A short-term eradication therapy for Helicobacter pylori acute gastritis

BACKGROUND AND AIMS: Acute gastritis, caused by an initial infection of Helicobacter pylori (H. pylori), may resolve spontaneously, but the infection sometimes becomes chronic. We examined the efficacy of a short-term H. pylori eradication therapy on acute gastritis. METHODS: Among the 15 patients with hemorrhagic acute gastritis who were randomly allocated to group A (eradication therapy) or group B (Lansoprazole, LPZ), 10 of them started to receive treatment within 1 day after the disease onset. The other five patients began the eradication therapy 4-6 days after disease onset (group C). Eradication therapy consisted of a daily oral administration of each of 30 mg lansoprazole (LPZ), once a day; 400 mg clarithromycin, twice a day; 1000 mg amoxicillin, twice a day; and 300 mg rebamipide, three times a day, for one week. If the endoscopy was normal, medication was stopped for the following 4 weeks before gastric endoscopy was performed again in order to assess H. pylori eradication. RESULTS: All group A patients were cured after the 1-week treatment and therefore, they became H. pylori negative. Group B and C patients had erosions or ulcers after the 1-week treatment and so received an additional 3-week administration of LPZ. Four weeks later, their gastritis was cured and except for one group B patient, they became H. pylori-negative. CONCLUSION: In patients with acute gastritis, caused by an initial H. pylori infection, eradication therapy was efficacious in achieving early healing. This therapy should be started as soon as possible after disease onset.     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

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

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

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

幽门螺杆菌相关性胃炎患者血清胃蛋白酶原检测的临床价值

背景幽门螺杆菌(Helicobacter pylori,Hp)可引起胃黏膜细胞的慢性炎症,并诱导胃黏膜细胞分泌胃蛋白酶原,导致血液中胃蛋白酶原含量的变化。目的探讨Hp相关性胃炎患者血清胃蛋白酶原含量变化的临床价值。方法对经胃镜和病理证实为浅表性胃炎和萎缩性胃炎的患者按照Hp阳性及阴性进行分组,采用ELISA法对其血清PGⅠ、PGⅡ含量进行检测,血清Hp-IgG抗体采用定性分析法。结果无论浅表性胃炎或萎缩性胃炎,Hp阳性组同阴性组之间比较,差异均有显著意义(P0.05);在萎缩性胃炎组中,血清PGⅠ含量较浅表性胃炎组者中明显降低,两者相比差异有显著意义(P0.05)。结论Hp感染慢性胃炎患者血清中PGⅠ、PGⅡ含量明显增加,PGⅠ含量的变化可以反映胃黏膜病变的程度。     

Omeprazole attenuates neutrophil-endothelial cell adhesive interaction induced by extracts of Helicobacter pylori

In this study, the influence of omeprazole on the adhesive activity of neutrophils, provided by an extract of Helicobacter pylori, was determined. Human neutrophils were collected from peripheral blood and labelled with a fluorochrome. Helicobacter pylori (NCTC 11637) was cultured and its water extract was obtained by centrifugation of the bacterial suspension. Neutrophils were incubated with the extract in a plastic plate. Percentage adherence was calculated by measuring the fluorescence of floating and adherent cells. Rat mesenteric venule was prepared on an intravital microscope and the number of neutrophils which adhered to venular endothelium was counted. Neutrophil adherence to the plastic plate was increased by the presence of H. pylori extract. Pretreatment with omeprazole significantly decreased this adherence in a dose-dependent manner (10(-6)-10(-4)mol/L). Neutrophil adherence to the mesenteric venule was also increased by H. pylori extract and significantly inhibited by omeprazole. These results indicate that the neutrophil-endothelial adhesive interaction is inhibited by omeprazole, suggesting that omeprazole prevents neutrophil recruitment to the gastric mucosa associated with H. pylori infection.     

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...     

