Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

胃窦部幽门螺杆菌清除对萎缩性胃炎病理改变的影响

目的通过对幽门螺杆菌（Hp）相关的萎缩性胃炎病人Hp清除治疗前后胃窦部黏膜病理改变的分析，来确定Hp对其炎症程度、活动性（中性粒细胞浸润）、腺体萎缩和肠上皮化生的影响。方法106例Hp相关的萎缩性胃炎患者接受Hp清除治疗，对其治疗前后胃窦部黏膜的病理变化进行分析，分析标准按96悉尼系统评定。结果在62例治疗成功组中，治疗后胃黏膜的炎症程度及活动性较治疗前明显减轻，但腺体萎缩及肠上皮化生未减轻。在44例治疗失败组中，治疗前后胃黏膜的炎症程度、活动性、腺体萎缩及肠化均没有变化。且随着Hp感染时间的延长，腺体萎缩和肠化还可加重。结论Hp的清除治疗可使萎缩性胃炎患者胃黏膜的炎症程度及活动度减轻，对此类病人应行Hp清除治疗。     

Effect of Hewei-Decoction on chronic atrophic gastritis and eradication of Helicobacter pylori

AIM: To demonstrate the effect of Hewei-Decoction (Decoction for regulating the stomach) on chronic atrophic gastritis (CAG) and eradication of Helicobacter pylori. METHODS: Ninety patients with CAG entering the investigation were divided into six differentiation syndromes, based on their major symptoms and signs. Hewei-Decoction was taken by all the patients orally for 4 or 8 wk. The efficacy was assessed by both the composite accumulation of reduced scores of major symptoms and the eradication of H pylori.X2 test was used to compare the efficacy between H pylori-positive and negative cases, and to disclose the relationship between efficacy and eradication of H pylori. RESULTS: In patients with six different syndrome types, the efficacy of Hewei-Decoction was 91.67% (11/12), 92.86% (13/14), 97.22% (35/36), 87.50% (14/16), 75.00% (6/8), 75.00% (3/4) respectively. The rate of highly efficacious was 58.33% (7/12), 50.00% (7/14), 77.78% (28/36), 62.50% (10/16), 12.50% (1/8) and 25.00% (1/4), respectively. The total efficacy was 91.11% (82/90), and the rate of highly efficacious was 60.00% (54/90). The eradication rate of H pylori was 67.86% (38/56). The therapeutic effect of Hewei-Decoction was better in H pylori positive cases than that in H pylori-negative cases with the total effect of 96.43% vs 82.35% (P<0.05). In 56 H pylori positive cases, the therapeutic effect was better in H pylori eradicated cases than that in H pylori-existent cases with the total effect of 97.37% vs 72.22% (P<0.01). CONCLUSION: Hewei-Decoction is effective in most cases of all the syndrome types. The results indicate that eradication of H pylori is one of the important mechanisms for alleviation of symptoms and signs. Also, the decoction is efficacious in H pylori-negative cases.     

中西医结合根除幽门螺杆菌对萎缩性胃炎核因子-κB表达的影响

[目的]观察以胃舒散为主的三联疗法（胃舒散、呋喃唑酮和克拉霉素）治疗幽门螺杆菌（Hp）阳性慢性萎缩性胃炎（CAG）的临床效果及其对核因子-κB（NF-κB）表达的影响。[方法]41例Hp阳性CAG患者服用胃舒散2．0g，呋喃唑酮0．1g，各3次／d，克拉霉素0．25g，2次／d，1周后再继服胃舒散4周。治疗前及治疗结束1年后行内镜及病理组织学检查，取活检观察病理组织学改变及NF-κB表达变化，采用银染色法、^14C-尿素呼气试验或快速尿素酶试验检测Hp。[结果]三联疗法结束1年后，Hp根除率为85．4％；根除Hp能显著减轻患者胃窦部慢性炎症（P〈0．05）和活动程度（P〈0．01），下调NF-κB表达（P〈0．01），但胃炎的萎缩和肠化生等病理无明显改变。[结论]以胃舒散为主的三联疗法对Hp有较高根除率。根除Hp可抑制NF-κB的表达，减轻活动性炎症，但近期观察对萎缩、肠化生等病理改变无明显作用。     

