CHANGES IN MUCOSAL PHOSPHOLIPID‐RELATED PROTECTION IN SOME GASTRIC DISEASES

Background: Phospholipids play an important role in gastric mucosal protection. The purpose of the present study was to investigate changes in various phospholipids in the fundic and pyloric gland mucosae of patients with gastric mucosal disease. Methods: One hundred and five patients with superficial gastritis, duodenal ulcer, gastric ulcer or gastric cancer were studied. Patients underwent endoscopy to obtain biopsy specimens from both the fundic and pyloric gland mucosae. The phospholipid contents were measured by high performance liquid chromatography. Results: Total phospholipid level was significantly greater in the fundic gland mucosa than in the pyloric gland mucosa (P = 0.037), and the level in the fundic gland mucosa was high in all four gastric diseases studied. The difference was significant in patients with gastric ulcers (P = 0.0156). Total phospholipid levels were the highest in superficial gastritis, followed by duodenal ulcer, gastric ulcer and gastric cancer. In all four gastric diseases, phosphatidylserine (PS), phosphatidylethanolamine (PE), and phosphatidylcholine (PC) levels were high, while phosphatidylinositol, lysophosphatidylcholine, and sphingomyelin levels were low. The PE and PC levels were higher in the fundic gland mucosa than in the pyloric glandular mucosa, whereas the PS level was higher in the pyloric gland mucosa than in the fundic gland mucosa. Conclusions: The fundic gland mucosa has stronger phospholipid‐related protection than the pyloric gland mucosa, based on the levels of mucosal phospholipids. The main phospholipids for gastric mucosal protection are PC and PE (in the fundic gland mucosa) and PS (in the pyloric gland mucosa). Phospholipid‐related protection is strong in superficial gastritis and duodenal ulcer, but is reduced in the pyloric gland mucosa in patients with gastric ulcers, and in both gastric gland mucosae in patients with gastric cancer.     

胃十二指肠疾病幽门螺杆菌检出的意义

目的:研究幽门螺杆菌(Hp)与消化性溃疡及慢性胃炎致病的关系。方法:因胃十二指肠疾病而做胃镜的患者,采取胃粘膜进行组织快速检菌,一分钟尿素酶(1min UT)试验和血清间接免疫荧光法进行检菌分析。结果:对5000例胃及十二指肠疾病Hp的组织检出率为88.1％。1min UT阳性率为62.9％,两种检菌法有显著差异(P<0.01)。十二指肠溃疡Hp检出为96.0％,胃癌和萎缩性胃炎Hp感染率为50.0％和59.2％,而1min UT只有41.5％阳性率。结论:胃癌和萎缩性胃炎均有粘膜层萎缩,腺体减少、粘液分泌功能降低,Hp茵不能适应强酸环境下生存。十二指肠溃疡和慢性胃炎多伴引起幽门口水肿和幽门变型,胃排空减缓。是导致Hp茵高检出率的重要因素。     

Epithelial cell proliferation in human fundic and antral mucosae

Epithelial cell proliferation in the fundic and antral mucosae was studied in 19 duodenal ulcer patients, 11 patients having undergone fundic superselective vagotomy for duodenal ulcer, and 10 controls. This was achieved throughin vitro incorporation of tritriated thymidine in mucosal biopsies and radioautography. Except for increased fundic mucosal height, duodenal ulcer patients did not differ from controls for all parameters studied. In vagotomized patients, as compared to the other two groups, the labeling index was significantly enhanced in the innervated antral mucosa where atrophic gastritis developed, but there was no change in the labeling index and no worsening of mucosal inflammation in the denervated fundic mucosa. The only abnormality in the latter was a striking expansion, towards the surface, of the proliferative area within the fundic pit. The labeling indices and the degree of gastritis in gastric mucosae are significantly correlated in control and duodenal ulcer patients. After superselective vagotomy, this correlation still existed in antral mucosa (r=0.88, P<0.001) but not in fundic mucosa. If findings in antral mucosa, after superselective vagotomy, seemed related to gastritis lesions, those in fundic mucosa were not and may indicate an alteration due to the vagotomyper se.This work was supported by the Institut de la Santé et de la Recherche Médicale (INSERM), France.     

