十二指肠溃疡患者H pylori根治前后NO、TNFα含量和NOS表达的变化及意义

目的:观察H pylori感染对十二指肠溃疡(DU)患者NOS、NO和TNFα的影响,探讨H.pylori感染、NO和TNFα在DU中的作用和意义. 方法:随机选择经电子胃镜和病理检查确诊的H pylori阳性DU患者60例,采用快速尿素酶试验、组织涂片Gram染色和Warthin-Starry银染色进行Hpylori检测.用兰索拉唑+ 阿莫西林+克拉霉素治疗7 d,于H pylori根治前后检测血清NO、TNFα的含量、免疫组化法检测胃窦黏膜eNOS 和iNOS蛋白的表达,并与内镜和病理检查证实胃黏膜大致正常H.pylori阴性的15名健康志愿者作对照观察. 结果:Hpylori根治率为82.14%(46/56),溃疡愈合率89.28% (50/56).正常人胃黏膜以eNOS表达为主、iNOS表达很少,NO、TNFα含量少,H pylori感染后胃黏膜eNOS、iNOS表达和NO、TNFα含量较正常对照增加(3568.78±624.34.238.43±72.92与2448.27±723.31,138.53±59.65; P<0.001),iNOS表达更显著.H pylori根除后,eNOS、iNOS的表达以及No和TNFα含量(2908.74±717.58, 142.43±58.63)均低于治疗前(P<0.001),但iNOS和NO仍高于正常对照组(P<0.05). 结论:iNOS过度表达和NO、TNFα含量增加可能在消化性溃疡的发病机制中发挥一定作用,有可能是Hpylori感染导致消化性溃疡的发病机制之一.NO在溃疡的愈合中也起一定作用.

H pylori and gastric cancer: Shifting the global burden

Infection with H pylori leads to a persistent chronic in?ammation of the gastric mucosa, thereby increasing the risk of distal gastric adenocarcinoma. Numerous studies have determined a clear correlation between H pylori infection and the risk of gastric cancer; however, general eradication is not recommended as cancer prophylaxis and time points for treatment remain controversial in different areas of the world. Prevalence rates in Western countries are decreasing, especially in younger people (< 10%); and a decline in distal gastric adenocarcinoma has been observed. Risk groups in Western countries still show considerably higher risk of developing cancer, especially in patients infected with cagA + strains and in persons harboring genetic polymorphism of the IL-1B promoter (-511T/T) and the corresponding IL-1 receptor antagonist (IL-1RN*2). Thus, general eradication of all infected persons in Western countries not recommended and is limited to risk groups in order to achieve a risk reduction. In contrast, infection rates and cancer prevalence are still high in East Asian countries. A prevention strategy to treat infected persons may avoid the development of gastric cancer to a large extent and with enormous clinical importance. However, studies in China and Japan indicate that prevention of gastric cancer is effective only in those patients that do not display severe histological changes such as atrophy and intestinal metaplasia. Thus, prophylactic strategies to prevent gastric cancer in high risk populations such as China should therefore especially aim at individuals now at younger age when the histological alterations caused by the bacterial infection was still reversible. In countries with a low prevalence of gastric cancer, risk groups carrying cagA+ strains and IL-1 genetic polymorphisms should be identi?ed and treated.

Antimicrobial activity of Sapindus mukorossi and Rheum emodi extracts against H pylori: In vitro and in vivo studies

