Helicobacter pylori infection as a cause of gastritis,duodenal ulcer,gastric cancer and nonulcer dyspepsia: a systematic overview.

OBJECTIVE: To evaluate current evidence for a causal relation between Helicobacter pylori infection and gastritis, duodenal ulcer, gastric cancer and nonulcer dyspepsia. DATA SOURCES: A MEDLINE search for articles published in English between January 1983 and December 1992 with the use of MeSH terms Helicobacter pylori, gastritis, duodenal ulcer, gastric cancer, dyspepsia and clinical trial; abstracts were excluded. Six journals and Current Contents were searched manually for pertinent articles published in that time frame. STUDY SELECTION: Original studies with at least 25 patients, case reports and reviews that examined the relation between H. pylori and the four gastrointestinal disorders; 350 articles were on gastritis, 122 on duodenal ulcer, 44 on gastric cancer and 96 on nonulcer dyspepsia. DATA EXTRACTION: The quality of the studies was rated independently on a four-point scale. The strength of the evidence was assessed using a six-point scale for each of the eight established guidelines for determining a causal relation. DATA SYNTHESIS: There was conclusive evidence of a causal relation between H. pylori infection and histologic gastritis. Koch''s postulates for the identification of a microorganism as the causative agent of a disease were fulfilled for H. pylori as a causative agent of gastritis. There was strong evidence that H. pylori is the main cause of duodenal ulcers not induced by nonsteroidal anti-inflammatory drugs, but all of Koch''s postulates were not fulfilled. There was moderate epidemiologic evidence of an association between chronic H. pylori infection and gastric cancer. There was a lack of convincing evidence of a causal association between H. pylori and nonulcer dyspepsia. CONCLUSIONS: The evidence supports a strong causal relation between H. pylori infection and gastritis and duodenal ulcer and a moderate relation between such infection and gastric cancer. Further studies are needed to clarify the role of H. pylori in these disorders. Thus far, there is no evidence of a causal relation between H. pylori and nonulcer dyspepsia.     

Changes in gastric mucosa after vagotomy and gastrojejunostomy for duodenal ulcer.

Gastric mucosa was studied histologically in 141 patients. Eighty two had undergone vagotomy and gastrojejunostomy between 15 and 25 years previously for duodenal ulcer, and 59 control patients had a long history (minimum 15 years) of duodenal ulcer treated medically. No carcinoma was found in either group. Two patients with severe dysplasia and 13 patients with moderate dysplasia were found in the study group, compared with none in the control group (p less than 0.01). Intestinal metaplasia was seen in 44 (53%) of the study group and 16 (27%) of the control group (p less than 0.01). Atrophy and gastritis were more severe (p less than 0.01 for atrophy; p = 0.05 for gastritis) in the study group. Gastric mucosal changes were more severe after surgical treatment for duodenal ulcer than after medical treatment, and possibly a high incidence of gastric carcinoma may occur 25 years after vagotomy and gastrojejunostomy.     

幽门弯曲菌与慢性胃炎和消化性溃疡关系的系列研究

我院自1986年6月至1989年6月检查了634例病人的胃粘膜,从幽门弯曲菌(CP)的细菌学、致病性、病理学、诊断方法及药物治疗等方面进行了研究,探讨CP与慢性胃炎及消化性溃疡的关系。结果发现CP有两种形态并与空弯菌不同,不产生肠毒素;消化性溃疡的CP检出率为80.9％,慢性胃炎为41.6％,显著高于正常胃粘膜(3.7％);CP与消化性溃疡、慢性胃炎,十二指肠炎特别是活动性炎症有密切关系;CP对胃型上皮或粘液有某种亲和性;观察到上皮细胞破溃处有大量细菌聚集,CP有致细胞病变的能力。用阿的平代替吖啶橙荧光染色,并制成CP感染快速诊断试剂盒。呋喃唑酮促进溃疡愈合,使45～73％病例CP消失,50～70％胃炎好转。但有复发,根除CP有困难。     

Helicobacter pylori infection,mucosal atrophy and intestinal metaplasia in Asian populations: a comparative study in age-, gender- and endoscopic diagnosis-matched subjects

