Helicobacter pylori eradication in the healing of atrophic gastritis: A one-year prospective study

Objective. Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. Material and methods. Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58±12.6 years (mean±SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. Results. Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). Conclusions. Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.     

Recovery of gastric function after Helicobacter pylori eradication in subjects with body atrophic gastritis: prospective 4-year study

BACKGROUND: The relationship between Helicobacter pylori (H. pylori) eradication and atrophic changes in the gastric mucosa has not yet been fully defined. Although studies report a partial restoration of serum pepsinogen I (sPGI) levels after eradication, it is not clear if this finding reflects gastric mucosal healing on a morphological level. AIM: To assess alterations in gastric function after H. pylori eradication on moderate/severe body atrophic gastritis by determination of sPGI levels. METHODS: Twenty-three dyspeptic patients, selected from 284 consecutive H. pylori positive patients, with histological features of moderate/severe body atrophic gastritis and sPGI < 25 microg/L (11 men, mean age: 51.8 years, range: 29-79 years), underwent an upper gastrointestinal endoscopy with gastric biopsies and sPGI determination at baseline. All patients underwent eradication therapy. Serum pepsinogen I was measured again after 6 months, and at 1, 2, 3 and 4 years after eradication therapy. RESULTS: Mean sPGI levels prior to eradication were 11.9 microg/L (range: 4-23 microg/L). Six months after eradication therapy, mean sPGI levels significantly increased to 17.4 microg/L (P = 0.04). At the completion of the study, 4 years after eradication, sPGI levels increased from 17.4 to 32.7 microg/L (P = 0.01). A significant progressive increase in sPGI levels was observed from 6 months to 1 year (17.4 to 23.9 microg/L) and from 1 to 2 years (23.9 to 26.0 microg/L, P = 0.01). Serum pepsinogen I levels higher than the cut-off value of 25 microg/L were observed at various time-points: 6.3% of patients at 6 months (1/16), 33.3% (5/15) at 1 year, 50% (7/14) at 24 months, 66.7% (6/9) at 36 months and 87.5% (7/8) at 4 years. CONCLUSION: After H. pylori eradication, subjects with body atrophic gastritis showed long-term improvement of physiological gastric function, reflected by significantly and continually increasing sPGI levels over a 4-year period.     

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.     

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。     

Helicobacter pylori eradication combined with folic acid in the treatment of chronic atrophic gastritis: a long-term follow-up study

正Objective To investigate the clinical and pathological outcome of gastric mucosa lesions in chronic atrophic gastritis treated with Helicobacter pylori(H.pylori)eradication combined with folic acid(three months treatments).Methods From December 2009 to December2010,outpatients with chronic atrophic gastritis were selected and divided into H.pylori positive group and H.     

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.     

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。     

根除Hp与疗胃煎剂对Hp相关CAG治疗作用

目的研究根除Hp与疗胃煎剂对Hp相关CAG的治疗作用.方法实验研究,90 g～110 g,二级Wistar大鼠70只,随机分为疗胃煎剂治疗组(三种不同剂量)、三九胃泰对照组、单纯根除Hp组、自然恢复组与正常组(各10只).采用灌胃接种SS1Hp菌株,灌胃水杨酸钠溶液,交替自由饮用50mL/L乙醇与5 mmol/L去氧胆酸钠溶液的综合方法制备Hp相关CAG动物模型.模型制备成功后均先根除Hp,以三九胃泰为对照进行疗胃煎剂治疗,12 wk疗程结束后,处死动物进行Hp感染,病理组织学检查与粘膜氨基己糖含量检测.临床研究,34例经内镜、病理证实的Hp阳性CAG患者随机分为疗胃煎剂治疗组和硫糖铝对照组,治疗前后分别进行病理组织学及化验指标检测.结果实验研究结果显示,疗胃煎剂中、高剂量组大鼠粘膜萎缩程度较三九胃泰组,自然恢复组及单纯根除Hp组明显减轻[粘膜上皮层厚度(pm)分别为97±14,96±13,73±11,66±12,74±10,P＜0.05],中剂量组粘膜氨基己糖增加,与自然恢复组比较(22.53±4.37)mg/gvs(12.21±2.40)mg/gP＜0.05.自然恢复组Hp均为阳性,粘膜固有层有较明显炎症细胞浸润.其他各实验组Hp阴性,粘膜固有层无明显炎症反应.临床研究结果显示,疗胃煎剂对萎缩病变治疗有效率75%(15/20)明显高于硫糖铝组29%(4/14)(P＜0.01),粘膜氨基己糖含量增加(41.21±7.73,49.72±12.61,P＜0.05).硫糖铝对照组治疗前后无明显变化.结论疗胃煎剂具有增强胃粘膜屏障功能作用,可增加氨基己糖含量,能增加粘膜固有层厚度,是治疗CAG的有效药物.     