Enzyme Immunoassay of Gastric Luminal Prostaglandin E2 in Duodenal Ulcer Disease

A highly sensitive enzyme immunoassay was used to determine gastric juice prostaglandin E2 (PGE2) levels in control subjects with or without gastritis and in both active or inactive duodenal ulcer patients. Mean pentagastrin-stimulated PGE2 concentration was significantly lower in patients with duodenal ulcer than in control subjects considered as a whole group (with or without gastritis). However, no such difference was found between duodenal ulcer patients and controls showing histologically normal gastric mucosa. On the other hand, controls with chronic superficial gastritis had PGE2 levels significantly higher than those of histologically normal subjects and duodenal ulcer patients. Therefore, it seems unlikely that an absolute gastric PGE2 deficiency is involved in the pathogenesis of duodenal ulcer disease. However, the possibility that PGE2 synthesis could be deficient in relation to the prevailing level of mucosal inflammation cannot be excluded.     

Gastric mucosal prostaglandin E2 levels in gastric non-ulcer and ulcer patients with chronic renal failure or without renal disease, and in healthy subjects

Investigations were carried out as to whether a disturbance in the formation of cytoprotective prostaglandin (PG) E2 in gastric mucosa is implicated in chronic renal failure. PGE2-like immunoactivity in gastric mucosal specimens was measured in individuals with chronic renal failure (creatine clearance less than 10 ml/min), in individuals without any renal disease, presenting either gastric ulceration or not, as well as in healthy subjects. Regardless of the group of patients, compared to normal mucosa a significant decrease in PGE2-like immunoactivity (about 50-70%) was found in mucosa from atrophic gastritis but not from superficial gastritis. Whenever patients of the control group or patients with kidney disease suffered from ulcers, PGE2-like immunoactivity showed a decrease of about 60-70% in the non-ulcerated mucosa compared to that of non-ulcer subjects. Moreover, ulcer patients showed the same frequency of gastritis and similar mucosal PGE2-like immunoactivity in their non-ulcerated mucosa. Furthermore, compared to the tissue from the ulcer edge, independent of the presence of renal disease, a relative deficiency of PGE2-like immunoactivity of about 50-60% was detected in the non-ulcerated mucosa of ulcer patients. We therefore conclude that chronic renal failure probably has no impact on PGE2 formation in the gastric mucosa. All told, relative mucosal PGE2 deficiency in gastric ulcer disease seems not to be correlated with chronic renal failure.     

慢性胃炎及消化性溃疡诱生型一氧化氮合酶表达和Hp感染的意义

目的探讨一氧化氮在慢性胃炎及消化性溃疡发病机制中的作用，以及ＮＯ和Ｈｐ感染的关系．方法用免疫组化法对正常对照者６例，慢性胃炎５６例及消化性溃疡患者１６例的胃粘膜标本进行检测，观察ｉＮＯＳ表达强度．并用改良Ｇｉｅｍｓａ法同步检测Ｈｐ感染状况．结果ｉＮＯＳ染色定位于胞质，在正常人胃及十二指肠粘膜细胞和腺体均有表达．慢性浅表性胃炎组呈过度表达，其平均表达强度明显高于对照组及慢性萎缩性胃炎组（Ｐ＜００１）．慢性萎缩性胃炎组平均表达水平和对照组比较差异无显著性（Ｐ＞００５）．慢性胃炎组ｉＮＯＳ表达强度与其Ｈｐ分级间呈明显正相关（Ｐ＜００５）．消化性溃疡组平均表达水平较对照组增强（Ｐ＜００５），其ｉＮＯＳ表达强度和Ｈｐ分级间相关性不明显（Ｐ＞００５）．结论ｉＮＯＳ活性增强和过度表达可能在慢性胃炎和消化性溃疡的发病机制中发挥一定作用，并可能是Ｈｐ感染导致慢性胃炎的相关发病机制之一．     

Peptic ulcer and chronic gastritis: their relation to age and sex, and to location of ulcer and gastritis