幽门螺杆菌形成空泡细胞毒素的提纯与特征分析

运用水油提、盐析及凝胶过滤色谱法对幽门螺杆菌ＹＣ－１１株所分泌的形成空泡细胞毒素进行了提取。纯化的形成空泡细胞毒素在ＳＤＳ－聚丙烯酰胺凝胶电泳中表现为单一条带，分子量约为８７０００，在ＰＨ２．４～６．４的环境中表现高细胞毒性。     

Helicobacter pylori cagA, iceA and vacA status in Taiwanese patients with peptic ulcer and gastritis

BACKGROUND: Helicobacter pylori causes chronic gastritis, peptic ulcer, gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma. Different genotypes of H. pylori are confirmed from diverse geographical areas. Its association with clinical diseases remains controversial. The aim of the present study was to investigate the H. pylori vacuolating cytotoxin (vacA) alleles, cytotoxin-associated gene (cagA) and iceA, in patients with peptic ulcer and gastritis. METHODS: We enrolled patients with peptic ulcer and chronic gastritis. Biopsy specimens were obtained from the antrum and lower body of the stomach. DNA extraction and polymerase chain reaction (PCR) were used to detect the presence or absence of cagA and to assess the polymorphism of vacA and iceA. RESULTS: A total of 133 patients (57 gastric ulcer, 52 duodenal ulcer, 24 chronic gastritis) had positive PCR results from biopsy specimens. Concerning genotypes, we found cagA (79% in the antrum, 92% in the body) and iceA1 (73% in the antrum, 82.8% in the body) strains in the majority of patients. The dominant vacA subtype was s1a (74.4% in the antrum, 75% in the body), followed by s1c (51.1% in the antrum, 60.5% in the body). In the middle region, the m2 strain dominated (49.6% in the antrum, 41.4% in the body), followed by m1T (19.5% in the antrum, 9.5% in the body). Mixed infection occurred in 89 patients (67%). There was no statistical difference in genotypes among the three groups. CONCLUSION: In Taiwan, H. pylori with positive cagA and iceA1 was found in the majority of cases. H. pylori with vacA s1a strains was the most common vacA subtype, followed by s1c, while s1b was rare. In the middle region, the m2 subtype was predominant followed by m1T. There was no significant association between genotypes and clinical diseases.     

Histological analysis of gastritis and Helicobacter pylori infection in patients with early gastric cancer: a case-control study

BACKGROUND AND AIMS: Infection with Helicobacter pylori is associated with an increased risk of gastric adenocarcinoma. However, most patients with H. pylori infection will not develop gastric cancer. The aims of the present study were to examine which histological features, including H. pylori infection, would increase the risk of gastric cancer using a case-control study. METHODS: Three gastric biopsy specimens were taken from 72 patients with early gastric cancer and 72 age- and sex-matched control subjects. The grade of gastritis was examined according to the updated Sydney System. The presence of H. pylori infection was determined by serology and histology. Odds ratio (OR) of developing gastric cancer was calculated for H. pylori positivity and histological features using conditional logistic regression. For patients with H. pylori infection, histological features in cancer patients and control subjects were compared. RESULTS: The OR of the presence of mononuclear cell infiltration in the corpus and intestinal metaplasia in the angulus were significantly elevated. The grade of mononuclear cell infiltration in the corpus and antrum was significantly higher in both types of cancer patients than controls. Glandular atrophy and intestinal metaplasia were increased in patients with intestinal-type cancer in the angulus and antrum. Bacterial density in the corpus and polymorphonuclear cell infiltration in the antrum were increased in patients with diffuse-type cancer. CONCLUSIONS: Severe chronic gastritis induced by H. pylori infection seems to be associated with diffuse-type gastric cancer. Glandular atrophy and intestinal metaplasia, which occur in gastric mucosa with chronic inflammation, are significantly associated with intestinal-type 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。     

Helicobacter pylori infection and gastric function in patients with fundic atrophic gastritis