AIM: To evaluate the antibacterial activity of Sapindus mukorossi (S. mukorossi) and Rheum emodi (R. emodi). METHODS: Powders of S. mukorossi and R. emodi were extracted successively with petroleum ether, benzene, chloroform and ethanol and were concentrated in vacuum. The disk diffusion method was used for in vitro studies and in vivo studies were performed on male Wister rats. Thirty resistant clinical isolates of H pylori, as determined by their antibiotic sensitivity patterns by E-test, along with two Gram +ve (S. aureus, B. subtilis) and two Gram -ve (E. coli, P. vugaris) organisms were screened for their susceptibility patterns against these extracts. RESULTS: In our screening, all 30 resistant isolates and the other four organisms (two Gram +ve S. aureus, B. subtilis and two Gram -ve, E. coli, P. vugaris) were sensitive to the test compounds. It was found that ethanol and chloroform extracts of S. mukorossi and ethanol and benzene extracts of R. emodi inhibited H pylori at very low concentrations. In the in vitro study, the isolates showed a considerable zone of inhibition at very low concentrations (10 μg/mL) for both the extracts. In the in vivo study, the H pylori infection was cleared with minimal doses of extracts of S. mukorossi (2.5 mg/mL) and R. emodi (3.0 mg/mL) given orally for seven days. CONCLUSION: We can conclude from this study that the extracts of S. mukorossi and R. emodi inhibited the growth of pylori in vitro and, in in vivo studies, the H pylori infection cleared within seven days at very low concentrations. We also found that H pylori did not acquire resistance against these herbal extracts even after 10 consecutive passages.

Th immune response induced by H pylori vaccine with chitosan as adjuvant and its relation to immune protection

AIM:To study the immunological protective effect of H pylori vaccine with chitosan as an adjuvant and its mechanism.METHODS:Female BALB/c mice were randomly divided into seven groups and orally immunized respectively with PBS,chitosan solution,chitosan particles,H pylori antigen,H pylori antigen plus cholera toxin(CT),H pylori antigen plus chitosan solution,H pylori antigen plus chitosan particles once a week for four weeks.Four weeks after the last immunization,the mice were challenged twice by alive H pylori(1 × 109 CFU/mL)and sacrificed.Part of the gastric mucosa was embedded in paraffin,cut into sections and assayed with Giemsa staining.Part of the gastric mucosa was used to quantitatively culture H pylori.ELISA was used to detect cytokine level in gastric mucosa and anti-H pylori IgG1,IgG2a levels in serum.RESULTS:In the groups with chitosan as an adjuvant,immunological protection was achieved in 60% mice,which was significantly higher than in groups with H pylori antigen alone and without H pylori antigen(P < 0.05 or 0.001).Before challenge,the level of IFN and IL-12 in gastric mucosa was significantly higher in the groups with chitosan as an adjuvant than in the control group and the group without adjuvant(P < 0.05 or 0.005).After challenge,the level of IFN and IL-12 was significantly higher in the groups with adjuvant than in the groups without adjuvant and antigen(P < 0.05 or 0.001).Before challenge,the level of IL-2 in gastric mucosa was not different among different groups.Afterchallenge the level of IL-2 was significantly higher in the groups with adjuvant than in the control group(P < 0.05 or 0.001).Before challenge,the level of IL-10 in gastric mucosa was significantly higher in the groups with chitosan as an adjuvant than in other groups without adjuvant(P < 0.05 or 0.01).After challenge,the level of IL-10 was not different among different groups.Before challenge,the level of IL-4 in gastric mucosa was significantly higher in the groups with chitosan as an adjuvant than in other groups without adjuvant(P < 0.05).After challenge,the level of IL-4 was significantly higher in the groups with chitosan particles as an adjuvant than in the group with CT as an adjuvant(P < 0.05),and in the group with chitosan solution as an adjuvant,the level of IL-4 was significantly higher than that in control group,non-adjuvant group and the groups with CT(P < 0.05 or 0.001).The ratio of anti-H pylori IgG2a/IgG1 in serum was significantly lower in the groups with chitosan as an adjuvant than in the groups with CT as an adjuvant or without adjuvant(P < 0.01).CONCLUSION:H pylori vaccine with chitosan as an adjuvant can protect against H pylori infection and induce both Th1 and Th2 type immune response.