The progression, age-behaviour and profiles of chronic gastritis were studied in 460 patients with active gastric or duodenal ulcer, and in 226 patients with ulcer scar. The results were compared with those obtained from a sample of subjects representing the general population. In patients with ulcer or ulcer scar, the progression of chronic gastritis was more rapid in antrum than in body mucosa, and was more rapid in patients with proximal ulcer in those with distal ulcer or in controls. In the body the progression of gastritis was significantly slower in patients with duodenal or juxtapyloric ulcer than in patients with proximal ulcer or in nonulcer controls: body gastritis tended to remain on the same level at all ages whereas it showed a steady progression with age in the nonulcer controls. The degree of gastritis showed a tendency to increase along the shift of ulcer to more proximal in the stomach; the prevalence of gastritis of pure B type (moderate or severe atrophy in antrum, but no atrophy in body mucosa) correspondingly increased along this shift. Severe antral atrophic gastritis was found in 7 per cent of proximal active gastric ulcers and in 20 per cent of proximal ulcer scars. The progression of antral and body gastritis was on the whole more rapid in males than in females irrespectively of the location of ulcer. We conclude that gastritis in different types of ulcers shows characteristic patterns of distribution, dynamics and progression with age. The high prevalence of severe grades of atrophic antral gastritis may also be of significance in regard to the pathogenesis of gastric cancer.     

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.     

Etiology and management of chronic gastritis

There are reasons to believe that chronic antral gastritis and chronic body gastritis are different clinical conditions. While both are associated with aging, chronic antral gastritis is much more commonly associated with gastric or duodenal ulcer. The natural history of chronic antral gastritis in asymptomatic normals and patients with peptic ulcer appears the same. Chronic body gastritis deteriorates rapidly with age in patients with gastric ulcer, but does not progress in patients with duodenal ulcer. With spontaneous healing of duodenal ulcer, chronic antral gastritis improves but persists. All these observations suggest that gastric ulcer, duodenal ulcer, and chronic antral gastritis are involved in a common mucosal inflammatory process. C. pylori occurs commonly on the antral mucosa affected by chronic gastritis, but is found to a much less extent at the site of peptic ulceration, and spontaneous ulcer healing is not affected by the presence of the organisms. It remains to be established whether C. pylori is the cause of chronic antral gastritis, is an aggravating factor of the gastritis, or is simply an inhabitant of the inflamed antral mucosa. Other known associations of chronic gastritis include pernicious anemia, bile reflux, and gastric cancer. Whether chronic antral or body gastritis is associated with clinical symptoms remains controversial. Histological improvement can be obtained with the use of prostaglandins, sucralfate, or bismuth compounds, which have one common property--they all possess mucosal-protective mechanisms.     

Gastric mucosal PGE2 levels in gastric nonulcer and ulcer patients with chronic renal failure or without renal diseases and in healthy subjects

PGE2-like immunoactivity in mucosal specimens from gastric corpus and antrum was measured in individuals with chronic uremia or without renal diseases in absence or presence of gastric ulcerations and in healthy subjects. Regardless the group of patients, compared to normal mucosa, a significant decrease in PGE2-like immunoactivity (50-70%) was found in mucosa from atrophic, but not from superficial gastritis. Whenever patients of the control group or patients with renal diseases suffered from ulcers, PGE2-like immunoactivity, compared to nonulcer subjects, revealed a decrease of about 60-70% in the nonulcerated mucosa. Compared to nonulcerated mucosa, the tissue of the ulcer rim in all patients with gastric ulcer showed a relative increase in PGE2-like immunoactivity, eg, PGE2-like immunoactivity was twice as high in tissue from the ulcer rim. The output of PGE2-like immunoactivity into the gastric juice of subjects without renal diseases was comparable to that found in patients with chronic uremia in both basal and pentagastrin-stimulated conditions. We therefore conclude that gastric mucosal formation is probably not influenced by chronic uremia.     

Low peptic ulcer and high gastric cancer prevalence in a developing country with a high prevalence of infection by Helicobacter pylori

We compared the prevalence rates of peptic ulcer (duodenal and gastric) and gastric cancer in 1,796 dyspeptic Peruvian patients with those reported in 2,883 similar patients from developed countries. The prevalence of total peptic ulcer was significantly lower, and that of gastric cancer significantly higher, in the Peruvian patients. The prevalence of gastric ulcer was lower but not significantly so. We deduced that the significantly lower prevalence of total peptic ulcer was directly related to the low prevalence rate of duodenal ulcer. We hypothesize that the reason for these differences was probably a higher prevalence of Helicobacter pylori-associated chronic atrophic gastritis with hypochlorhydria in the Peruvian patients. Hypochlorhydria decreases the predisposition to peptic ulcer (especially duodenal ulcer), and chronic atrophic gastritis may predispose an individual to gastric cancer.     

