Influence of various proton pump inhibitors on intestinal metaplasia in noneradicated Helicobacter pylori patients

AM: Intestinal metaplasia (IM) is more often found in patients with Helicobacterpylori(Hpylori) infection, while eradication of H pylori results in significant reduction in the severity and activity of chronic gastritis. We aimed to determine in patients with unsuccessful eradication of Hpylori the role of various proton pump inhibitors (PPIs) having different mechanisms in the resolution of IM. METHODS: We confirmed endoscopically and pathohistologically (Sydney classification) the IM in 335 patients with gastritis before and after medication for eradication of H pylori (Maastricht Protocol 2002). H pylori infection was determined by using histology, urease test and culture. Control endoscopy and histology were done after 30 d and thereafter (within 1 year). Unsuccessful eradication was considered if only one of the three tests (histology, urease and culture) was negative after therapy protocol. We used omeprazole, pantoprazole, lansoprazole in therapy protocols (in combination with two antibiotics). RESULTS: We found no significant difference in resolution of IM by using different PPI between the groups of eradicated and noneradicated patients (P<0.4821 and P<0.4388, respectively). CONCLUSION: There is no significant difference in resolution of intestinal metaplasia by different proton pump inhibitors.     

Effects of Helicobacterpylori eradication on atrophic gastritis and intestinal metaplasia： A 3-year follow-up study

AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM). METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system. RESULTS: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pylori-infected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P<0.01). However, the grade of IM increased in H pylori -infected group (P<0.05). CONCLUSION: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.     

根除幽门螺杆菌对胃黏膜肠化的影响

目的　幽门螺杆菌 (Hp)感染可导致慢性活动性胃炎进一步发展为慢性萎缩性胃炎、胃黏膜肠化、最终发展成肠型胃癌。通过 5年随访 ,探讨根除Hp是否对胃黏膜肠化逆转、发生及发展有影响。方法　将 1996年快速尿素酶试验及组织学方法检测Hp均为阳性的 398例病人随机分为治疗组和对照组。治疗组 2 0 1例 ,进行根除Hp治疗 ;对照组 197例 ,给予安慰剂 ;服药前及 5年后分别从胃窦部及胃体部取材检测胃炎、胃炎活动性及肠化。结果　 5年后治疗组中 15 1/2 0 1例Hp为阴性 ,对照组中 16 1/197例Hp为阳性 ;治疗组中Hp被根除的病人胃炎活动性的检出率明显减少 ,与对照组持续Hp感染者比较 ,差异有显著性 (P <0 .0 0 0 1) ;对照组中持续Hp感染者 5年后肠化检出率与自身 5年前、治疗组成功根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (P均 <0 .0 0 1) ,治疗组根除Hp的病人 5年前后比较差异无显著性 ;对照组中持续Hp感染者胃窦部 5年后肠化检出率与自身 5年前、治疗组根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (分别为P <0 .0 0 1,P <0 .0 0 1和P<0 .0 1) ,治疗组根除Hp感染的病人 5年前后比较差异无显著性 ;对照组持续Hp感染的病人与治疗组根除Hp感染的病人胃窦部肠化新增及新减情况比较无差异。 结论　 5年     

Future candidates for indications of Helicobacter pylori eradication: Do the indications need to be revised?

Since the discovery of Helicobacter pylori in 1982, the development of several treatment guidelines has allowed a consensus on the indications for H. pylori eradication. Beyond these currently accepted indications, including various upper gastrointestinal disorders and extragastric diseases, a significant amount of new information regarding H. pylori eradication is emerging. Certain types of acute gastritis, such as nodular gastritis, hypertrophic gastritis, Ménétrier's disease, hemorrhagic gastritis, and granulomatous gastritis are reversible after H. pylori eradication. Further, for chronic gastritis, closed-type atrophic gastritis and complete-type intestinal metaplasia appear to be more reversible after H. pylori eradication than open-type atrophic gastritis and incomplete-type intestinal metaplasia. Eradication can also be considered in subjects younger than 40 years who have a family history of gastric cancer and in subjects with long-term medications that might lead to bleeding (antiplatelet agents) or atrophy (proton pump inhibitors). Emerging evidence indicates that H. pylori eradication could be an effective treatment for some extragastric diseases that are unresponsive to conventional therapy. In such conditions, routine screening for eradication of H. pylori has not previously been recommended; a "test-and-treat" approach is suggested in the aforementioned situations. Given that H. pylori eradication is effective when the gastritis is reversible, future indications should be expanded to include acute gastric lesions that show marked improvement upon H. pylori eradication rather than just focusing on chronic gastric lesions. Future indications for H. pylori eradication should focus more on reversible lesions before preneoplastic conditions develop.     