Influence of H pylori on plasma ghrelin in patients without atrophic gastritis

AIM:To determine the association between H pylori infection and serum ghrelin levels in patients without atrophic gastritis.METHODS:Fifty consecutive patients(24 males and 26 females)with either H pylori-positive gastritis(n = 34)or H pylori-negative gastritis(n = 16)with normal gastric acid secretion determined by 24-h pHmetry and without atrophic gastritis in histopathology were enrolled in this study.Thirty-four H pylori-infected patients were treated with triple therapy consisting of a daily regimen of 30 mg lansoprazole bid,1 g amoxicillin bid and 500 mg clarithromycin bid for 14 d,followed by an additional 4 wk of 30 mg lansoprazol treatment.H pylori infection was eradicated in 23 of 34(67.6%)patients.H pylori-positive patients were given eradication therapy.Gastric acidity was determined via intragastric pH catethers.Serum ghrelin was measured by radioimmunoassay(RIA).RESULTS:There was no signifficant difference in plasma ghrelin levels between H pylori-positive and H pylori-negative groups(81.10 ± 162.66 ng/L vs 76.51 ± 122.94 ng/L).In addition,there was no significant difference in plasma ghrelin levels and gastric acidity levels measured before and 3 mo after the eradication therapy.CONCLUSION:H pylori infection does not influence ghrelin secretion in patients with chronic gastritis without atrophic gastritis.

H pylori and host interactions that influence pathogenesis

H pylori is probably the most prevalent human patho- gen worldwide. Since it was initially suggested in 1983 by Marshall and Warren to be implicated in gastritis and peptic ulcer disease, H pylori has also been implicated in gastric carcinoma and was classified as a class I car- cinogen. In the last two decades, a noteworthy body of research has revealed the multiple processes that this gram negative bacterium activates to cause gastroduo- denal disease in humans. Most infections are acquired early in life and may persist for the life of the individual. While infected individuals mount an inflammatory re- sponse that becomes chronic, along with a detectable adaptive immune response, these responses are ineffec- tive in clearing the infection. H pylori has unique features that allow it to reside within the harsh conditions of the gastric environment, and also to evade the host immune response. In this review, we discuss the various virulence factors expressed by this bacterium and how they inter- act with the host epithelium to influence pathogenesis.

Dyslipidemia and H pylori in gastric xanthomatosis

AIM: To investigate the relationship among gastric xanthomatosis (GX), H pylori, dyslipidemia, and gastritis in Korea, a well-known H pylori endemic area. METHODS: A total of 771 patients who had undergone gastroduodenoscopy by one endoscopist were included in this study. Among them, 54 patients with GX were assessed for H pylori infection and their endoscopic characteristics and serum lipid profiles. The findings were compared with 54 age-and sex-matched control subjects without GX. RESULTS: The prevalence of GX was 7% (54/771) with no sex difference. GX was mainly single (64.8%) and located in the antrum (53.7%). The mean diameter was 7 ± 3 mm. Mean body mass index (BMI) of patients with GX was 23.1 ± 2.8 and no one was above 30. Compared with the controls, lipid profiles of GX group showed significantly lower HDL-cholesterol (48.8 ± 12.3 vs 62.9 ± 40.5, P = 0.028) and higher LDL-cholesterol (112.9 ± 29.9 vs 95.9 ± 22.4, P = 0.032). The level of total serum cholesterol, triglyceride and the existence of dyslipoproteinemia were not related to the presence of GX. However, GX showed a close relationship with endoscopically determined atrophic gastritis and histologic severity (24/53, 44.4% vs 8/54, 14.8%, P = 0.0082). H pylori infection and bile reflux gastritis were not significantly related with GX. CONCLUSION: The prevalence of GX is 7% and it may be an increasing entity in Korea. Moreover, dyslipidemia and atrophic gastritis are found to be related to GX, but H pylori infection is not.