Update on the pathologic approach to the diagnosis of gastritis, gastric atrophy, and Helicobacter pylori and its sequelae

Biopsy sampling of the gastric mucosa at diagnostic endoscopy provides information that cannot be obtained otherwise. The most common indication for gastric biopsy is the need to know whether the patient is infected with Helicobacter pylori or not and whether the stomach is gastritic or not. Microscopic examination of gastric biopsy specimens gives, in addition to H. pylori status, information about the grade, extent, and topography of gastritis- and atrophy-related alterations in the gastric mucosa. This information provides further possibilities for the assessment of risk and likelihood of various gastric disorders. The presence of atrophy (loss of mucosal glands) results in failures in secretory functions of the corresponding mucosa and leads to errors in the homeostasis of normal gastric physiology. The grade of atrophy of the corpus mucosa linearly correlates with peak and maximal output of acid. The presence of advanced (moderate or severe) corpus atrophy indicates an extremely hypochlorhydric or achlorhydric stomach in which, for example, ordinary peptic ulcer is unlikely or impossible in spite of a possible H. pylori infection. Some well characterized and common topographic phenotypes of H. pylori gastritis and atrophic gastritis can be delineated as follows: Predominance or restriction of the H. pylori-related inflammation in antrum, in association with a nonatrophic corpus mucosa--of which phenotype is the most common--and with an increased risk of peptic ulcer disease, duodenal ulcer in particular ("duodenal ulcer phenotype" of gastritis); the presence of atrophic gastritis in corpus of the stomach ("corpus predominant gastritis"), which indicates a low risk of peptic ulcer and a reduction in the capacity of the patient to secrete acid; the occurrence of advanced atrophic gastritis and intestinal metaplasia multifocally in the stomach (advanced "multifocal atrophic gastritis"), which are features of a gastritis type and which also indicate a low acid secretion capacity and an increased risk of gastric neoplasias ("gastric cancer phenotype of gastritis"), suggesting a need for a careful exclusion of concomitant presence of small focal neoplastic or dysplastic lesions; and the presence of normal and healthy gastric mucosa, which indicates an extremely low risk of both peptic ulcer disease or gastric cancer and, therefore, is a finding of high clinical relevance. The presence of duodenal or gastric ulcer in conjunction with normal, healthy gastric mucosa suggests either aspirin or nonsteroidal antiinflammatory drugs to be the most likely cause of the ulcer.     

The pathophysiology of peptic ulcer disease

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. if they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acidpepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.     

The Distribution of Helicobacter pylori in Human Gastric Mucosa in vivo

Abstract: To estimate the distribution of Helicobacter pylori in human gastric mucosa in vivo, the phenol red dye spraying endoscopy lias been successfully developed and is performed after an oral and/or intravenous premedication of famotidine 20mg. This technique was conducted on 25 patients with chronic, atrophic gastritis, on 21 patients with a gastric ulcer and on 14 patients with duodenal ulcers. The red color changes which occurred on the gastric mucosa were classified into three types; the diffuse staining type, the regional staining type and the patchy staining type. In the chronic gastritis group, the diffuse staining type, the regional staining type and the patchy staining type occurred in 11 patients (44%), 7 patients (28%) and 2 patients (8%), respectively. The remainder of the patients' mucosa was unstained. In addition, the regional staining type occurred most frequently in the gastric ulcer group, while the diffuse staining type was dominant in the duodenal ulcer group. Notably, a recurrent and intractable ulcer was surrounded by regional staining fields in the stomach, and showed a diffuse staining at the antrum of the duodenum. These facts suggest that Helicobacter pylori prevented ulcer healing. This concurs with the results of our previous experimental study which found that the low concentration NH₃ solution, produced by Helicobacter pylori, prevented an acetic acid ulcer healing in rats and resulted from the suppression of the cell kinetics of the regenerative epithelial cells and the fibroblasts in the connective tissues at the ulcer margins.     