Maastricht Ⅱ treatment scheme and efficacy of different proton pump inhibitors in eradicating Helicobacter pylori

AIM: The Maastricht Ⅱ criteria suggest the use of amoxicillin and clarithromycin in addition to a proton pump inhibitor over 7-10 d as a first line therapy in the eradication of Helicobacter pylori(H pylori). For each proton pump inhibitor, various rates of eradication have been reported. The present study was to compare the efficacy of different proton pump inhibitors like omeprazole, lansoprazole and pantoprazole in combination with amoxicillin and clarithromycin in the first line eradication of H pylori and to investigate the success of H pylori eradication in our district.METHODS: A total of 139 patients were included having a Helicobacter pylori(+) gastroduodenal disorders diagnosed by means of histology and urease test. Besides amoxicillin (1 000 mg twice a day) and clarithromycin (500 mg twice a day), they were randomized to take omeprazole (20 mg twice a day), or lansoprazole (30 mg twice a day), or pantoprozole (40 mg twice a day) for 14 d. Four weeks after the therapy, the eradication was assessed by means of histology and urease test. It was evaluated as eradicated if the H pylori was found negative in both. The complaints (pain in epigastrium, nocturnal pain, pyrosis and bloating)were graded in accordance with the Licert scale. The compliance of the patients was recorded.RESULTS: The eradication was found to be 40.8% in the omeprazole group, 43.5% in the lansoprazole group and 47.4% in the pantoprazole group. Sixty-three out of 139patients (45%) had eradication. No statistically significant difference was observed between the groups. Significant improvements were seen in terms of the impact on the symptom scores in each group.CONCLUSION: There was no difference between omeprazole, lansoprazole and pantoprazole in H pylori eradication, and the rate of eradication was as low as 45%.Symptoms were improved independent of the eradication in each treatment group. The iow eradication rates suggest that the antibiotic resistance or the genetic differences of the microorganism might be in effect. Further studies are required to verify these suggestions.     

Maastricht Ⅱ treatment scheme and efficacy of different proton pump inhibitors in eradicating Helicobacter pylori

AIM: The Maastricht Ⅱ criteria suggest the use of amoxicillin and clarithromycin in addition to a proton pump inhibitor over 7-10 d as a first line therapy in the eradication of Helicobacter pylori (Hpylori). For each proton pump inhibitor, various rates of eradication have been reported. The present study was to compare the efficacy of different proton pump inhibitors like omeprazole, lansoprazole and pantoprazole in combination with amoxicillin and clarithromycin in the first line eradication of Hpylonand to investigate the success of H pylonrieradication in our district. METHODS: A total of 139 patients were included having a Helicobacter pylori (+) gastroduodenal disorders diagnosed by means of histology and urease test. Besides amoxicillin (1000 mg twice a day) and darithromycin (500 mg twice a day), they were randomized to take omeprazole (20 mg twice a day), or lansoprazole (30 mg twice a day), or pantoprozole (40 mg twice a day) for 14 d. Four weeks after the therapy, the eradication was assessed by means of histology and urease test. It was evaluated as eradicated if the Hpyloriwas found negative in both. The complaints (pain in epigastrium, nocturnal pain, pyrosis and bloating) were graded in accordance with the Licert scale. The compliance of the patients was recorded. RESULTS: The eradication was found to be 40.8% in the omeprazole group, 43.5% in the lansoprazole group and 47.4% in the pantoprazole group. Sixty-three out of 139 patients (45%) had eradication. No statistically significant difference was observed between the groups. Significant improvements were seen in terms of the impact on the symptom scores in each group. CONCLUSION: There was no difference between omeprazole, lansoprazole and pantoprazole in H pylori eradication, and the rate of eradication was as low as 45%. Symptoms were improved independent of the eradication in each treatment group. The low eradication rates suggest that the antibiotic resistance or the genetic differences of the microorganism might be in effect. Further studies are required to verify these suggestions.     