Relationship between the cytotoxin-associated gene-A status of H pylori strains and cerebral infarction in European Caucasians and Chinese Han: A meta-analysis

AIM:To study the relationship between the cytotoxin-associated gene-A (CagA) status of H pylori strains and cerebral infarction among European Caucasians and Chinese Han by conducting a meta-analysis. METHODS:Ten case-control studies, with data on a total of 907 cases and 966 controls, were retrieved and considered;disqualified studies were excluded. The included studies were then tested for heterogeneity, and a meta-analysis was performed. RESULTS:The combined data revealed CagA-bearing strains of H pylori which cause chronic infection are associated with an increased risk of cerebral infarction (OR = 2.66, 95% CI:2.17-3.26), but no such relationship was found with CagA-negative strains (OR = 0.74, 95% CI:0.49-1.10) in the overall population. We performed subgroup analyses, dividing the overall population into European Caucasians and Chinese Han subgroups, and analyzed the studies according to their subgroup classification. Through the subgroup analysis, an association between cerebral infarction and CagA-bearing strains was found in both subgroups (OR = 2.60, 95% CI:1.93-3.49 in Chinese Han;OR = 2.71, 95% CI:2.05-3.59 in European Caucasians), but no significant association was found between cerebral infarction and CagA-negative strains (OR = 0.81, 95% CI:0.45-1.48 in Chinese Han;OR = 0.64, 95% CI:0.37-1.09 in European Caucasians).CONCLUSION:These results suggest CagA-bearing strains of H pylori are significantly associated with susceptibility to cerebral infarction in Chinese Han and European Caucasians, but that CagA-negative strains are not a definite predisposing factor in either subgroup. The magnitude of this association with cerebral infarction needs to be confirmed by prospective studies and combined studies of H pylori eradication.

Expression of mutant type-p53 products in H pylori-associated chronic gastritis

AIM:To investigate the mutation of p 53 immuno-histochemically in non-tumorous gastric mucosa with H pylori infection before and after H pylori eradication therapy.METHODS:53 subjects(36 male,17 female,mean age ± SEM,57.1 ± 12.1)undergoing endoscopic examination were included in this study.42 of 53 patients were H pylori-positive,and 11 were H pylori-negative.All H pylori-positive patients had successful eradication therapy.Biopsy specimens were taken from five points of the stomach,as recommended by the updated Sydney system.Immunohistochemical studies were performed by using primary antibodies against p53(DO-7 and PAb240).RESULTS:p53(DO-7 and PAb240)immunoreactivity was shown in the neck region of the gastric pits,however,quite a few cells were found to be immunopositive for p 53(PAb240)in the H pylori-infected gastric mucosa.The proportion of patients immunopositive for p 53(PAb240)was significantly reduced 6 mo after eradication [28/42(66.7%)to 6/42(14.3%)](P < 0.05),while the biopsies taken from H pylori-negative patients showed no immunoreactivity for p53(PAb240).p53(PAb240)-positive patients were divided into two groups by the number of positive cells detected:one with more than six positive cells per 10 gastric pits(group A,n = 12),and the other with less than five positive cells per 10 gastric pits(group B,n = 30).Atrophy scores in group A were significant higher than those in group B at the greater curvature of the antrum(group A:2.00 ± 0.14 vs group B:1.40 ± 0.15,P = 0.012),the lesser curvature of the corpus(group A:2.00 ± 0.21 vs group B:1.07 ± 0.23,P = 0.017),and the greater curvature of the corpus(group A:1.20 ± 0.30vs group B:0.47 ± 0.21,P = 0.031).Group A showed significant higher intestinal metaplasia scores than group B only at the lesser curvature of the antrum(group A:2.10 ± 0.41 vs group B:1.12 ± 0.29,P = 0.035).CONCLUSION:H pylori-associated chronic gastritis expressed the mutant-type p53,which was significantly associated with more severe atrophic and metaplastic changes.H pylori eradication led to a significant reduction in the expression of the mutant-type p53.It is considered that H pylori-infected chronic gastritis is associated with a genetic instability that leads to gastric carcinogenesis,and H pylori eradication may prevent gastric cancer.