Assay of gastrin and somatostatin in gastric antrum tissues of children with chronic gastritis and duodenal ulcer

AIM: To study the expressions of gastrin (GAS) and somatostatin (SS) in gastric antrum tissues of children with chronic gastritis and duodenal ulcer and their role in pathogenic mechanism. METHODS: Specimens of gastric antrum mucosa from 83 children were retrospectively analyzed. Expressions of GAS and SS in gastric antrum tissues were assayed by the immunohistochemical En Vision method. RESULTS: The expressions of GAS in chronic gastritis Hp group (group A), chronic gastritis Hp- group (group B), the duodenal ulcer Hp group (group C), duodenal ulcer Hp- group (group D), and normal control group (group E) were 28.50 4.55, 19.60 2.49, 22.69 2.71, 25.33 4.76, and 18.80 2.36, respectively. The value in groups A-D was higher than that in group E. The difference was not statistically significant. The expressions of SS in groups A-E were 15.47 1.44, 17.29 2.04, 15.30 1.38, 13.11 0.93 and 12.14 1.68, respectively. The value in groups A-D was higher than that in group E. The difference was also not statistically significant. CONCLUSION: The expressions of GAS and SS are increased in children with chronic gastritis and duodenal ulcer.     

Link betweenHelicobacter pylori-associated gastritis and duodenal ulcer

We examined the interrelationships among the degree of fundic mucosal atrophy, the prevalence ofHelicobacter pylori in the gastric antrum, the gastric juice, and the duodenum with and without gastric metaplasia, in 20 duodenal ulcer patients and 20 non-duodenal ulcer patients. The detection rates ofH. pylori in the antrum, the gastric juice, and the duodenum were significantly higher in duodenal ulcer patients (80%, 65%, and 60%) than in non-duodenal ulcer subjects (50%, 20%, and 5%). The frequency ofH. pylori was significantly lower in the gastric juice (30%) and the duodenum (10%) in non-duodenal ulcer patients with antralH. pylori, compared with those in duodenal ulcer patients with antralH. pylori. All of seven patients with both gastric metaplasia andH. pylori infection in the duodenum had duodenal ulcer, whereas only 1 of 14 patients without either gastric metaplasia orH. pylori infection in the duodenum had duodenal ulcer. There was normal or mild atrophic mucosa in the fundus of duodenal ulcer patients withH. pylori in the antrum, whereas moderate or severe atrophic mucosa in non-duodenal ulcer patients withH. pylori gastritis. These results suggest that the preserved fundic mucosa, gastric metaplasia in the duodenum, and a greater load ofH. pylori to the duodenum through the gastric juice may be prerequisites for the formation of duodenal ulcers.     

Upper gastrointestinal mucosal lesions in chronic renal failure.

The upper gastrointestinal mucosa was studied endoscopically in 182 patients (140 males, 42 females) with chronic renal failure prior to hemodialysis. Endoscopy revealed normal mucosa in 77 patients (42.3%), inflammatory mucosal lesions in 88 (48.4%), peptic ulcer in 16 (8.8%; duodenal 15, gastric 1) and Barrett's ulcer in one patient. Upper gastrointestinal bleeding was noted at presentation in 16 (8.8%) cases and was associated with erosive gastritis, duodenitis and duodenal ulcer in 11, 3 and 2 patients respectively. Thus patients with chronic renal failure had a high prevalence of inflammatory mucosal changes.     

幽门螺杆菌cagG基因在胃黏膜中的表达及其意义

目的 研究cagG基因在不同上消化道疾病患者中的分布及其与幽门螺杆菌(Helico-bacter pylori,Hp)感染相关疾病的关系。方法 合成特异性引物,应用聚合酶链式反应(PCR)法扩增145株分离培养自上消化道疾病患者的Hp菌株cagG片段,其中慢性胃炎72例,胃溃疡17例,十二指肠球部溃疡48例,复合溃疡8例。比较cagG阳性、阴性的胃黏膜炎症程度。结果 Hp菌株cagG片段总检出率为91.7％(133/145),在慢性胃炎、胃溃疡、十二指肠溃疡、复合性溃疡中cagG阳性率分别为90.3％。88.2％、93.8％和 100.0％,各组间差异无显著性意义:(P>0.05)。结论 cagG有较高的保守性,在不同的消化道疾病患者的Hp中均有较高的检出率,在不同疾病中的分布无特异性,与胃黏膜炎症程度无明显关系,cagG尚不能单独作为某种疾病致病的相关基因。     

Gene distribution of cagⅡ in Helicobacter pylori-infected patients of Zhejiang Province