根除幽门螺杆菌前后对痘疹样胃炎治疗效果的比较

目的:评价痘疹样胃炎根除幽门螺杆菌(H.pylori)后的治疗效果以及病理变化情况,明确根除H.pylori对痘疹样胃炎的治疗意义.方法:325例痘疹样胃炎患者根据H.pylori检测结果分为阳性组(标准三联或四联疗法)与阴性组(单纯抑酸),比较治疗效果;阳性组根据复查胃镜H.pylori的结果再分为两组,比较病理情况...     

幽门螺杆菌根除对门脉高压性胃病患者预后的影响

目的:探讨幽门螺杆菌(Helicobacter pylori,H pylori)根除对门脉高压性胃病(portal hypertension gastric disease,PHGD)患者疗效．方法:106例PHGD患者,均为H pylori阳性,随机分为:对照组 50例,仅服用奥美拉唑;H pylori根除组56例,口服奥美拉唑和克拉霉素及阿莫西林,试验结束时所有患者均行胃镜复查及14C 呼气试验．结果:试验前46例患者(45．8％)内镜检查发现糜烂性胃炎,试验结束后H pylori根除组50例患者H pylori阴性(95．9％),对照组3例转阴(6．1％),两组H pylori根除率差异显著(P<0．01)．H pylor根除组16例失效,对照组有7例失效,两者相比差异显著(29．8％ vs 14．3％,P<0．05)．对照组患者胃体萎缩及胃体肠化较H pylori根除组明显增多．结论:H pylori根除可降低质子泵抑制剂(PPI)治疗PHGD的疗效,但H pylori根除对PHGD患者胃体糜烂及胃体肠化有防治作用.     

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.     

幽门螺杆菌感染胃黏膜病变基因表达和细胞生物学行为

目的　研究幽门螺杆菌(Helicobacterpylori,Hp)感染胃黏膜病变的多基因表达和细胞生物学行为。方法　327例患者经胃镜及手术的胃黏膜病变标本,应用免疫组化染色法,检测p53、p16、bcl-2和环氧合酶同工酶-2(COX-2)蛋白的表达。Hp感染由快速尿素酶试验结合组织学检查/     

Recent success of pantoprazole -or lansoprazole- based clarithromycin plus amoxicillin treatment in the eradication of Helicobacter pylori.

BACKGROUND/AIMS: There are some reports showing that resistance of Helicobacter pylori (H. pylori) to clarithromycin has increased in recent years. We aimed to investigate the current success of a most popular first-line eradication regimen by using two different proton pump inhibitors: lansoprazole and pantoprazole. METHODS: Ninety patients with H. pylori-positive functional dyspepsia were randomized to receive pantoprazole 40 mg b.i.d. or lansoprazole 30 mg b.i.d. in addition to amoxicillin 1,000 mg and clarithromycin 500 mg twice daily for 14 days in a multicenter study. H. pylori infection was determined by histological examination and a rapid urease test. A follow-up endoscopy was performed to assess the H. pylori eradication six weeks after the end of therapy. RESULTS: Seventy-nine patients completed the study protocol properly. The H. pylori eradication rates according to per protocol analysis were 70% in group pantoprazole, amoxicillin and clarithromycin (28/40) and 69.2% in group pantoprazole, amoxicillin and clarithromycin (27/39). The eradication rates according to intention to treat analysis were 62.2% and 60% in lansoprazole, amoxicillin, clarithromycin, pantoprazole, amoxicillin, clarithromycin groups, respectively. The eradication rates were similar in both protocols (p>0.05). CONCLUSIONS: The most popular first-line eradication protocols of H. pylori achieved only a moderate success in the current study. Alternative therapy options are needed instead of clarithromycin-based triple treatment for eradication of H. pylori. The choice of proton pump inhibitor is not important in the eradication rate of H. pylori.     