Clinical role and importance of fluorescence in situ hybridization method in diagnosis of H pylori infection and determination of clarithromycin resistance in H pylori eradication therapy

H pylori is etiologically associated with gastritis, gas-tric and duodenal ulcers, gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. Eradicating H pylori may convert rapidly the outcome of related diseases with the use of more accurate diagnostic molecular tests. Indeed some of the tests cannot give the evidence of current infection; H pylori can be detected by noninvasive and invasive methods, the latter requiring an endoscopy. Eradication failure is a big problem in H pylori infection. Recently, clarithromycin resistance in H pylori strains is increasing and eradicati-on therapy of this bacterium is becoming more difficult. Molecular methods have frequently been applied besides phenotypic methods for susceptibility testing to detect clarithromycin resistance due to mutations in the 2143 and 2144 positions of 23S rRNA gene. Fluorescence in situ hybridization (FISH) method on paraffin embedded tissue is a rapid, accurate and cost-effective method for the detection of H pylori infection and to determine clarithromycin resistance within three hours according to the gold standards as a non-culture method. This method can also be applied to fresh biopsy samples and the isolated colonies from a culture of H pylori, detecting both the culturable bacillary forms and the coccoid forms of H pylori, besides the paraffin embedded tissue secti-ons. This technique is helpful for determining the bac-terial density and the results of treatment where clarith-romycin has been widely used in populations to increase the efficacy of the treatment and to clarify the treatment failure in vitro.

H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease

AIM: To determine the overall prevalence of H pylori and CagA positive H pylori infection and the prevalence of other bacterial and viral causes of chronic infection in patients with coronary heart disease (CHD), and the potential role of anti-heat-shock protein 60 (Hsp60) anti- body response to these proteins in increasing the risk of CHD development. METHODS: Eighty patients with CHD and 160 controls were employed. We also compared the levels of anti- heat-shock protein 60 (Hsp60) antibodies in the two groups. The H pylori infection and the CagA status were determined serologically, using commercially available enzyme-linked immunosorbent assays (ELISA), and a Western blotting method developed in our laboratory. Systemic antibodies to Hsp60 were determined by a sandwich ELISA, using a polyclonal antibody to Hsp60 to sensitise polystyrene plates and a commercially available human Hsp60 as an antigen. RESULTS: The overall prevalence of H pylori infec- tion was 78.7% (n = 63) in patients and 76.2% (n = 122) in controls (P = 0.07). Patients infected by CagA- positive (CagA+) H pylori strains were 71.4% (n = 45) vs 52.4% of infected controls (P = 0.030, OR = 2.27). Sys-temic levels of IgG to Hsp60 were increased in H pylori- negative patients compared with uninfected controls (P < 0.001) and CagA-positive infected patients compared with CagA-positive infected controls (P = 0.007). CONCLUSION: CagA positive H pylori infection may concur to the development of CHD; high levels of anti- Hsp60 antibodies may constitute a marker and/or a con- comitant pathogenic factor of the disease.

