根除幽门螺杆菌对胃窦黏膜萎缩和肠上皮化生逆转影响的前瞻性研究

目的 探讨根除幽门螺杆菌(Hp)对逆转胃窦黏膜萎缩和肠上皮化生(肠化生)病理改变的作用.方法 对行胃镜检查的门诊患者,于胃窦处取黏膜活检行病理学检查,并确定Hp感染状态.将Hp感染的慢性胃炎伴胃窦黏膜萎缩或(和)肠化生患者作为入选对象并分为两组,一组行Hp根除治疗,为Hp根除组(48例);另一组未行抗Hp治疗,为对照组(38例).分别在1年和5年后对两组患者进行胃镜随访,并在同一部位取材,根据2次病理结果的不同分为逆转和未逆转两种情况.结果 胃窦黏膜萎缩逆转率在Hp根除组显著高于对照组(37.1%比12.0%).5年后Hp根除组的胃窦黏膜萎缩逆转率显著高于1年后,45岁以下者显著高于45岁以上者.而在对照组中,胃窦黏膜萎缩逆转和随访的时间及年龄无明显关系.在2次随访中,肠化生逆转率在Hp根除组和对照组间差异均无统计学意义(P>0.05).结论 根除Hp尚不能逆转胃窦黏膜肠化生,但对逆转胃窦黏膜萎缩有作用,这种作用与随访观察时间及患者的年龄有关.因此,对有Hp感染的胃窦黏膜萎缩者应及早行根除Hp治疗.     

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.     

幽门螺杆菌相关性胃部疾病的病理变迁

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

Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori gastritis

OBJECTIVE: Helicobacter pylori and duodenogastric reflux (DGR) are both associated with chronic gastritis, peptic ulcer and gastric cancer. The nature of their interrelationship remains unclear. H. pylori eradication has also been reported to result in new or worsening acid gastro-oesophageal reflux (GOR). The aim of this study was to investigate the relationship between GOR, DGR and H. pylori infection. METHOD: 25 patients with H. pylori gastritis underwent ambulatory 24-hour oesophageal and gastric pHmetry and gastric bilirubin monitoring before and 12 weeks after H. pylori eradication, confirmed by 14C urea breath testing (UBT). Ten healthy subjects served as a control group. RESULTS: There were no differences between patient and control groups for gastric alkaline exposure or gastric bilirubin exposure (P> 0.25 in all categories). Oesophageal acid reflux was higher in the study group (P< 0.02). No differences were detected in oesophageal acid reflux, gastric alkaline exposure, or gastric bilirubin exposure (P = 0.35, 0.18 and 0.11, respectively) before and after eradication. CONCLUSIONS: Acid GOR is not increased by H. pylori eradication. DGR in patients with H. pylori gastritis is similar to that in healthy, non-infected subjects. H. pylori eradication produces no change in GOR or DGR. In patients with chronic gastritis, H. pylori infection and DGR appear to be independent of each other.     

根除幽门螺杆菌对胃溃疡愈合质量及复发的影响研究

目的探讨幽门螺杆菌（Helicobacter pylori，Up）对胃溃疡愈合质量及复发的影响。方法120例坳阳性活动期胃溃疡患者，口服泮托拉唑、阿莫西林、甲硝唑一周后，继续口服泮托美拉唑5周。治疗结束后复查胃镜取病理组织学检查并检测Hp根除情况，对比却根除组与却根除失败组内镜下溃疡愈合形态差异和愈合质量（包括内镜下再生黏膜成熟度和再生黏膜组织学成熟度）。所有患者随诊1年以上了解溃疡复发情况。结果治疗后92例胃溃疡患者月p检测阴性，坳根除率为80．43％；却根除组与跏根除失败组在内镜下愈合率方面的差异无显著性意义（P〉0．05），但两组在再生黏膜成熟度和再生黏膜组织学成熟度方面的差异有显著性意义（P〈0．01）。坳根除组1年溃疡复发率为4．35％，却根除失败组为21．43％，两组差异有显著性意义（P〈0．05）。结论根除Hp可提高胃溃疡的愈合质量，减少溃疡病复发。     

