情况。结果对照组Hp阳性表达率(72.5%)与观察组(12.5%)差异显著(P<0.005)。结论 Hp感染在十二指肠溃疡发生发展中起着重要作用,而与十二指肠癌发生关系不大。     

Helicobacter pylori infection in patients with ulcer recurrence after partial gastrectomy

BACKGROUND/AIMS: Recurrent ulceration of the stomach occurs in some patients after surgery for peptic ulcer disease. The aim of this study is to evaluate the association of Helicobacter pylori infection with ulcer recurrence in patients after partial gastrectomy due to peptic ulcer disease. METHODOLOGY: A total of 186 patients after partial gastrectomy with Billroth I or Billroth II anastomosis presenting with dyspepsia or bleeding were included. An ulcer recurrence was documented by endoscopic examination. Biopsy specimens were taken from the remnant gastric bodies in all patients. H. pylori infection was diagnosed by either a positive biopsy urease test or the presence of the microorganism on histology. RESULTS: Eighty-three (44.6%) patients among the 186 patients had recurrent ulcers. H. pylori infection was found in 29 (36%) patients in the ulcer group and 42 (41%) patients in the non-ulcer group. The incidence of H. pylori infection did not differ significantly between the two groups (P>0.05). CONCLUSIONS: H. pylori infection may not play an important role in the pathogenesis of recurrent ulcer after partial gastrectomy. Other factors should be studied further.     

Relationship between Helicobacter pylori infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer

BACKGROUND: The aim of this study was to determine whether the amount of Helicobacter pylori and the extent of gastric metaplasia in the duodenal mucosa play critical roles in the pathogenesis of duodenal ulcer. METHODS: Duodenal and gastric biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer, gastric ulcer or chronic gastritis. The extent of gastric metaplasia was evaluated histologically and endoscopically using the methylene blue test. In this study, we performed competitive polymerase chain reaction, a highly sensitive and quantitative method for determining the amount of H. pylori gastric and duodenal mucosa. The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in the three patient groups were compared. The correlation between the amount of H. pylori in the duodenum and gastric antrum and extent of gastric metaplasia were also determined. RESULTS: The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in patients with duodenal ulcer were much higher than in patients with gastric ulcer or chronic gastritis. A positive correlation was found between the amount of H. pylori in the duodenum and the extent of gastric bulb and that in the antrum. CONCLUSIONS: The findings of this study indicate that H. pylori colonization in the duodenal bulb may play a critically important role in the pathogenesis of duodenal ulcer and that the amount of H. pylori in the duodenal bulb may be related to the amount of H. pylori in the gastric antrum and the extent of gastric metaplasia in the duodenal bulb.     

Endoscopic duodenitis, gastric metaplasia and Helicobacter pylori

BACKGROUND AND AIMS: The purpose of this study was to investigate the relationship between gastric metaplasia and Helicobacter pylori in patients with endoscopic duodenitis. METHODS: The subjects were 57 patients with endoscopic duodentitis with or without H. pylori-associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori-positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria. RESULTS: There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori-positive and -negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori-negative group, whereas the incomplete type was frequently observed in the H. pylori-positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation. CONCLUSIONS: The complete type of gastric metaplasia occurred frequently without H. pylori infection, whereas the incomplete type was frequently associated with H. pylori infection.     

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.     

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.     

Cyclooxygenase-2 expression in early gastric cancer, intestinal metaplasia and Helicobacter pylori infection

Cyclooxygenase (COX) is the crucial enzyme for synthesis of prostaglandins and occurs in two isoforms COX-1 and COX-2. Whilst COX-1 is constantly expressed in the gastrointestinal tract in large quantities and probably maintains mucosal integrity through constant generation of prostaglandins, COX-2 is induced principally during inflammation. In early gastric cancer and in intestinal metaplasia the expression of COX-2 in patients infected by Helicobacter pylori is increased in intestinal type compared to diffuse type gastric cancer and in intestinal metaplasia. In tumours of mixed type, COX-2 is also increased in the intestinal component compared to the diffuse component. Whilst there has been success of COX-2 inhibition for chemoprevention in colon cancer, a similar role in gastric cancer needs to be carefully assessed in the light of reported adverse effects and whether the precancerous condition, intestinal metaplasia, can truly regress.     

胃粘膜肠化中幽门螺杆菌感染与PCNA,c-erbB-2的表达

目的研究肠化胃粘膜幽门螺杆菌（Ｈｐ）阳性率与ＰＣＮＡ,ｃｅｒｂＢ２表达率之间关系,以探讨Ｈｐ感染在胃肠化发生、发展中作用．方法经病理检查证实的慢性胃炎伴肠化１１６例,对照组非溃疡性消化不良．应用改良ＷａｒｔｈｉｎＳｔａｒｙ法检测Ｈｐ,免疫酶组化ＳＰ法检测ＰＣＮＡ,ｃｅｒｂＢ２的表达,比较Ｈｐ阳性组和阴性组间ＰＣＮＡ,ｃｅｒｂＢ２的阳性表达率．结果胃粘膜肠化者Ｈｐ感染率增高（５８６％ｖｓ１８８％,χ２＝１０７９,Ｐ＜００１）,肠化胃上皮内少见Ｈｐ粘附,Ｈｐ阳性组ＰＣＮＡ,ｃｅｒｂＢ２表达高于阴性组（４８／６８ｖｓ１２／４８,χ２＝９０５,Ｐ＜００５;３６／７４ｖｓ２／４２,χ２＝１３２８,Ｐ＜００１）．结论Ｈｐ感染促进胃粘膜肠化,并使肠化胃粘膜细胞增殖迅速而启动恶性变,故Ｈｐ感染可能促进胃癌的形成．     

Intestinal metaplasia of gastric cardia and carditis in Japanese patients with Helicobacter pylori infection

AIM: The purpose of this study was to determine the prevalence of intestinal metaplasia of the gastric cardia in Japanese patients with Helicobacter pylori infection. METHODS: One hundred and fifty-seven patients with H. pylori infection participated in this study. Four biopsy specimens were taken from antrum, lesser and greater curvatures of stomach, and cardia for histological examination. The patients were divided into three groups: those < or = 39 years of age (group A), those 40-59 years old (group B), and those > or = 60 years of age (group C). RESULTS: The proportions of the patients with intestinal metaplasia of the gastric cardia in the three groups were 12, 39, and 65%, respectively. Their intestinal metaplasia of gastric cardia scores were 0.2, 0.54, and 0.81, respectively (significant difference among groups A, B, and C: p < 0.05), according to the updated Sydney classification. CONCLUSION: The prevalence of intestinal metaplasia of the gastric cardia and carditis in Japanese patients with H. pylori infection was similar to that of metaplasia of antrum and lesser curvature of the stomach.     

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS:. Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS:. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.     

Hp感染与十二指肠溃疡复发及再出血关系的研究

目的探索Hp感染与十二指肠溃疡复发及再出血的关系.方法对58例已治愈并清除Hp感染的十二指肠溃疡患者进行跟踪,症状复发者及时做胃镜检查和Hp检测.结果2年内十二指肠溃疡复发率77.6%(45/58例),其中Hp+86.7%(39/45例),Hp-13.3%(6/45例),P＜0.01;溃疡合并再出血18例,占40%,其中Hp+94.4%,Hp-5.6%,P＜0.01.结论Hp感染是十二指肠溃疡复发及再出血的重要因素.