H pylori infection causes chronic pancreatitis in Mongolian gerbils

AIM: To investigate whether chronic H pylori infection has the potential to induce pancreatitis in the Mongolian gerbil model, and whether it is dependent on an intact type Ⅳ secretion system. METHODS: Mongolian gerbils were infected with wild type (WT) H pylori typeⅠstrain B128 or its isogenic mutant B128 ?cagY (defective type Ⅳ secretion). After seven months of infection, H pylori was reisolated from antrum and corpus and H pylori DNA was analyzed by semi- nested polymerase chain reaction (PCR). Inflammation and histological changes were documented in the gastric antrum, corpus, and pancreas by immunohistochemistry. Cytokine mRNA, gastric pH, plasma gastrin, amylase, lipase, and glucose levels were determined. RESULTS: The H pylori infection rate was 95%. Eight infected animals, but none of the uninfected group, developed transmural inflammation and chronic pancreatitis. Extensive interstitial fibrosis and inflammation of the pancreatic lobe adjacent to the antrum was confirmed by trichrome stain, and immuno- histochemically. Pro-inflammatory cytokine mRNA was significantly increased in the antral mucosa of all infected gerbils. In the corpus, only cytokine levels of WT-infected animals and those developing transmural inflammation and pancreatitis were significantly increased. Levels of lipase, but not glucose or amylase levels, were significantly reduced in the pancreatitis group. H pylori DNA was detected in infected antral and corpus tissue,but not in the pancreas. CONCLUSION: H pylori infection is able to induce chronic pancreatitis in Mongolian gerbils independently of the type Ⅳ secretion system, probably by an indirect mechanism associated with a penetrating ulcer.

Association between the presence of H pylori in the liver and hepatocellular carcinoma: A meta-analysis

AIM: To evaluate the arguments for and against the possible roles of H pylori in hepatocellular carcinoma (HCC). METHODS: We performed a systematic review of all relevant studies published in the literature. A total of 103 clinical trials and reports were identified, but only 10 trials qualified under our selection criteria. A meta-analysis was carried out by a biostatistician according to the Cochrane Reviewers’ Handbook recommended by The Cochrane Collaboration.RESULTS: Nine case-control studies and one retrospective cross sectional study were included in the final analysis. Overall the prevalence of H pylori infection was 53.3% (129 of 242) in cases and 10.4% (29 of 280) in controls, and the summary odds ratio for the association of H pylori infection with the risk for HCC (using the fixed-effects model, which accounted for the homogeneity across the 10 studies) was determined to be 13.63 (95% CI, 7.90-23.49).CONCLUSION: Our analysis showed a positive association between H pylori infection and the risk of HCC, with an indication of possible publication bias and possible confounders due to study designs that showed results of less pronounced associations.

H pylori eradication:A randomized prospective study of triple therapy with or without ecabet sodium

AIM: To investigate whether adding ecabet sodium to the standard triple therapy for H pylori infection improve eradication rate. METHODS: Two hundred and fifty-seven H pylori-infected patients were randomly assigned to standard triple therapy (group A, n = 129) or triple therapy plus ecabet sodium (group B, n = 128). Successful eradication was defined as a negative 13C-urea breath test 6-8 wk after completion of treatment. RESULTS: After completion of therapy, 194/257 patients showed negative 13C-urea breath test results. According to intention-to-treat analysis, the infection was eradicated in 93/129 (72.1%) patients in group A and 101/128 (78.9%) in group B (P = 0.204). Per-protocol analysis showed successful eradication in 93/118 (78.8%) patients from group A and 101/114 (88.6%) from group B (P = 0.044). There were no significant differences in the side effects experienced by the patients in the two treatment groups. CONCLUSION: Our results suggest that the addition of ecabet sodium improves the efficacy of the standard triple therapy for H pylori.

CagA+ H pylori infection is associated with polarization of T helper cell immune responses in gastric carcinogenesis