Helicobacter pylori infection and development of gastric cancer in Korea: long-term follow-up

BACKGROUND AND AIM: Infection of Helicobacter pylori is viewed as a major driver of progression to the precancerous state or to gastric cancer. This study was performed to investigate the effect of H. pylori infection on gastric cancer development and to determine to what extent H. pylori eradication is likely to reduce the prevalence of gastric cancer. METHODS: Gastric cancer development was investigated in 1790 Korean subjects who underwent gastroscopy and H. pylori testing between 1992 and 1998. The effects of H. pylori-positive and eradicated states on gastric cancer development were analyzed. RESULTS: Gastric cancer developed in 5 of the study cohort during a mean follow-up period of 9.4 years. All of these patients were positive for H. pylori infection, and 4 of the 5 had antral intestinal metaplasia (IM) at the time of study enrollment. One of these 5 patients was in an eradicated state when the gastric cancer was diagnosed, and had histologic IM before eradication therapy was performed. Gastric cancer was found to develop 10.9 times more frequently in the presence of IM than in its absence. CONCLUSIONS: The present study shows a close relationship between H. pylori infection and IM, and between IM and the development of gastric cancer. In addition, our finding suggests that chronic H. pylori infection looks like an important risk factor for the development of gastric cancer in Korea, where the prevalence of H. pylori remains high. This study indicates that to prevent gastric cancer H. pylori eradication is best performed before the development of IM.     

Helicobacter pylori infection and chronic immune thrombocytopenic purpura: long-term results of bacterium eradication and association with bacterium virulence profiles

Eradication of Helicobacter pylori may lead to improvement of chronic immune thrombocytopenic purpura (ITP), although its efficacy over time is uncertain. We report the results of H pylori screening and eradication in 75 consecutive adult patients with ITP. We also used molecular methods to investigate lymphocyte clonality and H pylori genotypes in the gastric biopsies from 10 H pylori-positive patients with ITP and 19 H pylori-positive patients without ITP with chronic gastritis. Active H pylori infection was documented in 38 (51%) patients and successfully eradicated in 34 (89%) patients. After a median follow-up of 60 months, a persistent platelet response in 23 (68%) of patients with eradicated infection was observed; 1 relapse occurred. No differences in mucosal B- or T-cell clonalities were observed between patients with ITP and control participants. Of note, the frequency of the H pylori cagA gene (P = .02) and the frequency of concomitant H pylori cagA, vacAs1, and iceA genes (triple-positive strains; P = .015) resulted statistically higher in patients with ITP than in control participants. All asymptomatic H pylori-positive patients with ITP were suffering from chronic gastritis. Our data suggest a sustained platelet recovery in a proportion of patients with ITP by H pylori eradication alone. Overrepresentation of specific H pylori genotypes in ITP suggests a possible role for bacterium-related factors in the disease pathogenesis.     

Antralization at the edge of proximal gastric ulcers： Does Helicobacterpyloriinfection play a role？

AIM: To determine the prevalence of antralization at the edge of proximal gastric ulcers, and the effect of H. pylori eradication on the mucosal appearances. METHODS: Biopsies were taken from the antrum, body and the ulcer edge of patients with benign proximal gastric ulcers before and one year after treatment. Gastric mucosa was classified as antral, transitional or body type. H. pylori positive patients received either triple therapy, or omeprazole. RESULTS: Patients with index ulcers in the incisura, body or fundus (n=116) were analyzed. Antral-type mucosa was more prevalent at the ulcer edge in H. pylori-positive patients than H. pylori-negative patients (93 % vs 60 %, OR=8.95, 95 %CI: 2.47-32.4, P=0.001). At one year, there was a significant reduction in the prevalence of antralization (from 93 % to 61 %, P=0.004) at the ulcer edge in patients with H. pylori being eradicated. However, there was no difference in the prevalence of antralization at the ulcer edge in those with persistent infection. CONCLUSION: H. pylori infection is associated with antralization at the edge of proximal gastric ulcers, which may be reversible in some patients after eradication of the infection.     