In the present study we evaluated the relation among histology, H. pylori, IgG to H. pylori, gastric emptying, and acid secretion in 43 patients with fundic atrophic gastritis. On the basis of gastric acid secretion, patients were divided into three subgroups: patients with preserved acid secretion (Group 1), patients with hypochlorhydria (Group 2), and patients with achlorhydria (Group 3). Fundic glandular atrophy was more severe in hypoachlorhydric patients than in those with preserved acid secretion (P < 0.05 vs Group 2, P < 0.005 vs Group 3). H. pylori colonization was found in 94% of patients in Group 1, in 61% of patients in Group 2, and in only 8% of patients in Group 3 (P < 0.001 vs Group 1, P < 0.05 vs Group 2). Conversely, serological positivity to H. pylori was high in all three subgroups of patients (100% in Group 1, 77% in Group 2, 92% in Group 3). Gastric emptying was delayed in atrophic patients, particularly in those with hypoachlorhydria. Our data suggest that fundic atrophic gastritis represents a possible end stage of H. pylori infection, characterized by a progressive disappearance of the bacterium and a progressive deterioration of gastric functions.     

慢性萎缩性胃炎免疫状态与幽门螺杆菌感染的关系

本文对１１０例老年人慢性萎缩性胃炎检测幽门螺杆菌及免疫球蛋白ＩｇＡ、ＩｇＧ，Ｔ细胞标民，和超氧化物歧化酶等局部粘膜免疫状态。结果显示老年ＣＡＧ的ＨＰ感染率比非老年ＣＡＧ的ＨＰ感染率为低。局部粘膜ＩｇＡ、ＩｇＧ阳性增强，且体液免疫ＩｇＡ、ＩｇＧ强于细胞免疫ＴｕｃＨＬ，有ＳＯＤ减弱现象。示感染ＨＰ的老年ＣＡＧ患者存在粘膜免疫功能亢进，以及清除自由基能力下降。     

慢性多灶萎缩性胃炎患者胃酸分泌与幽门螺杆菌感染及血清胃泌素的关系

目的 研究慢性多灶萎缩性胃炎(BAG)胃酸分泌与幽门螺杆菌(Hp)感染及血清胃泌素的关系.方法 将200例确诊的慢性胃炎患者根据病理结果分为轻度、中度、重度BAG组及对照组(非萎缩性胃炎组),监测各组患者24小时胃内pH值的变化情况,并检测其幽门螺杆菌及血清胃泌素的含量,各组间进行比较.结果 (1)150例BAG患者中,Hp感染阳性率70%,随着胃粘膜萎缩程度的加重,Hp感染阳性率逐渐上升;(2)各组间血清胃泌素值比较:轻度萎缩组与非萎缩性胃炎组比较差异无显著性(P＞0.05),其余各组问比较差异有显著性(P＜0.05;(3)各组pH值分析结果:BAC胃黏膜轻度萎缩时,pH≤2时间百分比较非萎缩性胃炎组升高,pH＞4时间百分比及pH平均值、pH中位值均较非萎缩性胃炎组降低,中度及重度萎缩时pH≤2时间百分比逐渐降低,pH＞4时间百分比及pH平均值、pH中位值逐渐升高.结论 BAG的发生与Hp感染有关,胃粘膜萎缩程度与Hp感染的严重程度有关;BAG胃黏膜轻度萎缩时,血清胃泌素含量无明显变化;中、重度萎缩时,血清胃泌素含量降低;BAc胃黏膜轻度萎缩时,胃酸分泌增多;随着胃黏膜萎缩程度的加重,胃酸分泌逐渐减少.     