AIM:To characterize the immune responses including local and systemic immunity induced by infection with H pylori,especially with CagA+ H pylori strains and the underlying immunopathogenesis. METHODS:A total of 711 patients with different gastric lesions were recruited to determine the presence of H pylori infection and cytotoxin associated protein A (CagA),the presence of T helper (Th) cells and regulatory T (Treg) cells in peripheral blood mononuclear cells (PBMCs),expression of plasma cytokines,and RNA and protein expression of IFN-γ and IL-4 in gastric biopsies and PBMCs were determined by rapid urease test,urea 14C breath test,immunoblotting test,flow cytometry ,real time RT-PCR and immunohistochemistry. RESULTS:Of the patients,629 (88.47%) were infected with H pylori ; 506 (71.16%) with CagA+ and 123 (17.30%) with CagA- strains. Among patients infected with CagA+ H pylori strains,Th1-mediated cellular immunity was associated with earlier stages of gastric carcinogenesis,while Th2-mediated humoral immunity dominated the advanced stages and was negatively associated with an abundance of Treg cells. However,there was no such tendency in Th1/Th2 polarization in patients infected with CagA- H pylori strains and those without H pylori infection. CONCLUSION:Polarization of Th cell immune responses occurs in patients with CagA+ H pyloriinfection,which is associated with the stage and severity of gastric pathology during the progression of gastric carcinogenesis. This finding provides further evidence for a causal role of CagA+ H pylori infection in the immunopathogenesis of gastric cancer.

H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: A retrospective study

AIM: To identify and evaluate the relative impact of H pylori infection and other risk factors on the occurrence of gastric ulcer (GU), duodenal ulcer (DU) and gastritis in Turkish patients. METHODS: A total of 4471 patients (48.3% female) out of 4863 attended the Samatya hospital in Istanbul (June 1999 - October 2003) were included. The records of H pylori status (CLO-test), endoscopic f indings of GU, DU and gastritis, personal habits (smoking, alcohol intake) and medication [non-steroidal anti-inflammatory drugs (NSAIDs), aspirin intake] were analyzed using multi-way frequency analysis. RESULTS: We have found that GU in the presence of H pylori had significant association with aspirin (P = 0.0001), alcohol (P = 0.0090) and NSAIDs (P = 0.0372). DU on the other hand had significant association with aspirin/ smoking/NSAIDs (P = 0.0259), aspirin/alcohol (P = 0.0002) and aspirin/smoking (P = 0.0233), also in the presence of H pylori. In the absence of H pylori GU had significant association with alcohol/NSAIDs (P = 0.0431), and NSAIDs (P = 0.0436). While DU in the absence of H pylori had significant association with smoking/alcohol/ NSAIDs (P = 0.0013), aspirin/NSAIDs (P = 0.0334), aspirin/alcohol (P = 0.0360). CONCLUSION: In the presence of H pylori, aspirin, alcohol and NSAIDs intake act as an independent risk factors that had an augmenting impact on the occurrence of GU and only together on the occurrence of DU in Turkish patients.

Red wine and green tea reduce H pylori- or VacA-induced gastritis in a mouse model

AIM: To investigate whether red wine and green tea could exert anti-H pylori or anti-VacA activity in vivo in a mouse model of experimental infection.METHODS: Ethanol-free red wine and green tea concentrates were administered orally as a mixture of the two beverages to H pylori infected mice, or separately to VacA-treated mice. Gastric colonization and gastric in? ammation were quantifi ed by microbiological, histopathological, and immunohistochemical analyses. RESULTS: In H pylori -infected mice, the red wine and green tea mixture significantly prevented gastritis and limited the localization of bacteria and VacA to the surface of the gastric epithelium. Similarly, both beverages significantly prevented gastric epithelium damage in VacA-treated mice; green tea, but not red wine, also altered the VacA localization in the gastric epithelium. CONCLUSION: Red wine and green tea are able to prevent H pylori -induced gastric epithelium damage, possibly involving VacA inhibition. This observation supports the possible relevance of diet on the pathological outcome of H pylori infection.

