Helicobacter pylori Infection Has No Role in the Pathogenesis of Reflux Esophagitis

In a prospective study of consecutive patientswith reflux esophagitis and/or hiatal hernia andBarrett's esophagus, the prevalence of Helicobacterpylori was assessed. Antral biopsy specimens werestudied and a serum sample for detection of IgGantibodies against Helicobacter pylori was taken. As areference group patients presenting with a normalesophagus, stomach, and duodenum were taken. Refluxesophagitis was diagnosed in 118 patients, hiatal herniawithout esophageal inflammation in 109, and Barrett'sesophagus in 13. Helicobacter pylori was present in 74(30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacterpylori was significantly lower in all groups comparedwith the reference group (P < 0.001). There was nodifference when patients with esophagitis, Barrett'sesophagus, or hiatal hernia were compared. Patients withesophagitis and Helicobacter pylori in their antrum aresignificantly older than esophagitis patients withoutconcomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). Itis concluded that the prevalence of Helicobacter pyloriinfection in patients with gastroesophageal refluxdisease is significantly lower than in the reference group, irrespective of the severity ofesophagitis. Helicobacter pylori infection has no rolein the pathogenesis of reflux esophagitis.     

One-Week Antibiotics versus Maintenance Acid Suppression Therapy for Helicobacter pylori-Associated Peptic Ulcer Bleeding

Bleeding peptic ulcer is the most importantcause of upper gastrointestinal bleeding. Our aim was tocompare the effect of anti-Helicobacter therapy withmaintenance treatment of H₂-receptorantagonist in the prevention of relapses of ulcer andbleeding. Patients with bleeding duodenal or gastriculcers and H. pylori infection were randomized toreceive either a one-week course of triple therapy with bismuth subcitrate, metronidazole, andtetracycline plus ranitidine or a six-week course ofranitidine 300 mg/day. After the ulcers healed, theantibiotic-treated patients were not given anymedication, whereas the ranitidine-treated patientscontinued to receive a maintenance dose of 150 mg/day.One hundred twenty-six patients were randomized toreceive anti- Helicobacter therapy and 124 patients toreceive long-term ranitidine. H. pylori eradication wasachieved in 98.2% in those who received triple therapyand 6.1% in those who received ranitidine (P <0.0001). At the six-week follow-up, ulcer healing was documented in 88.2% in those who receivedtriple therapy and 86.1% in those who receivedranitidine (P = 0.639). Recurrent ulcer developed innine of the ranitidine-treated patients and three ofthem presented with recurrent upper gastrointestinal bleeding.One patient in the antibiotic group developed recurrentulcer without rebleeding (P = 0.01). It is concludedthat eradication of H. pylori is sufficient for the prevention of recurrent bleedingulcers.     

Interleukin-8 Production in Primary Cultures of Human Gastric Epithelial Cells Induced by Helicobacter pylori

Interleukin-8 (IL-8) production by the gastricmucosa is increased in Helicobacter pylori infection.Previous studies indicated that H. pylori induces IL-8synthesis in cancer cell lines, and the ability of H. pylori to stimulate IL-8 production issupposed to be associated with cag A and other cagpathogenicity island genes, including pic B gene. In thepresent study, we investigated the induction of IL-8 in primary cultures of normal human gastricepithelial cells to elucidate the IL-8 induction by wildtype strains and by the pic B knockout strain. Humangastric epithelial cells were obtained from surgically resected specimens from four patients. Three H.pylori strains (TN2F4; type 1 clinical isolate, TN2F4m1;isogenic pic B mutant of TN2F4, Tx30a; type 2 strain)were cocultured with the normal gastric epithelial cells or the transformed MKN-28. IL-8 levels inculture medium were determined by enzyme immunoassay.Human gastric epithelial cells produced IL-8 at a 10 -50times higher level than MKN-28 did when cocultured with TN2F4. The mutant TN2F4m1 induced IL-8 atsignificantly lower levels than the parent strain. Cellsfrom four patients behaved similarly on IL-8 production.The results of the present study demonstrated the induction of IL-8 in normal gastricepithelial cells, suggesting that pic B gene product mayplay an essential role in vivo.     

中药治疗幽门螺杆菌相关性胃炎

幽门螺杆菌相关性慢性胃炎治疗是难题，本研究通过前瞻对照法探讨中药的疗效。经确诊的本病患者随机分入中医辨证治疗组和西药对照组，结果治疗组症状缓解率８５％，和西药组相近（Ｐ〉０．０５），但组织学改善率８０％，Ｈｐ根除率２５％，均优于西药组（Ｐ〈０．０５），说明中医治疗有一定优点。     