Does Helicobacterpylori eradication therapy for peptic ulcer prevent gastric cancer？

AIM： TO investigate the effects of Helicobacter pylori （H pylori） eradication therapy for treatment of peptic ulcer on the incidence of gastric cancer. METHODS： A multicenter prospective cohort study was conducted between November 2000 and December 2007 in Yamagata Prefecture, Japan. The study included patients with H pylori-positive peptic ulcer who decided themselves whether to receive Hpylori eradication （eradication group） or conventional antacid therapy （non-eradication group）. Incidence of gastric cancer in the two groups was determined based on the results of annual endoscopy and questionnaire surveys, as well as Yamagata Prefectural Cancer Registry data, and was compared between the two groups and by results of Hpylori therapy.RESULTS： A total of 4133 patients aged between 13 and 91 years （mean 52.9 years） were registered, and 56 cases of gastric cancer were identified over a mean follow-up of 5.6 years. The sex- and age-adjusted incidence ratio of gastric cancer in the eradication group, as compared with the non-eradication group, was 0.58 （95% CI： 0.28-1.19） and ratios by follow-up period （〈 1 year, 1-3 years, 〉 3 years） were 1.16 （0.27-5.00）, 0.50 （0.17-1.49）, and 0.34 （0.09-1.28）, respectively. Longer follow-up tended to be associated with better prevention of gastric cancer, although not to a significant extent. No significant difference in incidence of gastric cancer was observed between patients with successful eradication therapy （32/2451 patients, 1.31%） and those with treatment failure （11/639 patients, 1.72%）. Among patients with duodenal ulcer, which is known to be more prevalent in younger individuals, the incidence of gastric cancer was significantly less in those with successful eradication therapy （2/845 patients, 0.24%） than in those with treatment failure （3/216 patients, 1.39%）. CONCLUSION： H pylori eradication therapy for peptic ulcer patients with a mean age of 52.9 years at registration did not significantly decrease the incidence of gastric cancer.     

The effect of eradicating helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease

OBJECTIVES: Infection with Helicobacter pylori is a risk factor for the development of gastric cancer. However, it is not known whether eradication therapy can prevent the development of gastric cancer in persons in whom the cancer is not yet established. In the present study, we investigated whether the eradication of H. pylori in patients with peptic ulcer disease reduces the likelihood of their developing gastric cancer. METHODS: Prospective posteradication evaluations were conducted in 1,342 consecutive patients (1,191 men and 151 women; mean age: 50 yr) with peptic ulcer diseases who had received H. pylori eradication therapy. After confirmation of eradication, endoscopy and a urea breath test were performed yearly. RESULTS: A total of 1,120 patients completed more than 1-yr follow-up and were followed for up to 8.6 yr (a mean of 3.4 yr). Gastric cancer developed in 8 of 944 patients cured of infection and 4 of 176 who had persistent infection (p= 0.04; log-rank test). All the gastric cancer developed in patients with gastric ulcer, but none in patients with duodenal ulcer (p= 0.005; Fisher's exact test). In patients with gastric ulcer, persistent infection was identified as a significant factor for the risk of developing gastric cancer (hazard ratio: 3.35; 95% confidence interval: 1.00-11.22; p= 0.04; Cox's proportional-hazards model). CONCLUSION: H. pylori eradication may reduce their risk of developing gastric cancer in patients with gastric ulcer. Large-scale studies in additional populations of this important international public-health issue are warranted.     

Epithelial cell proliferation and glandular atrophy in lymphocytic gastritis： Effect of Hpyloritreatment