Background. It is known that the incidence and mortality rate of gastric cancer is high among Japanese and Chinese populations, but extremely low in Thai and Vietnamese populations. The aim of this study was to investigate the prevalence of Helicobacter pylori infection and the differences in the glandular atrophy and intestinal metaplasia scores in stomach specimens of Asian adult subjects of different races. Materials and Methods. Chinese, Thai, Vietnamese and Japanese patients were matched by age, gender and endoscopic diagnosis, in order to compare the differences in incidence of H. pylori‐related peptic ulcer disease and the prevalence of H. pylori infection among four Asian populations (n = 700). Glandular atrophy scores and intestinal metaplasia scores were also compared among four Asian populations divided into H. pylori‐positive cases (n = 120, 109, 145, 80, respectively) and H. pylori‐negative cases (n = 55, 66, 30, 95, respectively). Results. Among peptic ulcers, gastric ulcer was more frequently seen in Japanese subjects than in the other Asian populations examined. On the other hand, duodenal ulcer was more frequently seen in other Asian populations than in Japanese subjects. The prevalence of H. pylori infection was similar in the Japanese (Tokyo) and Chinese (Beijing and Fuzhou) populations. It was higher in Thai (Chiang Mai) subjects compared with Japanese subjects. On the other hand, Vietnamese (Ho Chi Minh) subjects had significantly lower rates of H. pylori infection than Japanese subjects. The glandular atrophy and intestinal metaplasia scores in the stomach were significantly higher in the H. pylori‐positive Japanese subjects than in H. pylori‐positive subjects belonging to other Asian populations, except for the higher glandular atrophy scores in Chinese rather than Japanese subjects. On the other hand, there were no significant differences in the glandular atrophy and intestinal metaplasia scores in the angulus of the stomach among H. pylori‐negative subjects belonging to the different Asian populations examined. Conclusions. Gastric ulcer was more common among Japanese subjects, while duodenal ulcer was more common among the other Asian populations examined. Japanese subjects with H. pylori infection showed more severe atrophic and metaplastic gastritis compared with that in other Asian subjects with H. pylori infection. These results may be related to the higher incidence of gastric cancer noted in Japanese subjects and the lower incidence of the cancer seen in Thai and Vietnamese patients.     

Occurrence of Campylobacter pylori in gastric mucosa and selected parameters of cell-mediated immunity in patients with duodenal ulcer and individuals with non-ulcerative dyspepsia]

The study was aimed at investigating a relationship between Campylobacter pylori infection in the gastric mucosa and selected parameters of cell-mediated immunity in patients with duodenal ulcer and the individuals with non-ulcerative dyspepsia. A relationship between Campylobacter pylori and gastritis has also been studied. Endoscopic and immunological tests were carried out in the group of 45 patients, including 14 patients with duodenal ulcer and 29 with non-ulcerative dyspepsia. Specimens of gastric mucosa were collected endoscopically for histological and bacteriological examinations. Immunological tests included an assessment of the number of lymphocytes T (and their subpopulations) forming active rosettes (ARFC); total - (TRFC) and theophylline-resistant in active rosettes fraction (ARFC-TR); total (TRFC-TR) and theophylline-sensitive lymphocytes in both fractions (ARFC-TS and TRFC-TS) in 1 mm3 of the peripheral blood. Results suggest, that there is correlation between an infection of the gastric mucosa by Campylobacter pylori and duodenal ulcer and gastritis. No correlation between the infection by Campylobacter pylori and examined parameters of immunity in both patients with duodenal ulcer and non-ulcerative dyspepsia was found.     

Helicobacter pylori. One bacterium and a broad spectrum of human disease! An overview.