AIM: To determine the prevalence of genotypes of cagⅡin Helicobacter pylori ( H pylori)-infected patients in Zhejiang Province and investigate the relationship between these genotypes and the types of gastroduodenal diseases.METHODS: One hundred and seventy one clinical isolates were collected from 70 chronic superficial gastritis, 31 chronic atrophic gastritis, 41 gastric ulcer, 21 duodenal ulcer, 3 gastric and duodenal ulcer, and 5 gastric adenocarcinoma patients. Polymerase chain reaction assays were performed for analysis of cagT, ORF13 and ORF10 genes in the cagⅡ region.RESULTS: Of 171 Hpyloriisolates from Zhejiang patients,159(93.0%) were positive for all the three loci. One isolate (0.6%) was negative for all the three loci, and 11(6.4%) were partially deleted in cagⅡ. The positive rates of cagT,ORF13and ORF10genes were 97.1%, 94.7% and 99.4%,respectively. In the strains isolated from the patients with diseases including chronic superficial gastritis, chronic atrophic gastritis, gastric ulcer and duodenal ulcer, the sitive rates of cagTwere 95.7%, 100.0%, 95.1% and 100.0%, respectively. The positive rates of ORF13 were 94.3%, 93.5%, 95.1% and 100.0%, respectively. The sitive rates of ORF10 were 98.6%, 100.0%, 100.0% and 100.0%, respectively. The three genes were all positive in the three H pylori strains isolated from the patients with both gastric and duodenal ulcer. In the five strains isolated from the patients with gastric adenocarcinoma,only one isolate was negative for ORF13. There were no significant differences of the cagT, ORF13and ORF10genes among the different gastroduodenal diseases including chronic superficial gastritis, chronic atrophic gastritis,gastric ulcer, duodenal ulcer, both gastric and duodenal ulcer and gastric adenocarcinoma (X2=3.098, P＞0.05 for cagT; X2=3.935, P＞0.05 for ORF13 and X2=6.328, P＞0.05for ORF10).CONCLUSION: The cagⅡis not a uniform and conserved entity. Although the genes in cagⅡ are highly associated with the gastroduodenal diseases, the clinical outcome of Hpylori infection is not reliably predicted by the three genes in cagⅡin patients from Zhejiang Province.     

Gene distribution of cagⅡ in Helicobacter pylori-infected patients of Zhejiang Province

AIM: To determine the prevalence of genotypes of cagⅡ in Helicobacter pylori( H pylon)-infected patients in Zhejiang Province and investigate the relationship between these genotypes and the types of gastroduodenal diseases.METHODS: One hundred and seventy one clinical isolates were collected from 70 chronic superficial gastritis, 31 chronic atrophic gastritis, 41 gastric ulcer, 21 duodenal ulcer, 3 gastric and duodenal ulcer, and 5 gastric adenocarcinoma patients. Polymerase chain reaction assays were performed for analysis of cagT, ORF13 and ORF10 genes in the cagⅡ region.RESULTS: Of 171 Hpyloriisolates from Zhejiang patients,159(93.0%) were positive for all the three loci. One isolate (0.6%) was negative for all the three loci, and 11(6.4%) were partially deleted in cagⅡ. The positive rates of cagT,ORF13 and ORF10 genes were 97.1%, 94.7% and 99.4%,respectively. In the strains isolated from the patients with diseases including chronic superficial gastritis, chronic atrophic gastritis, gastric ulcer and duodenal ulcer, the sitive rates of cagT were 95.7%, 100.0%, 95.1% and 100.0%, respectively. The positive rates of ORF13 were 94.3%, 93.5%, 95.1% and 100.0%, respectively. The sitive rates of ORF10 were 98.6%,100.0%,100.0% and 100.0%, respectively. The three genes were all positive in the three H pylori strains isolated from the patients with both gastric and duodenal ulcer. In the five strains isolated from the patients with gastric adenocarcinoma,only one isolate was negative for ORF13. There were no significant differences of the cagT, ORF13 and ORF10 genes among the different gastroduodenal diseases including chronic superficial gastritis, chronic atrophic gastritis,gastric ulcer, duodenal ulcer, both gastric and duodenal ulcer and gastric adenocarcinoma (χ^2=3.098, P＞0.05 for cagT;χ^2=3.935, P＞0.05 for ORF13 and χ^2=6.328,P＞0.05 for ORF10).CONCLUSION: The cagⅡ is not a uniform and conserved entity. Although the genes in cagⅡ are highly associated with the gastroduodenal diseases, the clinical outcome of Hpyloriinfection is not reliably predicted by the three genes in cagⅡ in patients from Zhejiang Province.