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

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

Lafutidine inhibits Helicobacter pylori-induced interleukin-8 production in human gastric epithelial cells

BACKGROUND AND AIM: Attachment of Helicobacter pylori to gastric epithelial cells leads to the production of chemokines, such as interleukin-8 (IL-8), which in turn activate and recruit neutrophils to the site of infection. Lafutidine [(+/-)-2-(furfurylsulfinyl)-N-(4-(4-(piperidinomethyl)-2-pyridyl)oxy-(Z)-2-butenyl)acetamide] is a new type of antiulcer drug that possesses an antisecretory action as well as gastroprotective activity, independent of its antisecretory action. In the present study, we examined the effects of lafutidine on H. pylori-induced IL-8 release and H. pylori adhesion to MKN45 cells. METHODS: MKN45 cells were stimulated with H. pylori, tumor necrosis factor (TNF)-alpha, or IL-1beta, then IL-6 and IL-8 levels in the culture supernatants were determined with a specific enzyme-linked immunosorbent assay kit. RESULTS: Lafutidine significantly inhibited both the release of IL-8 induced by H. pylori and the adhesion of H. pylori to cells in a dose-dependent manner. These properties of lafutidine are unrelated to the blockade of histamine H(2)-receptors, because the same effects have not been observed with other H(2)-receptor antagonists, such as cimetidine and famotidine. Lafutidine also significantly inhibited H. pylori-induced IL-6 release. Both TNF-alpha and IL-1beta-induced IL-8 releases, conversely, were little affected by lafutidine up to a concentration of 10(-5) M. CONCLUSIONS: These results suggest that lafutidine inhibits IL-8 release by inhibiting H. pylori adherence to gastric epithelial cells, indicating a novel mechanism by which lafutidine protects against the mucosal inflammation associated with H. pylori infection.     

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。     

Effects of clarithromycin,omeprazole and leminoprazole on gastric ulcer healing in Helicobacter pylori-infected rats

Abstract We examined whether a single inoculation of Helicobacter pylori can colonize the stomachs of ulcerated rats and delay their healing and whether an antibiotic drug and acid pump inhibitors can enhance the ulcer healing in infected rats. Ulcers were produced by a submucosal injection of acetic acid solution into the gastric wall. Helicobacter pylori (ATCC-43504) was inoculated into rats with and without gastric ulcers. The animals were killed 2, 4, 6, 8 or 10 weeks after the inoculation and the ulcerated area and H. pylori viability were determined. Each test drug and their combination was administered for 1 or 2 weeks after H. pylori inoculation. Helicobacter pylori could not colonize the stomachs of normal rats, but could colonize stomachs with ulcers for 10 weeks at an incidence of >80%. Spontaneous healing of gastric ulcers was delayed by H. pylori infection during these 10 weeks. Daily treatment with clarithromycin significantly and dose-dependently delayed ulcer healing in infected rats. Both omeprazole and leminoprazole significantly enhanced ulcer healing and inhibited the clarithromycin-delayed ulcer healing. We conclude that: (i) H. pylori can colonize rat stomachs with ulcers and delay ulcer healing; (ii) clarithromycin delays ulcer healing in H. pylori-infected rats; and (iii) acid pump inhibitors inhibited the clarithromycin-delayed ulcer healing.     