Since the historical rediscovery of gastric spiral Helicobacter pylori in the gastric mucosa of patients with chronic gastritis by Warren and Marshall in 1983, peptic ulcer disease has been largely viewed as being of infectious aetiology. Indeed, there is a strong association between the presence of H. pylori and chronic active gastritis in histology. The bacterium can be isolated in not less than 70% of gastric and in over 90% of duodenal ulcer patients. Eradication of the organism has been associated with histologic improvement of gastritis, lower relapse rate and less risk of bleeding from duodenal ulcer. The bacterium possesses several virulence factors enabling it to survive the strong acid milieu inside the stomach and possibly damaging host tissues. The sequence of events by which the bacterium might cause gastric or duodenal ulcer is still not fully elucidated and Koch's postulates have never been fulfilled. In the majority of individuals, H. pylori infection is largely or entirely asymptomatic and there is no convincing data to suggest an increase in the prevalence of peptic ulcer disease among these subjects. An increasingly growing body of literature suggests an association between colonization by H. pylori in the stomach and a risk for developing gastric mucosa-associated lymphoid tissue (MALT), MALT lymphoma, gastric adenocarcinoma and even pancreatic adenocarcinoma. The bacterium has been implicated also in a number of extra-gastrointestinal disorders such as ischaemic heart disease, ischaemic cerebrovascular disease, atherosclerosis, and skin diseases such as rosacea, but a causal role for the bacterium is missing. Eradication of H. pylori thus seems to be a beneficial impact on human health. Various drug regimens are in use to eradicate H. pylori involving the administration of three or four drugs including bismuth compounds, metronidazole, clarithromycin, tetracyclines, amoxycillin, ranitidine, omeprazole for 1-2 weeks. The financial burden, side effects and emergence of drug resistant strains due to an increase in the use in antibiotics for H. pylori eradication therapy need further reconsideration.     

Genetic polymorphisms of NOD1 and IL-8, but not polymorphisms of TLR4 genes, are associated with Helicobacter pylori-induced duodenal ulcer and gastritis

BACKGROUND: Intracellular pathogen receptor NOD1 is involved in the epithelial cell sensing Helicobacter pylori, which results in a considerable interleukin (IL)-8 production. The aim of this study was to evaluate the relationship between NOD1 and IL-8 genetic polymorphisms and the development of H. pylori-induced gastritis and duodenal ulcer (DU), as compared with TLR4 polymorphisms. MATERIALS AND METHODS: Eighty-five patients with DU and 135 patients with gastritis were enrolled in the study. Seventy-five serologically H. pylori-positive subjects without gastric or duodenal symptoms served as controls. The G796A (E266K) NOD1 polymorphism was determined by restriction fragment length polymorphism, and the -251 IL-8 polymorphism by amplification refractory mutation system method. The TLR4 (ASP/299/Gly and Thr/399/Ile) gene polymorphisms were examined by melting point analysis. RESULTS: AA homozygote mutant variants of NOD1 were detected in 20% of the H. pylori-positive patients with DU versus 7% of H. pylori-positive patients with gastritis and versus 6% of the H. pylori-positive healthy controls. The IL-8 heterozygote mutant variant was detected with a significantly higher frequency among the DU patients and those with gastritis than among the H. pylori-positive controls. However, no significant correlation concerning the frequency of the TLR4 gene polymorphism could be revealed between any group of patients and the controls. CONCLUSION: E266K CARD4/NOD1, but not the TLR4 gene polymorphism increases the risk of peptic ulceration in H. pylori-positive patients. The -251 IL-8 polymorphism was significantly associated with either gastritis or DU in H. pylori-infected subjects. Host factors including intracellular pathogen receptors and IL-8 production play an important role in H. pylori-induced gastric mucosal damage.     