AIM: Lymphocytic gastritis is commonly associated with Helicobacter pylori infection. The presence of glandular atrophy and foveolar hyperplasia in lymphocytic gastritis suggests abnormalities in cell proliferation and differentiation, forming a potential link with the suspected association with gastric cancer. Our aim was to compare epithelial cell proliferation and morphology in H pylori associated lymphocytic gastritis and H pylori gastritis without features of lymphocytic gastritis, and to evaluate the effect of H pylori treatment. METHODS: We studied 14 lymphocytic gastritis patients with H pylori infection. For controls, we selected 14 matched dyspeptic patients participating in another treatment trial whose H pylori infection had successfully been eradicated. Both groups were treated with a triple therapy and followed up with biopsies for 6-18 months (patients) or 3 months (controls). Blinded evaluation for histopathological features was carried out. To determine the cell proliferation index, the sections were labeled with Ki-67 antibody. RESULTS: Before treatment, lymphocytic gastritis was characterized by foveolar hyperplasia (P=0.001) and glandular atrophy in the body (P=0.008), and increased proliferation in both the body (P=0.001) and antrum (P=0.002). Proliferation correlated with foveolar hyperplasia and inflammation activity. After eradication therapy, the number of intraepithelial lymphocytes decreased in the body (P=0.004) and antrum (P=0.065), remaining higher than in controls (P<0.001). Simultaneously, the proliferation index decreased in the body from 0.38 to 0.15 (P=0.043), and in the antrum from 0.34 to 0.20 (P=0.069), the antral index still being higher in lymphocytic gastritis than in controls (P=0.010). Foveolar hyperplasia and glandular atrophy in the body improved (P=0.021), reaching the non-LG level. CONCLUSION: In lymphocytic gastritis, excessive epithelial cell proliferation is predominantly present in the body, where it associates with foveolar hyperplasia and glandular atrophy. These characteristic changes of lymphocytic gastritis are largely related to H pylori infection, as shown by their improvement after eradication. However, some residual deviation was still seen in lymphocytic gastritis, indicating either an abnormally slow improvement or the presence of some persistent abnormality.     

Duodenogastric reflux eradicates Helicobacter pylori after distal gastrectomy

BACKGROUND/AIMS: Patients who undergo distal gastrectomy often develop duodenogastric reflux and preoperative H. pylori infection is eradicated spontaneously after distal gastrectomy in some patients. However, whether a causal relationship exists has not yet been studied. This report examines the correlation between H. pylori eradication and the amount of duodenogastric reflux following distal gastrectomy. METHODOLOGY: Among 72 consecutive patients who underwent curative distal gastrectomy with radical lymphadenectomy for gastric cancer, 37 patients had H. pylori infection preoperatively and were included in this study. The period of bile reflux (percent time) into the gastric remnant was measured with the Bilitec 2000 under standardized conditions on the 14th day after the surgery. Endoscopic examination was performed to determine the presence of H. pylori infection on week 12 after surgery. RESULTS: The percent time was higher in patients whose H. pylori infection had been eradicated after distal gastrectomy (58.1+/-9.2%) than in patients who had H. pylori infection after distal gastrectomy (33.8+/-5.7%). CONCLUSIONS: Duodenogastric reflux correlates with spontaneous eradication of H. pylori infection following distal gastrectomy.     

Preoperative versus postoperative Helicobacter pylori eradication therapy in gastric cancer patients: a randomized trial

OBJECTIVES: Helicobacter pylori (H. pylori) eradication is strongly recommended for gastric cancer patients who undergo subtotal gastrectomy. The efficacy of proton pump inhibitor-based triple therapy for H. pylori eradication has not been adequately assessed in the gastric remnant. The aim of this study was to compare the efficacy of postoperative versus preoperative H. pylori eradication therapy. METHODS: A total of 138 distal gastric cancer patients with H. pylori infection were randomized to receive either preoperative (preop, N = 68) or postoperative (postop, N = 70) proton pump inhibitor-based triple therapy for H. pylori eradication. The regimen consisted of rabeprazole 10 mg, clarithromycin 500 mg, and amoxicillin 1,000 mg, all twice daily for 7 days. Eradication was assessed by rapid urease test and histology 12 wk after surgery. RESULTS: By intention-to-treat (ITT) analysis, H. pylori eradication rates were 84.6% (95% CI 73.5-92.4) in the preop group and 83.1% (95% CI 71.7-91.2) in the postop group (P= 0.99). By per protocol (PP) analysis, the rates were 87.3% (95% CI 76.5-94.4) in the preop group and 86.9% (95% CI 75.8-94.2) in the postop group (P= 0.99). In the postop group, eradication rates did not differ with reconstruction method (Billroth I vs II, 80.4%[95% CI 66.1-90.6]vs 89.5%[95% CI 66.9-98.7] by ITT analysis (P= 0.49), and 85.7%[95% CI 71.5-94.6]vs 89.5% (95% CI 66.9-98.7) by PP analysis, P= 0.99). CONCLUSIONS: In distal gastric cancer patients, the effect of proton pump inhibitor-based triple therapy for H. pylori eradication was not different whether given postoperatively or preoperatively.     