Prolonged use of proton pump inhibitors, CagA status, and the outcome of Helicobacter pylori gastritis

GOALS AND BACKGROUND: To assess whether prolonged use of proton pump inhibitors (PPIs) in patients infected with Helicobacter pylori has adverse effects on gastritis. STUDY: We studied 34 H. pylori-positive individuals with reflux esophagitis, Barrett esophagus, or nonulcer dyspepsia. Half of them were on maintenance treatment with PPIs (mean, 8 years) and half were not.H. pylori and CagA status were tested serologically. Gastric biopsies were classified histopathologically by the updated Sydney classification. RESULTS: Proton pump inhibitors in H. pylori gastritis are associated with significantly less antral inflammation and lower H. pylori density, regardless of CagA status. There was a tendency toward more antral atrophy in patients with the CagA strain who were undergoing maintenance treatment with PPIs (p = 0.08), but there was an opposite tendency in CagA-negative individuals (p = 0.08). Intestinal metaplasia was seen more frequently in CagA-positive, treated individuals (p = 0.028). CONCLUSIONS: These findings support the hypothesis that CagA status is important in the progression to atrophy and that maintenance treatment with PPIs accelerate this progression, while reducing inflammatory infiltration.     

Gastric mucosal morphological consequences of acid suppression: a balanced view

In the chapter, an analysis of the literature on the relationship between Helicobacter pylori, the use of proton pump inhibitors and the development of atrophic gastritis is presented, and the difficulties of classifying gastritis and the new possibilities of quantifying chronic inflammation by morphometric analysis are discussed. The issue surrounding the necessity of eradicating H. pylori in H. pylori-positive patients has still not been solved. Most studies have now accepted that proton pump inhibitors indeed accelerate the onset of atrophic gastritis in H. pylori-positive patients, but evidence against such an association was published in one recent (Scandinavian) study; conclusions from this study have, however, been challenged by several groups. Some data are available on the efficacy of H. pylori eradication with regard to the prevention of atrophy. The limited significance of the development of parietal cell protrusions and fundic gland cysts is better understood, but much less is known of the development and long-term consequence of H. pylori-induced autoimmune gastritis. Finally, recent studies in H. pylori-positive patients indicate that treatment with proton pump inhibitors may promote bacterial N-nitrosation formation. These data taken together suggest that the eradication of H. pylori may be based not only on morphological arguments, but also on bacterial alterations in the gastric milieu.     

Pre and post eradication gastric inflammation in Helicobacter pylori-associated duodenal ulcer.

BACKGROUND: Distribution and nature of gastritis are major determinants of clinical outcome of H. pylori infection. The gastric inflammatory changes associated with this infection in developing countries have not been systematically studied. AIMS: To evaluate the inflammatory changes in gastric antrum and corpus in patients with duodenal ulcer and H. pylori infection, before and after H. pylori eradication therapy. METHODS: Histology and H. pylori density were studied in gastric biopsies obtained from 53 consecutive patients with active duodenal ulcer and H. pylori infection. Biopsies were obtained before and 4 weeks after H. pylori eradication therapy, from the anterior and posterior walls of the antrum and corpus, and were evaluated according to the Sydney system. RESULTS: In the pre-H. py/ori eradication antral biopsies, chronic gastritis, active gastritis, atrophy, intestinal metaplasia (IM) and lymphoid follicles / aggregates were seen in 53 (100%), 49 (92%), 11 (21%), 7 (13%) and 28 (53%) patients, respectively. In the corresponding biopsies from gastric corpus, these changes were seen in 49 (92%), 23 (43%), 2 (4%), 2 (4%) and 8 (15%), respectively. All changes except IM were significantly more frequent and of higher grade in the antrum. The grade of chronic gastritis was significantly higher in antrum than corpus; the frequency of gastritis in the antrum and corpus was similar (100% vs. 92%). H. pylori density was also higher in the antrum and correlated well with the grades of chronic gastritis and activity at both sites. Eradication of H. pylori was achieved in 39 patients (74%), and led to significant decrease in gastritis; no change was seen in patients who did not eradicate the organism. CONCLUSIONS: Antral-predominant chronic gastritis and activity are present in more than 90% of patients with H. pylori infection associated with duodenal ulcer, and the grade of gastritis correlates with the density of the organism. Eradication therapy results in improvement of both chronic gastritis and activity.     

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.     