Seroprevalence of Helicobacter pylori and association with atrophic gastritis in patients with Sjögren’s syndrome

Abstract

To investigate the association between Helicobacter pylori (HP) infection and atrophic gastritis in Sjögren’s syndrome (SS), we conducted an age-matched case-control study examining serum HP-IgG antibodies and pepsinogen (PG) I and II levels using ELISA. The sera of 82 primary SS (1-SS), and 57 secondary SS (2-SS) were studied, as well as 198 controls having a diagnosis of connective tissue disease (CTD), except for SS which were obtained according to age. The titers of HP-IgG in 1-SS were significantly much higher than those in either 2-SS or control. The HP-IgG level revealed an exclusively positive correlation with the serum PG II level and a negative correlation with the PG I/II ratio. Serum PG II levels and PG I/II ratios were associated with the positivity of HP-IgG antibodies. The age-specific seroprevalence rates of HP infection in SS patients compared with controls showed a high positivity in patients less than 49 years old, but no difference among the higher age groups because of increasing positive rates with advancing age in the control. The matched odds ratio with HP infection in all SS (1-SS and 2-SS) and in 1-SS were 2.33 (95% CI: 1.43–3.81) and 2.75 (95% CI: 1.50–5.05), respectively. However, the positive PG I/II ratio did not show a statistically significant odds ratio for SS. We conclude that SS patients have a highly positive association with HP infection and that atrophic gastritis with SS may occur as a result of HP infection.     

Treatment of Helicobacter pylori infection in atrophic gastritis

Helicobacter pylori(Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis(AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows:(1) Cure of infection, resolution of inflammation and normalization of gastric functions;(2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and(3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric p H, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroupof patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG.     

Mouse model of gastric infection with cytotoxin-expressing strain of Helicobacter pylori in studying of pathogenesis of chronic gastric ulcer

Abstract Helicobacter pylori is a major risk factor for peptic ulcer, but studies on the role of H. pylori infection in gastric pathology are limited due to lack of convenient models resembling H. pylori infection in humans. We studied the effects of inoculation of conventional BALB/c mice with a toxigenic (cytotoxin associated gene A (cagA)+ and vacuolating cytotoxin gene A (vacA+) H. pylori strain on the course of healing of gastric ulcers. Following inoculation of toxigenic H. pylori or vehicle, gastric ulcers were produced in mice, which were then killed either at day 0 or after 2, 4, 7, 14 or 28 days and ulcer area and gastric blood flow (GBF) were determined. Gastric secretions from mice with chronic gastric fistulae were studied before and after inoculation with toxigenic H. pylori or vehicle (saline). The area (7 mm²) of ulcers in control mice decreased gradually and disappeared almost completely after 14 or 28 days. The ulcers in H. pylori-infected mice were present at all test days, showing a larger area than in vehicle control animals. The GBF in control mice rose gradually with decreasing ulcer size, being significantly higher at the ulcer margin than the ulcer crater. In contrast, the GBF in H. pylori-infected mice was significantly lower at the ulcer area than that in the vehicle controls but, again, the GBF at the ulcer margin was always higher than at the ulcer crater. Gastric acid output was reduced by more than 50% immediately after H. pylori inoculation and was accompanied by a significant increase in plasma gastrin release and a fall in gastric luminal somatostatin content. These secretory changes persisted at all test days. Oedema/congestion of surface epithelium appeared after 7 days and mucosal inflammatory infiltration appeared after 14 days, to further increase after 28 days, upon the induction of ulcer. Plasma interleukin (IL)-Iß and IL-12 were significantly elevated above the initial values compared with controls. Conventional mice with gastric ulcers can be successfully infected with an H. pylori strain expressing cagA and vacA cytotoxin and this infection markedly delays healing of the ulcers, probably due to the fall in GBF in the ulcer area, mucosal inflammation, cytokine release and impairment of the gastrin-somatostatin link.     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Effect of eradicating Helicobacter pylori on the development and reversion of atrophic gastritis in an animal study