慢性胃病患者胃蛋白酶原I、II水平与幽门螺旋杆菌感染的关系研究

目的:探讨慢性胃病患者胃蛋白酶原(PG)Ⅰ、PG Ⅱ水平与幽门螺旋杆菌(HP)感染的关系。方法:选取2012年12月-2016年12月期间我院收治的慢性胃病患者64例作为研究对象,根据疾病类型分为慢性胃炎组23例、胃溃疡组22例以及胃癌组19例。另取同期于我院接受体检的健康志愿者30例作为对照组,应用免疫比浊法测定各组血清PG Ⅰ与PG Ⅱ水平,采用快速尿激酶法测定各组HP感染情况,分别对比各组研究对象HP感染发生情况,血清PG Ⅰ、PG Ⅱ、PG Ⅰ/PG Ⅱ水平,HP感染情况与血清PG Ⅰ、PG Ⅱ、PG Ⅰ/PG Ⅱ水平关系。结果:慢性胃炎组、胃溃疡组以及胃癌组患者HP阳性率分别为60.87%、63.64%、78.95%,均明显高于对照组的13.33%(P0.05)。慢性胃炎组、胃溃疡组以及胃癌组患者血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平均低于对照组,且胃癌组低于慢性胃炎组与胃溃疡组(P0.05),慢性胃炎组和胃溃疡组血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平比较差异无统计学意义(P0.05),各组血清PG Ⅱ比较无统计学差异(P0.05)。各组研究对象HP阳性血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平均低于HP阴性(P0.05),而PG Ⅱ水平比较无统计学差异(P0.05),慢性胃炎组、胃溃疡组、胃癌组HP阳性血清PG Ⅰ水平低于对照组,且胃癌组低于慢性胃炎组、胃溃疡组(P0.05),胃溃疡组、胃癌组HP阳性血清PG Ⅰ/PG Ⅱ水平低于对照组,且胃癌组低于慢性胃炎组(P0.05)。结论:慢性胃病患者PG Ⅰ、PG Ⅱ水平异常降低,HP阳性患者PG Ⅰ、PG Ⅱ水平降低更为明显,随病变的程度增加,血清PG Ⅰ、PG Ⅰ/PG Ⅱ水平也呈现出下降的趋势。     

Clinical epidemiology and natural history of gastroesophageal reflux disease

In the MUSE classification of gastroesophageal reflux disease (GERD), esophagitis is assessed by the presence of metaplasia, ulcer, stricture, or erosion, each being graded as absent, mild or severe. Daily reflux symptoms affect about 4 to 7 percent of the population; erosive esophagitis occurs in about 2 percent; the prevalence rate of Barrett's metaplasia is 0.4 percent; and esophageal adenocarcinoma leads to two deaths per million living population. In persons with GERD symptoms, about 20 percent are found to have erosive esophagitis, while ulcers or strictures are found in less than 5 percent of all patients with erosive esophagitis. No clear-cut temporal progression exists between successive grades of disease severity, as the most severe grade of GERD is reached at the onset of the disease. Mild forms of GERD tend to be more common in women than men, while severe GERD characterized by erosive esophagitis, esophageal ulcer, stricture or Barrett's metaplasia are far more common in men than women. All forms of GERD affect Caucasians more often than African Americans or Native Americans. The prevalence of GERD is high among developed countries in North America and Europe and relatively low in developing countries in Africa and Asia. During the past three decades, hospital discharges and mortality rates of gastric cancer, gastric ulcer and duodenal ulcer have declined, while those of esophageal adenocarcinoma and GERD have markedly risen. These opposing time trends suggest that corpus gastritis secondary to Helicobacter pylori infection protects against GERD. This hypothesis is consistent with the geographic and ethnic distributions of GERD. Case-control studies also indicate that cases with erosive esophagitis are less likely to harbor active or chronic corpus gastritis than controls without esophagitis.     

Chronic gastritis associated with Helicobacter pylori. Correlation between histological and bacteriological findings.

Biopsy specimens of gastric and duodenal mucosa from 326 patients were examined bacteriologically and histologically to determine the correlation between chronic gastritis and H. pylori colonization. H. pylori was identified in 111 (66.5%) patients with evidence of chronic gastritis and in 97 (82.2%) individuals who had gastritis associated with other pathology (gastric o duodenal ulcer, carcinoma o bulboduodenitis). The spiral bacteria was found more frequently in specimens with chronic superficial gastritis (88/107) and no significant difference was observed between the grade of activity of gastritis and H. pylori colonization. Giemsa stain was the most suitable method for detecting H. pylori in histological sections. By electron microscopy the microorganism was seen on the surface of the gastric mucosa, beneath the mucous layer, and more occasionally in intercellular junctions and the gastric pit.     

Flow cytometric analysis of the cell cycle in chronic gastritis.

Flow cytometric cell cycle analysis was recorded in gastric biopsy specimens from patients with normal gastric mucosa (GM), superficial gastritis (SG) and chronic atrophic gastritis (CAG). Cell-cycle analysis showed significantly higher percentages of cells in S- and S+G2/M-phase in CAG than in SG and normal GM (P < 0.0001). Moreover, CAG with severe or moderate atrophy showed significantly higher percentages of cells in S-phase (P < 0.05) and S+G2/M-phase (P < 0.02) than CAG with mild atrophy in antrum. In fundus, even if this increase was observed, it did not reach statistical significance. Consideration of concomitant pathologic findings such as oesophagite, gastric or duodenal ulcer, duodenite or benign polyp allowed a better differentiation of CAG both in antrum and in fundus. Significantly higher S-phase was observed in CAG with severe or moderate atrophy than in CAG with mild atrophy (P < 0.05). No statistically significant results were observed in patients with normal gastric mucosa or chronic gastritis and a concomitant pathologic finding.     