Noninvasive tests as a substitute for histology in the diagnosis of Helicobacter pylori infection

BACKGROUND: Rapid urease tests for Helicobacter pylori have a sensitivity of 80% to 90%. Therefore histologic examination of gastric biopsies is recommended as a "backup" diagnostic test in rapid urease test-negative patients. However, noninvasive tests (urea breath test, serology, whole blood antibody tests) may provide a more rapid diagnosis and be less expensive but offer similar accuracy. METHODS: Sixty-seven patients (no prior treatment for H pylori, no proton pump inhibitors, antibiotics, or bismuth within 4 weeks) undergoing endoscopy for evaluation of dyspepsia symptoms and testing rapid urease test-negative by antral biopsy were enrolled. All had the following tests: gastric biopsies (2 antral, 1 fundus; H&E and Alcian Yellow stain) examined for gastritis and H pylori; (13)C-UBT; capillary blood for whole blood rapid antibody tests: FlexSure HP, QuickVue, AccuStat, and Stat-Simple Pylori; serum for FlexSure HP; HM-CAP enzyme-linked immunoassay. H pylori infection was diagnosed (reference standard) if chronic gastritis was present on histology and at least 2 of the 3 following tests were positive: urea breath test, H pylori organisms unequivocally demonstrated in biopsies on special stain, and/or enzyme-linked immunoassay. The test and treatment costs per patient were calculated. RESULTS: Of 67 patients with a negative rapid urease test, 4 were positive for H pylori. None had active peptic ulcer disease. Histology only identified 1 patient with organisms visible on special stain. Using chronic active gastritis (neutrophilic and mononuclear infiltrate) as a diagnostic criterion for H pylori, 6 patients would have been judged positive. However, only 2 of these were truly positive by the reference standard (positive predictive value 33%). Negative predictive value for presence of organisms and chronic active gastritis was 95% and 97%, respectively. All of the noninvasive tests identified all 4 truly positive patients correctly. Urea breath test and FlexSure whole blood assay yielded a substantial number of false-positive results (positive predictive value 31% and 36%, respectively); positive predictive value for the other tests ranged from 50% to 80%. All tests except histology had a negative predictive value of 100%. Histology was the most costly test (p < 0. 001 compared with all other tests), followed by urea breath test and HM-CAP serology (p < 0.001 compared with all rapid antibody tests). CONCLUSIONS: Whole blood or serum antibody testing is a rapid, accurate, and cost-effective means for establishing H pylori status in rapid urease test-negative patients. Whole blood or serology rapid antibody testing should substitute for histology when the patient has not been previously treated for H pylori.     

Effects of Helicobacter pylori eradication on the natural history of lymphocytic gastritis

BACKGROUND: Lymphocytic gastritis is characterised by an accumulation of lymphocytes in the surface epithelium of the stomach. Lymphocytic gastritis has been linked to coeliac disease and Helicobacter pylori infection. AIMS: To determine whether H pylori eradication leads to resolution of the lymphocytic infiltrate and clinical improvement in patients with lymphocytic gastritis, and to determine their HLA status. METHODS: The Leeds Dyspepsia Questionnaire (LDQ) was administered to 13 patients with lymphocytic gastritis. H pylori serology, (13)C urea breath test (UBT), and upper gastrointestinal endoscopy with sampling of the duodenum, antrum, and corpus were done in all cases and the HLA status was determined. Eleven patients had at least one positive test for H pylori. Patients with lymphocytic gastritis and H pylori infection were treated with a one week course of omeprazole, clarithromycin, and metronidazole. Gastric and duodenal intraepithelial lymphocyte (IEL) counts were performed, along with histological assessment of gastric and duodenal biopsies before and after H pylori eradication. RESULTS: Two months after treatment there was a significant reduction in gastric IEL counts in both antrum and corpus. There was no significant change in duodenal IEL counts before and after eradication. According to the Sydney grading there was significant improvement in corpus inflammation after eradication. The patients histologically H pylori positive before treatment became H pylori negative. Dyspepsia scores also improved significantly after treatment. CONCLUSIONS: H pylori eradication treatment in patients with lymphocytic gastritis causes significant improvement in the gastric IEL infiltrate, corpus inflammation, and dyspeptic symptoms. H pylori serology is frequently positive when histology and UBT are negative. Lymphocytic gastritis may represent a specific immune response to H pylori infection.     