幽门螺杆菌的根除与萎缩性胃炎形成和逆转的动物实验研究

目的 明确根除幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒ ｐｙｌｏｒｉ,Ｈｐ）对萎缩性胃炎的形成和逆转的影响。方法 １１０只２级Ｃ５７ＢＬ／６小鼠随机分为实验组（６０只）和对照组（５０只）。实验组感染Ｈｐ后又随机分为Ａ、Ｂ两组,并分别于感染后６个月和１２个月根除Ｈｐ。采用番尼系统、免疫组化及流式细胞术比较根除前后鼠腺胃黏膜组织学和细胞动力学。结果 （１）接受根除治疗的动物Ｈｐ检查均为阴性。根除Ｈｐ可明显     

HOGG1 polymorphism in atrophic gastritis and gastric cancer after Helicobacter pylori eradication

AIM:To investigate the association between Ser326Cys human oxoguanine glycosylase 1(hOGG1) polymorphism and atrophic gastritis and gastric cancer after Helicobacter pylori(H.pylori) eradication.METHODS:A total of 488 subjects(73 patients with gastric cancer,160 with atrophic gastritis after H.pylori eradication and 255 controls) were prospectively collected.Polymerase chain reaction-restriction fragment length polymorphism analysis was performed to distinguish hOGG1 Ser326Cys polymorphism.Statistical analys...     

Helicobacter pylori eradication versus one-year maintenance therapy: effect on relapse and gastritis outcome.

OBJECTIVE: The aim of this study was to determine ulcer healing and H. pylori eradication rates obtained with triple therapy (omeprazole, amoxicillin and clarithromycin). Ulcer relapsing rate one year after eradication was also assessed. Maintenance therapy with placebo was compared with ranitidine therapy and the effect of eradication on histological variables of the gastric mucosa was studied. METHODS: A prospective, double-blind parallel study was performed in 85 patients endoscopically diagnosed of duodenal ulcer H. pylori positive. Patients were randomized to a 7-days triple therapy (group A) or omeprazole plus antibiotic placebo (group B). All patients were treated only with omeprazole for the next three weeks. Patients with ulcer healing after treatment were entered in a one-year follow up phase with ranitidine placebo (group A) or ranitidine (group B). Endoscopy and biopsies were performed at baseline, after treatment (5 weeks) and after 12 months of follow-up or when relapsing symptoms appeared. RESULTS: Healing rate was 90.2% in group A and 85.7% in group B. Eradication rate was 78% in group A and 0% in group B. Out of 37 healed patients in group A, eradication was achieved in 29 and only one relapse was found (3.4%). Three out of eight patients with healing but without eradication relapsed at 12 months (35%) (p < 0.05). Histopathological results showed statistically significant differences (p < 0.05) between eradicated and non eradicated patients in terms of severity of inflammation and intestinal metaplasia, but not in terms of atrophy. CONCLUSIONS: H. pylori eradication is useful to prevent ulcer relapse and to improve gastric mucosa status.     

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.     