Interactions of the gastrotropic bacterium Helicobacter pylori with the leukocyte-endothelium adhesion molecules,the selectins--a preliminary report

The deleterious effects of Helicobacter pylori infection of the stomach are largely the result of a vigorous chronic inflammatory response, and include chronic gastritis, peptic ulceration and gastric cancer. We are exploring the possibility that carbohydrate components on H. pylori contribute to the persistent inflammation through interactions with leukocyte-endothelial adhesion molecules of the host. Lipopolysaccharides of most H. pylori strains contain sequences related to the Lewis (Le(x) or Le(a)) antigens. Carbohydrate sequences of this family encompass ligands for the leukocyte-endothelium adhesion molecules of the host, namely, the E- and P-selectins, which are expressed on inflamed endothelia, and L-selectin, which is constitutively expressed on leukocytes. Here we investigate H. pylori isolates from patients with chronic gastritis, duodenal ulcer and gastric cancer for their interactions with the selectins. Our results provide unequivocal evidence of interactions of isolates from each of the diagnostic groups with E- and L-selectins.     

慢性腹痛患儿C~(13)-尿素呼气试验与胃镜检查的临床意义

目的了解慢性腹痛患儿幽门螺杆菌(H.pylori)的感染状态及幽门螺杆菌感染患儿内镜下表现的特点。方法应用C13尿素呼气试验,对905例以慢性腹痛为主要症状的患儿进行检测,对C13呼气试验阳性者进行电子胃镜检查。结果905例慢性腹痛患儿中H.pylori呈阳性185例(20.44%),随年龄增长,其H.pylori阳性率升高,学年组已达高峰。对H.pylori阳性者进行胃镜检查结果显示十二指肠隆起病变47例占25.40%,结节性胃炎41例占22.1%,慢性浅表性`胃炎38例占20.5%,结节性胃炎伴十二指肠隆起病变23例占12.43%,十二指肠球部溃疡23例占12.4%。胃溃疡7例,占3.7%(其中包括1例复合性溃疡),结节性胃炎伴十二指肠炎6例,占3.2%。结论H.pylori感染为小儿慢性腹痛的主要原因之一,也是导致慢性胃炎及消化性溃疡的主要原因之一。C13尿素呼气试验方便,快速,无痛苦,无放射性,是一较好的H.pylori检测方法;对既有消化道症状同时C13呼气试验阳性者进行胃镜检查能够协助临床诊断及治疗。     

Gastric emptying of liquids in patients with peptic ulcer disease

This study was designed to determine the rates of gastric emptying of water, saline and a 20% glucose solution in patients with gastric and duodenal ulcers. In all subjects, gastric emptying was fastest after administration of the saline, slower with water and the slowest with glucose. Significant statistical differences (p less than 0.05) in emptying rates between normal subjects and the group with duodenal ulcer were seen when water and saline but not glucose were used. We conclude that inhibitory effects of the osmotic receptors are not changed in gastric and duodenal ulcer patients. However, the emptying rates were higher when osmotic stimulus was withheld.     