Effects of the myeloperoxidase 463 gene polymorphisms on development of atrophy in H pylori infected or noninfected gastroduodenal disease

AIM: To investigate the relationship between myelo- peroxidase polymorphisms as a host-related factor and atrophy caused by H pylori. METHODS: Our study enrolled 77 patients. Biopsy materials obtained during gastrointestinal endoscopies were evaluated for the presence of H pylori. Polymerase chain reaction-restriction fragment length polymorphism assay was used to characterize myeloperoxidase genotypes. RESULTS: Forty four patients (57.1%) were Hp (+) and 33 (42.9%) were Hp (-). Sixty six (85.7%) had GG genotype, 10 (12.9%) had GA genotype and 1 (1.29%) had AA genotype. The change in atrophy in relation to neutrophil infiltration was significant in Hp (+) patients (P = 0.0001). The change in atrophy in relation to neutrophil infiltration in patients with GG genotype was significant (P = 0.002). However, the change in atrophy in relation to neutrophil infiltration was not significiant in patients with Hp (+) GG genotype (r = 0.066, P = 0.63). CONCLUSION: Myeloperoxidase genotype is critical for development of atrophy in relation to the severity of inflammation. However, it is interesting to note that, H pylori does not show any additive effect on development of atrophy.

Eradication of H pylori infection in a rural population: One-day quadruple therapy versus 7-day triple therapy

瞄准：比较有标准 7-d 的四倍的治疗增加两倍的一天为在中国的一张农村人口的 H pylori 根除的治疗。方法：396 个病人与的一个总数(13 ) pylori 被分配进二的为 H 阳性的 C 脲呼吸测试组织：239 个病人收到了一天四倍的治疗(amoxicillin 2000 mg qid；灭滴灵 500 mg qid；枸橼酸铋 900 mg qid 和 lansoprazole 60 mg 从前每日) 并且 157 个病人收到了 7-d 标准三元组治疗(amoxicillin 1000 mg 出价；clarithromycin 500 mg 出价和 lansoprazole 30 mg 出价) 。所有病人经历了一(13 ) 六个星期估计 H pylori 感染的根除的 C-UBT 术后疗法。结果：229 个病人完成了一天治疗(95.8%) ， 148 个病人完成了 7-d 治疗(94.2%) 。一天治疗根除了在 64 个病人(27.95%) 的 H pylori 感染。相反， 103 个病人(69.59%) 是在 7-d 治疗以后否定的 H pylori (P 【 0.01 ) 。结论：这个预研项目建议与 7-d 标准治疗相比没有在 H pylori 感染的治疗的一天治疗的有益的效果。

Effects of H pylori therapy on erythrocytic and iron parameters in iron deficiency anemia patients with H pylori-positive chronic gastristis

AIM:To elucidate the influences of H pylori infection on oral iron treatment for iron deficiency anemia(IDA). METHODS:A total of 86 patients were divided into two groups:group A,receiving ferrous succinate combined with triple therapy for H pylori eradication,and group B(control),treated with ferrous succinate only.During treatment of IDA,dynamic changes in hemoglobin(Hb) level,mean corpuscular volume(MCV),mean corpuscular hemoglobin(MCH),serum iron(SI),and serum ferritin (SF)were compared between the groups. RESULTS:Hb was slightly higher in group A at d 14 after the start of triple therapy for H pylori eradication (P>0.05).After the therapy,the increase of Hb in group A became significantly faster than that in group B (P<0.05).At d 56,the mean Hb in group A returned to the normal level,however,in group B,it was lower than that in group A(P<0.05)although it had also increased compared with that before oral iron treatment.The MCV and MCH in group A recovered to the normal level,and were much higher than those in group B(P<0.05)at d 21.In Group B,the MCV and MCH remained at lower than normal levels until d 42 after the start of therapy. And then,they reached a plateau in both groups and the differences disappeared(P>0.05).The SF in group A was higher than that in group B(P<0.05)28 d after the treatment and its improvement was quicker in group A (P<0.05),and the difference between the two groups was even more significant(P<0.01)at d 56.The SI in group A was higher than that in group B(P<0.05)at d 14 and this persisted until d 56 when the follow-up of this research was finished. CONCLUSION:Treatment of H pylori can enhance the efficacy of ferrous succinate therapy in IDA patients with H pylori-positive chronic gastritis.