Surface hydrophobicity of gastric mucosa in Helicobacter pylori infection: effect of clearance and eradication.

Surface hydrophobicity of the gastric mucosa is reduced in peptic ulcer disease and Helicobacter pylori infection. This abnormality may be caused by H. pylori or may be an inherent defect. The aim of the present study was to clarify the relationship between H. pylori infection and mucosal hydrophobicity by examining the effect of eradication of the organism. H. pylori-positive patients with (n = 42) or without (n = 42) duodenal ulcer were randomized to receive ranitidine, bismuth, or bismuth plus antibiotics. Surface hydrophobicity of gastric mucosa was assessed by measurement of plateau-advancing contact angle. Measurements were performed at presentation, end of treatment, and 1 month later. Contact angle was unchanged after ranitidine (55 degrees vs. 56 degrees) but increased with bismuth (57 degrees-62 degrees; P < 0.05) and bismuth plus antibiotics (56 degrees-67 degrees; P < 0.0001). One month after treatment ended, contact angles in patients in whom H. pylori was not eradicated were not different from those before treatment (56 degrees vs. 56 degrees) but increased to a value similar to H. pylori-negative controls in patients in whom H. pylori was eradicated (56 degrees-69 degrees; P < 0.0001). It is concluded that reduced mucosal hydrophobicity in peptic ulcer disease is secondary to H. pylori infection and that this impaired mucosal defense provides a possible mechanism whereby H. pylori infection predisposes to acid/peptic digestion.     

Helicobacter pylori infection influences tumor growth of human gastric carcinomas

BACKGROUND: Helicobacter pylori infection is considered a risk factor for gastric carcinoma. However, the effect of eradication therapy in gastric carcinoma patients is not well known. The aim of this study was to investigate the relationship between H. pylori infection and tumor growth of gastric carcinoma. METHODS: Fifty-one patients with gastric carcinoma participated in the study. Thirty-three were H. pylori-positive, 6 were H. pylori-negative, and 12 were diagnosed with gastric carcinoma after eradication of H. pylori. To investigate tumor growth of gastric carcinoma, cell proliferation and angiogenesis of the tumors were evaluated by immunohistochemical techniques using Ki-67 and CD34. RESULTS: The Ki-67 labeling index was 47.9 +/- 2.6 (mean +/- s) in the H. pylori-positive group, 38.1 +/- 3.6 in the H. pylori-eradicated group, and 22.2 +/- 5.5 in the H. pylori-negative group. It was significantly lower in the H. pylori-eradicated and H. pylori-negative groups than in the H. pylori-positive one, and a significant difference was also found between the H. pylori-positive and H. pylori-eradicated groups. The microvessel counts were 62.5 +/- 3.0, 50.2 +/- 4.0, and 66.0 +/- 9.8 in the positive, eradicated, and negative groups, respectively. A significant difference was found between the H. pylori-positive and H. pylori-eradicated groups. CONCLUSION: Our results suggest that H. pylori infection is associated with cell proliferation, and its eradication may influence tumor vascularity of gastric carcinoma. Therefore, H. pylori eradication therapy may contribute to the suppression of tumor growth.     