小儿消化性疾病的胃电图变化及与临床特点和胃镜特征的关联性

目的:分析小儿消化性疾病的胃电图变化及与临床病理特征和胃镜特征的关联性。方法:选取2018年1月至2019年5月我院儿科收治的经胃镜和病理学两种方式诊断为消化性疾病的患儿54例为观察组,另选取无胃肠道疾病的健康儿童40例为对照组。比较两组胃电图参数(频率均值和波幅均值),54例胃电图诊断后纤维胃镜检查结果,分析消化性疾病患儿HP感染与临床病理特征、溃疡面积的关系。结果:各组胃病患者胃电慢波频率均值各不相同(P0.05),三组患者胃电慢波波幅均值相比差异具有统计学意义(P0.05);且浅表性胃炎组、胆汁反流性胃炎组患者胃电慢波频率均值、胃电慢波波幅均显著低于胃溃疡组(P0.05);浅表性胃炎组患者胃电慢波频率均值显著低于胆汁反流性胃炎组(P0.05)。胆汁反流性胃炎组患者胃电慢波波幅显著低于浅表性胃炎组(P0.05)。胃镜检查结果显示,其中浅表性胃炎的诊断符合率较高,达90.00%,胃溃疡符合率为60.71%,胆汁反流性胃炎符合率为83.33%。HP检测结果显示,HP阳性患儿占总例数的77.78%(42/54),HP阴性患儿占总例数的22.22%(12/54);HP阳性组患儿淋巴滤泡形成、胃黏膜萎缩、胃黏膜炎性活动的发生率明显高于HP阴性组,差异具有统计学意义(P0.01);HP阳性组溃疡范围2 cm的患儿比例明显高于HP阴性患儿,差异具有统计学意义(P0.01)。结论:小儿消化性疾病胃电图存在餐后NSWP的下降及节律过缓的上升,胃电图检查和胃镜检查在诊断上有较高的符合率,HP感染科引起胃黏膜组织学改变,可作为小儿消化性疾病的靶向治疗。     

Helicobacter pylori recurrence in patients with duodenal ulcer: Clinical, endoscopic, histologic, and genotypic aspects. A 10-year Brazilian series

BACKGROUND: Recurrence infection following successful eradication of Helicobacter pylori is usually low, except for countries with high prevalence of H. pylori. The aim of this study was to verify H. pylori recurrence rate in patients with duodenal ulcer after eradication and the possible relationship with environmental factors, histologic pattern of the mucosa and bacterial genotype. MATERIALS AND METHODS: One-hundred and ninety-four patients with an active duodenal ulcer and who were successfully treated for H. pylori infection from 1990 to 1999 were studied. A questionnaire was answered about their living conditions, and a 14C-urea breath test was performed. Patients with a positive breath test underwent an upper endoscopy to investigate for possible ulcer recurrence; gastric biopsy samples were than collected for rapid urease test and for histologic assessment. H. pylori vacA and cagA genotype was determined by polymerase chain reaction in those samples with positive urease test. RESULTS: H. pylori infection was detected in 11 patients (recurrence rate of 5.7%) that were not associated with the type of bacterial virulence. In 10 patients the ulcer was healed and all of them were clinically asymptomatic. In eight, histology showed an intensification of gastritis. All 11 patients had adequate housing and sanitary conditions and no other risk for H. pylori recurrence was identified. CONCLUSIONS: The recurrence rate of H. pylori in Brazil was higher than that reported in developed countries, but lower than usually reported in developing ones. Ulcer relapse rarely occurs even in long-term follow up.     

Genetic polymorphism of interleukin-8 (IL-8) is associated with Helicobacter pylori-induced duodenal ulcer

BACKGROUND AND AIMS: Helicobacter pylori infection almost invariably causes chronic gastritis, but only a proportion of the infected subjects develop peptic ulcers. The local inflammation associated with H. pylori infection is characterized by an increased production of the proinflammatory cytokines IL-1-B, IL-6, IL-8 and TNF-alpha. Since such cytokine production is often determined by the genetic polymorphism of regions regulating cytokine gene expression, we investigated the relationship between TNF-alpha and IL-8 polymorphisms and the development of duodenal ulcer disease. We also sought a correlation between the promoter polymorphism of the lipopolysaccharide (LPS) receptor CD14 and the formation of peptic ulcer, because CD14 plays a crucial role in the initiation of the cytokine cascade. METHODS: Genomic DNA extracted from the peripheral blood of 69 patients with H. pylori-positive duodenal ulcer disease and 47 H. pylori-positive healthy controls was analyzed for TNF-alpha -308 promoter polymorphism by RFLP, and for IL-8 -251 polymorphism by ARMS. Genetic polymorphism within the promoter of the CD14 gene was identified using the LightCycler instrument via melting point analysis. RESULTS: No significant correlation could be revealed between the TNF-alpha and CD14 promoter polymorphisms and the clinical outcome of H. pylori infection. The IL-8 A/T heterozygote mutant variant was detected with a significantly higher frequency (65.22%) among the ulcer patients than among the healthy, H. pylori-positive blood donors (36.17%), while the frequency of the normal allelic genotype (TT) was significantly higher in the control group (44.6% vs 15.9%). CONCLUSION: Analysis of the genetic predisposition to enhanced cytokine production revealed a significant association only for the IL-8 polymorphism. This observation draws attention to the possible importance of IL-8 polymorphism as a genetic predisposing factor in the pathomechanism of H. pylori-induced duodenal ulcer disease, and to the relative protection from duodenal ulcer disease that is associated with the TT genotype.     