叶酸联合幽门螺杆菌根除治疗慢性萎缩性胃炎的疗效观察

目的 探讨叶酸联合幽门螺杆菌(Hp)根除治疗对慢性萎缩性胃炎转归的影响.方法 选取2009年12月至2011年3月南京医科大学第一附属医院经胃镜及病理检查确诊的慢性萎缩性胃炎患者184例,其中Hp阳性90例,阴性94例.Hp阳性患者分为A组43例和B组47例.A组予标准三联Hp根除治疗后再予叶酸治疗3个月.B组和Hp阴性者均予叶酸治疗3个月.各组治疗前、口服叶酸1个月、口服叶酸3个月时分别进行临床症状评分并行t检验.各组治疗前及停药3个月时分别接受胃镜检查,并就胃镜下评分、病理评分行t检验.治疗前及停药3个月时分别抽取55例Hp阴性者静脉血并以ELISA法检测血清胃蛋白酶原(PG)Ⅰ、PGⅡ及胃泌素17水平.结果 所有患者经叶酸治疗1个月时的临床症状评分(1.55±0.04)与治疗3个月时(1.15±0.03)相比差异有统计学意义(t=8.18,P＜0.01).治疗结束时,A组临床症状评分(1.06±0.04)低于B组(1.56±0.08),差异有统计学意义(t=6.00,P＜0.01).所有患者治疗前胃镜下评分(1.57±0.95)与治疗后(1.00±0.76)相比差异有统计学意义(t=11.12,P＜0.01).所有患者治疗前后黏膜炎性反应、活动性、萎缩、肠上皮化生、不典型增生分级评分比较差异均有统计学意义(t值分别=5.51、6.90、7.53、6.34、2.90,P值均＜0.01).55例Hp阴性者治疗前血清PGⅠ水平[(1.03±0.19) nmol/L]低于治疗后[(2.24±0.33) nmol/L],差异有统计学意义(t=3.19,P＜0.01).55例Hp阴性者治疗后胃泌素17水平[(0.86±0.05)nmol/L]较治疗前[(0.47±0.05)nmol/L]增高,差异有统计学意义(t=5.33,P＜0.01).结论 叶酸联合Hp根除治疗对萎缩性胃炎的转归有利,可促进血清PG及胃泌素的分泌.     

Role of gastritis pattern on Helicobacter pylori eradication

Helicobacter pylori eradication rate following standard triple therapy is decreasing. Identification of predictive factors of therapy success would be useful for H. pylori management in clinical practice. This study aimed to evaluate the role of different gastritis patterns on the efficacy of the currently suggested 14-day triple therapy regimen. One-hundred and seventeen, consecutive, non-ulcer dyspeptic patients, with H. pylori infection diagnosed at endoscopy, were enrolled. All patients received a 14-day, triple therapy with lansoprazole 30?mg, clarithromycin 500?mg and amoxicillin 1?g, all given twice daily. Bacterial eradication was assessed with ¹³C-urea breath test 4?C6?weeks after completion of therapy. H. pylori infection was cured in 70.1% at ITT analysis and 83.7% at PP analysis. The eradication rate tended to be lower in patients with corpus-predominant gastritis as compared to those with antral-predominant gastritis at both ITT (66.1 vs 74.5%) and PP (80.4 vs 87.2%) analyses. The multivariate analysis failed to identify factors associated with therapy success. However, 14-day triple therapy does not achieve acceptable H. pylori cure rate in Italy, and should be not recommended in clinical practice.     

Healing of lymphocytic gastritis by eradication of Helicobacter pylori

BACKGROUND: It is not yet clear whether lymphocytic gastritis might not be a sequela of Helicobacter pylori (Hp) infection. The aim of the present pilot study was, therefore, to investigate whether lymphocytic gastritis can be cured by Hp eradication, which, if affirmed, would provide indirect evidence for an etiopathogenic relationship. PATIENTS AND METHODS: 98 of 220 patients with lymphocytic gastritis diagnosed between 1988 and 1998 were investigated at least twice, with 61 of them undergoing Hp eradication treatment. In 29 of these patients, the pretreatment histological work-up using the Warthin-Starry silver stain revealed Hp colonisation, while in the remaining 32 patients the biopsies from the antrum and corpus were negative for Hp. The other 37 patients received no treatment, and served as a control group. RESULTS: Both in the group with Hp-positive, and in the group with Hp-negative histology prior to treatment, eradication treatment led to healing of the gastritis, i.e. to regression of the gastritis parameters including normalisation of the intra-epithelial lymphocyte count, in 93.1% and 84.3% of the cases, respectively. In the control group the histological findings did not change. CONCLUSIONS: The results of our retrospective study support the notion that most cases of lymphocytic gastritis might be a consequence of Hp infection. This, however, needs to be clarified definitively by a prospective, randomized, double-blind study.