OBJECTIVE : To investigate the effect of eradicating Helicobacter pylori on the development and reversion of atrophic gastritis in an animal study. METHODS : One hundred and ten grade II C57BL/6 female mice were randomly divided into experimental (60 mice) and control (50 mice) groups. The mice in the experimental group were infected with the SS1 H. pylori strain, then randomly subdivided into group A and group B (30 mice in each group). Group A and group B received a dose of standard bismuth triple therapy 6 and 12 months after infection, respectively. Ten mice in each group were killed before the therapy, then at 3 and 6 months after completion of the therapy (a total of 30 mice). The histopathological features of the glandular stomach were graded using a method analogous to the Sydney system and kinetic changes in the mucosal epithelial cells of the glandular stomach were examined using anti‐BrdU immunohistochemical staining and flow cytometry. RESULTS : All mice that received eradication therapy tested negative for Helicobacter pylori. Significant improvement in chronic active gastritis was observed after the eradication of H. pylori in both groups A and B. Atrophic changes were not seen at any time interval in group A, whereas in group B, atrophic changes were seen 12 months after H. pylori infection and no significant changes in the degree of atrophy were observed 3 and 6 months after the eradication of H. pylori. The cell kinetic indices (S‐phase cell percentage, proliferation index and labeling index) in the experimental group before the eradication of H. pylori were significantly higher than those in the control group at any time (P < 0.01), and significantly decreased 3 months after the eradication of H. pylori compared with those before therapy (P < 0.01). The cell kinetic indices showed no significant difference 6 months after the eradication of H. pylori compared with those in the control group at the same time intervals (P > 0.05). CONCLUSIONS : The present study suggests that the eradication of H. pylori can reduce gastric mucosal inflammation and change the epithelial cell kinetics of the stomach. It was found that early treatment can prevent the formation of mucosal atrophy. When atrophy has established, eradication of H. pylori can no longer reverse the change but may prevent its progress.     

Screening of atrophic gastritis and gastric cancer by serum pepsinogen, gastrin-17 and Helicobacter pylori immunoglobulin G antibodies

OBJECTIVE: Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin‐17 (G‐17) and H. pylori‐immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer. METHODS: A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non‐atrophic gastritis) served as a control group. Serum samples for PGI and II, G‐17, and H. pylori‐IgG antibodies estimation were analyzed by ELISA. RESULTS: PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P < 0.01). For the best discrimination of atrophic gastritis, the cut‐off values of PGI and PGR were 82.3 µg/L and 6.05, respectively. The PGI, PGR and G‐17 values were related significantly with the grades and/or sites of atrophic gastritis (P < 0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G‐17 level, and patients with atrophic antral gastritis had low G‐17 level. G‐17 increased significantly in the gastric cancer group (P < 0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G‐17 level between them. The positivity rate of H. pylori‐IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P < 0.001), while there was no difference in G‐17 level between them. The positivity rates of H. pylori‐IgG antibodies were over 85% in all other four groups. CONCLUSIONS: Low serum PGI, PGR and G‐17 values are biomarkers of atrophic antral gastritis. Atrophic corpus gastritis can be screened by lower serum PGI, PGR and high G‐17 values. [Correction added after online publication on 2 February 2007: the preceding sentence has replaced one that read ‘Atrophic be screened by serum PGI and PGR values’]. Gastric cancer can be screened on the basis of increased serum G‐17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.     

Allelic variation in the vacA gene of Helicobacter pylori isolated from Chinese patients

OBJECTIVE : To characterize the vacA alleles present in Chinese Helicobacter pylori strains and to compare the allelic variation in the vacA gene of Chinese strains with that of Western strains. METHODS : Twenty‐two single colonies of H. pylori isolated from five biopsy specimens with different gastric disorders were characterized for the expression of VacA protein and for evaluating the cytotoxic activity in HeLa cells. Five representative strains were selected and the vacA gene was amplified by PCR and subjected to automatic DNA sequencing using a primer walking strategy. RESULTS : Four strains expressed the VacA protein. Only one of the five strains induced vacuole degeneration in HeLa cells. All five vacA genes coded for identical signal peptides of the sla allele and had similar sequences encoding a 37 kDa subunit and outer membrane exporter. One of the five strains expressed a VacA protein with a middle region of the m1 allele and the others of the m2 allele. The four m2 allele strains had little vacuolating activity in HeLa cells. Phylogenetic analysis indicated that the homology of the Chinese vacA genes was 97.6–99.2% compared with 91.3–92.0% in the Western strains. CONCLUSIONS : There are allelic variations in the vacA gene between Chinese and Western H. pylori. Chinese H. pylori strains form a phylogenetically independent cluster separated from Western isolates. The m2‐type strains seem to be more prevalent in China. Cytotoxicity in HeLa cells appear to associate with the middle region but not the signal sequence.