Effect of Helicobacter pylori eradication on the outcome of reflux esophagitis and chronic gastritis in the elderly. A randomized, multicenter, eight-month study

BACKGROUND: The effect of Helicobacter pylori eradication on the clinical outcome of esophagitis in elderly patients is controversial. AIM: To evaluate the effect of H. pylori eradication on clinical outcome of esophagitis and on chronic gastritis and its activity. MATERIALS AND METHODS: Sixty-one symptomatic elderly patients with esophagitis and H. pylori infection were randomized into two groups. Group 1 (PPI-only, 30 patients) was treated with pantoprazole 40 mg daily for 2 months followed by pantoprazole 20 mg daily for a further 6 months; group 2 (PPI + eradication, 31 patients) was treated as group 1 plus a 1-week course of amoxicillin 1 g twice daily and clarithromycin 250 mg twice daily. Endoscopy with gastric biopsies, 13C-UBT and clinical visits were repeated after 2 and 8 months. RESULTS: After 8 months, the intention-to-treat H. pylori eradication rates were 19.2% in group 1 vs. 80.7% in group 2 (p < 0.0001). No differences between group 1 and group 2 were observed in symptoms improvement (77 vs. 77%, p = n.s.) and healing rates of esophagitis (92.3 vs. 88.5%, p = n.s.). A significant decrease in the prevalence of moderate/severe chronic gastritis (from 52.2 to 4.7%, p = 0.002) and its activity (from 38 to 4.7%, p = 0.02) was observed in the antrum of patients of group 2, and not in patients of group 1. While a nonsignificant reduction in the chronic gastritis activity (from 28.6 to 4.7%, p = 0.09) was observed in the corpus of the eradicated patients of group 2, conversely a significant worsening of the chronic gastritis activity was found in the corpus of group 1 patients (from 25 to 60%, p = 0.05). CONCLUSION: The eradication of H. pylori infection does not affect the clinical outcome of esophagitis, while it improves chronic gastritis and its activity in elderly patients on short- and long-term treatment with PPIs. These findings suggest that H. pylori infection should be eradicated in elderly patients with esophagitis who need maintenance treatment with PPI.     

Helicobacter pylori eradication in the African setting, with special reference to reinfection and duodenal ulcer recurrence.

The aim of this study was to determine the effect of Helicobacter pylori eradication on the natural history of duodenal ulcer disease, and to determine the incidence of reinfection in adult patients where H pylori had been eradicated in a community with a high prevalence of the infection. An investigator blinded study, with 24 month endoscopic follow up, in subjects where H pylori had been eradicated, and similarly treated subjects where it had not been eradicated was conducted at a tertiary referral hospital. The patients consisted of a volunteer sample of 48 patients with endoscopically proved active duodenal ulcer disease. Duodenal ulcers were healed with omeprazole, 20 mg/day. After endoscopically confirmed healing, patients were treated with either one (17 patients) or two weeks (31 patients) of 'triple therapy'. H pylori status (urease reaction, histological tests, and culture of antral biopsy specimens) was determined at entry, four weeks after the finish of triple therapy and six, 12, and 24 months after this, or whenever an endoscopically proved recurrent duodenal ulcer was found. The main outcome measures were the recurrence of duodenal ulceration, over 24 months in the eradicated and non-eradicated groups and the incidence of reinfection by H pylori in the eradicated group during this follow up period. Five patients in the eradicated group experienced a duodenal ulcer relapse, of which only three were unexplained (1 = reinfected, 1 = gastrinoma). Fifteen of 21 patients in the non-eradicated group relapsed over the same period (p < 0.001). Only two of 27 patients in the eradicated group were reinfected during the 24 month follow up period. It is concluded that H pylori eradication is an effective treatment strategy for the longterm treatment of duodenal ulcer disease, even in the high prevalence, African setting. Reinfection is uncommon.     