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。     

非溃疡性消化不良及慢性非萎缩性胃炎幽门螺杆菌感染4年前后比较

目的了解成都地区非溃疡性消化不良(NUD)及慢性非萎缩性胃炎(NAG)患者幽门螺杆菌(H.pylori)感染情况及变化趋势。方法纳入经胃镜检查确诊为NUD及NAG患者共2 403例,其中2008年1 042例,2012年1 361例。将NAG患者分为非糜烂性胃炎(NEG)、平坦糜烂性胃炎(FEG)及隆起糜烂性胃炎(REG)三组。所有患者以ASSURE快速血清学方法检测H.pylori感染状态。结果 4年后H.pylori现症感染总体检出率显著下降(35.1%vs 24.8%,P0.01),在NUD、所有NAG患者及FEG患者中均显著下降(P0.05)。H.pylori现症感染检出率FEG患者明显高于同期REG、NEG、NUD患者(P0.05)。REG患者与同期NEG、NUD患者比较,差异无统计学意义(P0.05)。4年后FEG、REG患者H.pylori既往感染率明显升高(FEG:3.5%vs 10.8%,REG:5.2%vs 12.9%,P0.05)。结论 2008年至2012年成都地区NUD及NAG患者H.pylori现症感染率显著下降,FEG、REG H.pylori既往感染率明显升高。NAG患者中可能FEG与H.pylori感染关系更为密切。     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

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

Evaluation of combined antibiotic-omeprazole therapies in Helicobacter pylori-infected Mongolian gerbils

Mongolian gerbils are a laboratory host for gastric colonization with Helicobacter pylori, showing gastritis followed by typical gastric ulcer after infection with H. pylori. In such gerbils, we evaluated combined therapies of amoxicillin (AMPC) and clarithromycin (CAM) as antibiotics, and omeprazole (OPZ) as a H⁺/K⁺ adenosine triphosphatase (ATPase) inhibitor. The gerbils were orally inoculated with 2 × 10⁸ bacilli of ^{H. pylori} ATCC 43504. Four weeks after inoculation, the infected gerbils were orally treated singly with OPZ, AMPC, and CAM, and their insufficient efficacy on bacterial clearance was confirmed by a polymerase chain reaction technique, and by a culture method. In contrast, combined therapy of OPZ plus either AMPC or CAM showed significant bacterial clearance, demonstrating the efficacy of this combined therapy in the gerbil model. Mongolian gerbils are suggested to be useful for the pharmacological evaluation of anti-H. pylori compounds. Received Mar. 11, 1997; accepted June 27, 1997     

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

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

A topographic study of Helicobacter pylori density, distribution and associated gastritis

BACKGROUND AND AIMS: The topographic distribution and density of Helicobacter pylori and associated gastritis in the stomach were studied in order to determine which biopsy sites are likely to provide the maximum yield so as to reduce the fallacious results due to sampling error. METHODS: Fifty patients with upper gastrointestinal symptoms were studied. Eleven gastric biopsies from predetermined sites were obtained and subjected to ultra-rapid urease test, imprint cytology and histology. Haematoxylin and eosin stain was used for defining gastritis and other associated histopathological details. Loeffler's methylene blue stain was used to confirm the presence of H. pylori in imprint smears and histological sections. RESULTS: All 50 patients had H. pylori infection and evidence of chronic gastritis at one or more of the 11 biopsy sites. Maximum and minimum percentage positivity were observed at A3 (antral lesser curvature) and B4 (corpus greater curvature), respectively. Various sites in decreasing order of percentage positivity were A3 > A2 > A1 > A4 > B3 > B1 > A5 > B6 > B5 > B2 > B4. Among the biopsies obtained from the corpus, B3 (corpus lesser curvature) was the site with maximum positivity. A3 and B4 had a statistically significant difference in percentage positivity (P < 0.0001) for H. pylori and gastritis. The maximum and minimum density scores of H. pylori and gastritis were found in A3 and the B4, respectively. A3 had a significantly higher (P < 0.0001) mean density score than any other site in the stomach. The difference in the grading of H. pylori between A3 and B3 (sites of maximum positivity in antrum and corpus) was statistically significant (P < 0.0001). A statistically significant (P < 0.001) positive correlation between increasing grades of H. pylori and gastritis was observed at the site of maximum density. Eighty per cent of the patients had antral predominant gastritis and in 82%, H. pylori was predominantly observed in antral biopsies. CONCLUSION: It is concluded that two biopsies taken from A3 are sufficient for confirmation of presence of H. pylori and associated gastritis for initiation of treatment. However, additional biopsies from B3 will help in deciding the topographic pattern of gastritis.