Relationship of gastric metaplasia and age, sex, smoking and Helicobacter pylori infection in patients with duodenal ulcer and duodenitis

Gastric metaplasia is one of the factors in duodenal ulcer appearance. The aim of this study was to investigate the frequency of gastric metaplasia and its connection with age, sex, cigarette smoking and H. pylori infection. In the study 216 patients were included. There were 98 patients with duodenal ulcer, 60 with duodenitis, and 58 healthy control subjects. There was no statistically significant difference in gastric metaplasia frequency according to age and sex. Gastric metaplasia was statistically more significant in patients with duodenal ulcer (p < 0.01). In all the subjects cigarette smoking did not significantly influence gastric metaplasia. In smokers with duodenal ulcer, and those who besides duodenal ulcer and smoking had H. pylori infection gastric metaplasia was more frequent (p < 0.01). However, in patients with duodenal ulcer, there was no statistically significant difference of gastric metaplasia related to H. pylori presence. It may be suggested that H. pylori infection is not of indispensable significance for gastric metaplasia appearance.     

Higher number of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> CagA EPIYA C phosphorylation sites increases the risk of gastric cancer,but not duodenal ulcer

Background  

Helicobacter pylori infection is one of the most common infections worldwide and is associated with gastric cancer and peptic ulcer. Bacterial virulence factors such as CagA have been shown to increase the risk of both diseases. Studies have suggested a causal role for CagA EPIYA polymorphisms in gastric carcinogenesis, and it has been shown to be geographically diverse. We studied associations between H. pylori CagA EPIYA patterns and gastric cancer and duodenal ulcer, in an ethnically admixed Western population from Brazil. CagA EPIYA was determined by PCR and confirmed by sequencing. A total of 436 patients were included, being 188 with gastric cancer, 112 with duodenal ulcer and 136 with gastritis.     

MDR1 C3435T polymorphism has no influence on developing Helicobacter pylori infection-related gastric cancer and peptic ulcer in Japanese

AIMS: P-glycoprotein, the gene product of multidrug-resistant transporter-1 (MDR1), confers multidrug resistance against antineoplastic agents but also affects the kinetic disposition of some drugs and carcinogens. MDR1 C3435T polymorphism influences the development of colon cancer and adult acute myeloid leukemia by the association with transporting carcinogen. The aim of this study was to clarify the association of MDR1 C3435T polymorphism with susceptibility to gastric cancer and peptic ulcers in patients with Japanese H. pylori infection. MAIN METHODS: We assessed the MDR1 C3435T polymorphism in H. pylori-positive gastritis alone patients (n=150), gastric cancer (n=292), gastric ulcer (n=215), and duodenal ulcer (n=163) and H. pylori-negative subjects (n=168) as control by a PCR-based method. KEY FINDINGS: No significant difference existed in frequencies of MDR1 C3435T polymorphisms between H. pylori-negative controls and H. pylori-positive gastritis alone patients. Moreover, MDR1-3435 T allele carriage didn't affect the risk of gastric cancer or peptic ulcer development. The age- and sex-adjusted odds ratios (ORs) of MDR1 3435 T allele carriers relative to the C/C genotype group for gastric cancer, gastric ulcer and duodenal ulcer risk were 0.96 (95%CI: 0.56-1.66), 1.16 (95%CI: 0.72-1.84) and 1.00 (95%CI: 0.61-1.62), respectively. SIGNIFICANCE: In this preliminary data, the association with MDR1 C3435T polymorphism and risk for developing H. pylori-related gastric cancer and peptic ulcer in Japanese was low. P-glycoprotein might not be involved in the carcinogenesis of H. pylori-related gastric cancer.