Inability to noninvasively diagnose gastric intestinal metaplasia in Hispanics or reverse the lesion with Helicobacter pylori eradication

BACKGROUND: Helicobacter pylori infection has been linked with the development of gastric adenocarcinoma and its precursor lesion, intestinal metaplasia (IM). The presence of gastric IM is not associated with symptoms, which makes identification of individuals with this lesion difficult. It is not clear whether eradication of H. pylori infection leads to reversal of gastric IM or the potential decrease in the risk of cancer in these patients. GOALS: The purpose of this pilot study was to define the prevalence of gastric IM in a population at high risk for gastric cancer (Southwestern Hispanics), examine the ability of noninvasive testing to identify individuals with the lesion, and determine whether eradication of H. pylori infection reverses gastric IM in this population. STUDY: Subjects from the Tucson metropolitan area were recruited, and baseline data, including the presence of upper gastrointestinal (UGI) symptoms, urinary sodium, and serum pepsinogen levels, were obtained. Upper endoscopy was performed and six gastric biopsies from specific anatomic sites were obtained, followed by methylene blue staining with targeted biopsies from blue-stained mucosa. Biopsies were evaluated for the presence of H. pylori infection and gastric IM. A subset of patients with gastric IM were treated to eradicate H. pylori infection. Follow-up exams with methylene blue staining, including biopsies for histology and rapid urease testing, were performed for up to 48 months. RESULTS: There were 84 subjects with a mean age of 53.0 years; 24 (29%) had gastric IM and 65 (77%) had H. pylori. There was no significant association between gastric IM and age, gender, UGI symptoms, H. pylori, or urine sodium. There was an association identified between gastric IM and a decreased pepsinogen I:II ratio (p = 0.03). Of the 11 individuals with gastric IM treated for H. pylori infection, 9 had successful therapy and underwent at least 2 follow-up examinations. The mean length of follow-up was 3.3 years. Eight of the nine (89%) had gastric IM identified histologically at the final endoscopic exam. CONCLUSIONS: H. pylori infection and gastric IM are frequent findings in Southwestern Hispanics, a high-risk population for gastric cancer. Noninvasive testing is not clinically useful in distinguishing individuals within this group who harbor gastric IM. Although eradication of H. pylori infection may lead to a decrease in the amount of gastric IM in some individuals, the lesion may be detected in the majority of individuals after more than 3 years of follow-up. These data suggest that therapy for H. pylori may not eliminate the risk of gastric cancer once IM has developed.     

Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.

BACKGROUND: Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability. AIM: To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression. METHODS/SUBJECTS: Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer. RESULTS: All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged. CONCLUSIONS: Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.     

Histological changes of gastric atrophy and intestinal metaplasia after Helicobacter pylori eradication]

BACKGROUND/AIMS: Long-term Helicobater pylori infection results in atrophic gastritis and intestinal metaplasia, and increases the risk of gastric cancer. However, it is still controversial that eradication of H. pylori improves atrophy or metaplasia. Therefore, we investigated histological changes after the H. pylori eradication in patients with atrophy or metaplasia. METHODS: One hundred seven patients who received successful eradication of H. pylori infection in Hanyang University, Guri Hospital from March 2001 to April 2006, were enrolled. Antral biopsy was taken before the eradication to confirm the H. pylori infection and grade of atrophy or metaplasia by updated Sydney System. After a certain period of time, antral biopsy was repeatedly taken to confirm the eradication and investigate histological changes of atrophy or metaplasia. RESULTS: Mean age of the patients was 55.3+/-11.3, and average follow-up period was 28.7+/-13.9 months. Endoscopic diagnosis included gastric ulcer, duodenal ulcer, non-ulcer antral gastritis. Atrophy was observed in 41 of 91 and their average score was 0.73+/-0.92. After the eradication of H. pylori, atrophy was improved (0.38+/-0.70, p=0.025). However, metaplasia which was observed in 49 of 107, did not significantly improve during the follow-up period. Newly developed atrophy (7 of 38) or metaplasia (18 of 49) was observed in patients who without atrophy or metaplasia initially. Their average scores were slightly lower than those of cases with pre-existing atrophy or metaplasia without statistical significance. CONCLUSIONS: After the eradication of H. pylori infection, atrophic gastritis may be improved, but change of intestinal metaplasia is milder and may take longer duration for improvement.