Role of Helicobacter pylori infection in gastric carcinogenesis:Current knowledge and future directions

Helicobacter pylori(H. pylori) plays a role in the patho-genesis of gastric cancer. The outcome of the infection depends on environmental factors and bacterial and host characteristics. Gastric carcinogenesis is a multistep process that is reversible in the early phase of mucosal damage, but the exact point of no return has not been identified. Therefore, two main therapeutic strategies could reduce gastric cancer incidence:(1) eradication of the already present infection; and(2) immunization(prior to or during the course of the infection). The success of a gastric cancer prevention strategy depends on timing because the prevention strategy must be introduced before the point of no return in gastric carcinogenesis. Although the exact point of no return has not been identified, infection should be eradicated before severe atrophy of the gastric mucosa develops. Eradication therapy rates remain suboptimal due to increasing H. pylori resistance to antibiotics and patient noncompliance. Vaccination against H. pylori would reduce the cost of eradication therapies and lower gastric cancer incidence. A vaccine against H. pylori is still a research challenge. An effective vaccine should have an adequate route of delivery, appropriate bacterial antigens and effective and safe adjuvants. Future research should focus on the development of rescue eradication therapy protocols until an efficacious vaccine against the bacterium becomes available.     

In Dyspeptic Patients without Gastric Phase III of the Migrating Motor Complex,Helicobacter pylori Eradication Produces no Short-term Changes in Interdigestive Motility Pattern

Background: The relationship between Helicobacter pylori infection and interdigestive gastroduodenal motility in functional dyspepsia is still uncertain. Recent data from a large series documented that in dyspeptic patients without gastric phase III of the interdigestive migrating motor complex (MMC), the prevalence of bacterial infection was significantly higher. Since most H. pylori-positive dyspeptic patients have coexisting chronic gastritis, whether or not dyspepsia per se rather than bacterial colonization or chronic inflammation of the gastric mucosa may account for the observed interdigestive motility pattern is unknown. Our aim was to compare the interdigestive gastroduodenal motility pattern and dyspeptic symptoms before and 1 month after bacterial eradication in 20 H. pylori-positive dyspeptic subjects with chronic non-atrophic gastritis and without gastric phase III of the MMC, who were randomly allocated to receive eradication treatment (n = 10) or not (n = 10). Methods: Upper GI endoscopy with duplicate biopsies in antrum and corpus, 240-min interdigestive gastroduodenal manometric recording and symptoms assessment were performed before and 1 month after the treatments; bacterial eradication was confirmed by 13C-urea breath test. Results: After H. pylori eradication, neither in the incidence of antral and duodenal phase III of MMC nor in the phase II motility index values were any changes observed. Symptomatic improvement was recorded in both groups, with no significant differences between eradicated patients and controls. Conclusions: In dyspeptic patients with chronic non-atrophic gastritis and without gastric phase III of MMC, H. pylori eradication influences neither the interdigestive motility pattern nor the symptoms in the short-term period.     

In dyspeptic patients without gastric phase III of the migrating motor complex, Helicobacter pylori eradication produces no short-term changes in interdigestive motility pattern

BACKGROUND: The relationship between Helicobacter pylori infection and interdigestive gastroduodenal motility in functional dyspepsia is still uncertain. Recent data from a large series documented that in dyspeptic patients without gastric phase III of the interdigestive migrating motor complex (MMC), the prevalence of bacterial infection was significantly higher. Since most H. pylori-positive dyspeptic patients have coexisting chronic gastritis, whether or not dyspepsia per se rather than bacterial colonization or chronic inflammation of the gastric mucosa may account for the observed interdigestive motility pattern is unknown. Our aim was to compare the interdigestive gastroduodenal motility pattern and dyspeptic symptoms before and 1 month after bacterial eradication in 20 H. pylori-positive dyspeptic subjects with chronic non-atrophic gastritis and without gastric phase III of the MMC, who were randomly allocated to receive eradication treatment (n = 10) or not (n = 10). METHODS: Upper GI endoscopy with duplicate biopsies in antrum and corpus, 240-min interdigestive gastroduodenal manometric recording and symptoms assessment were performed before and 1 month after the treatments; bacterial eradication was confirmed by 13C-urea breath test. RESULTS: After H. pylori eradication, neither in the incidence of antral and duodenal phase III of MMC nor in the phase II motility index values were any changes observed. Symptomatic improvement was recorded in both groups, with no significant differences between eradicated patients and controls. CONCLUSIONS: In dyspeptic patients with chronic non-atrophic gastritis and without gastric phase III of MMC, H. pylori eradication influences neither the interdigestive motility pattern nor the symptoms in the short-term period.