慢性浅表性胃炎脾胃湿热证胃粘膜病理、幽门螺杆菌感染及胃粘膜分泌特点

[目的]探讨慢性浅表性胃炎脾胃湿热证与胃粘膜的病理改变、胃粘膜分泌白细胞介素-8(IL-8)、肿瘤坏死因子α(TNF-α)和分泌型免疫球蛋白A(sIgA)、及幽门螺杆菌(HP)感染的关系。[方法]选择55例慢性浅表性胃炎患者为观察对象,其中脾胃湿热证35例,脾虚证20例,并设无临床症状者15例为正常对照组,检测胃粘膜病理组织学改变,观察胃粘膜组织中IL-8、TNF-α和sIgA水平以及HP感染情况。[结果]脾胃湿热证患者的HP感染率、胃粘膜炎症程度要高于脾虚证组和正常组(P<0.05或P<0.01);脾胃湿热证胃粘膜组织中的IL-8、TNF-α要高于脾虚证组(P<0.05或P<0.01),而sIgA却低于脾虚证组(P<0.01);在脾胃湿热证中,HP阳性者的胃粘膜炎症程度明显重于阴性者(P<0.01),且HP阳性者胃粘膜组织中的IL-8、TNF-α要高于阴性者(P<0.05),而sIgA在两组间无显著性差异(P>0.05)。[结论]脾胃湿热证的胃粘膜呈现一种活动性炎症改变,这可能与局部炎症因子(IL-8、TNF-α)分泌增加、防御因子(sIgA)分泌减少有关;而HP感染可能是引起和加重脾胃湿热证内在病理变化的因素之一。     

Preoperative Work-up in Asymptomatic Patients Undergoing Roux-en-Y Gastric Bypass: Is Endoscopy Mandatory?

Background: We aimed to determine before Roux-en-Y gastric bypass (RYGBP) in asymptomatic morbidly obese patients: 1) the prevalence of abnormal findings at upper gastrointestinal (UGI) endoscopy; 2) Helicobacter pylori (HP) status; 3) clinical consequences of these findings; and 4) associated costs. Methods: We retrospectively reviewed 468 consecutive patients, excluded those with UGI symptoms, drug intake or previous UGI endoscopy/surgery, and analyzed findings in the 319 remaining patients (68%). Results: There were abnormal findings in 147 patients (46%), including 54 hiatal hernias and 146 parietal (i.e. mucosal or submucosal) lesions. The most significant were 7 ulcers and 2 gastric polyposis. HP was detected (using CLO-test) in 124 patients (39%). Histopathological examination of biopsies was abnormal in 109/161 patients (68%), and disclosed mainly chronic gastritis (n=98). Abnormal findings were more frequent in HP-positive compared to HP-negative patients (94 vs 51%, P<0.001). Findings had clinical implications in only 4% of patients: delayed surgery (7 ulcers), prophylactic gastrectomy (2 gastric polyposis), unnecessary work-up (3 irrelevant/false-positive diagnoses), and inclusion in a screening program (1 Barrett's esophagus). Mean cost of complete UGI work-up was 389 €/patient. Conclusion: Asymptomatic morbidly obese patients frequently harbour UGI lesions warranting UGI work-up before RYGBP. However, routine endoscopy presents drawbacks. We propose a less invasive strategy which reduces costs and limits false-positive results and the subsequent investigations that they require. In our series, it would have missed two gastric polyposis only, for which no formal recommendation has yet been issued. This strategy could be a valuable alternative to routine UGI endoscopy before RYGBP in asymptomatic patients.     

Helicobacter pylori Stool Antigen Test (Clinical Evaluation and Cost Analysis of a New Enzyme Immunoassay)

Noninvasive tests for Helicobacter pylori areincreasingly used. Recently, an enzyme immunoassay forH. pylori detection in feces has been put on the market.Aim of this multicenter study was to evaluate the usefulness of this novel test as apredictor of H. pylori status in the pretreatmentsetting. Three hundred consecutive patients wereenrolled. None of the patients had received anyeradicating treatment in the last 12 months, and all underwentgastroscopy with biopsies of the antrum and body forhistology (H) and rapid urease test (RUT). H. pyloristatus was defined positive (or negative) if both H and RUT were positive (or negative). When H and RUTgave conflicting results, the patients were classifiedas H. pylori indeterminate. A stool specimen wascollected for each patient and tested by using a novel enzyme immunoassay for H. pylori detection(HpSAT). Sensitivity, specificity, and diagnosticaccuracy of the test were calculated, as was the cost ofeach assay. H. pylori status was positive in 159patients, negative in 131, and indeterminate in 10. HpSATgave evaluable results (positive or negative) in 293patients, and doubtful results in 7 (2.3%). Sensitivity,specificity, and diagnostic accuracy of HpSAT were 96.8%, 89.7%, and 93.6% respectively.Considering the H. pylori-indeterminate patients aspositive, the percentages were 95.8%, 98.7%, and 93.2%respectively. The cost for each assay was about US $27. These results suggest that HpSAT is anoninvasive, simple, reliable, fast, and cheap methodfor evaluating H. pylori status in the pretreatmentsetting.     

Osmotic Effect of Honey on Growth and Viability of Helicobacterpylori

Honey from New Zealand and Saudi Arabia atconcentrations approximating 20% (v/v) inhibit thegrowth of H. pylori in vitro. The anti-H. pylori effectinvolves both hydrogen peroxide- andnon-peroxide-mediated killing mechanisms. This study was designed todetermine whether the anti-H. pylori activity of honeydiffered regionally (honey from Texas, Iowa, and NewZealand) and to determine whether this activity was due to the presence of hydrogen peroxide.Broth dilution susceptibility tests were performed usingsolutions of honey prepared in BHI broth ranging inconcentration from 5 to 35% (v/v) in 5% increments. Control solutions containing glucose, fructose,and combined glucose/fructose solutions in ratios of1:1.23 were also prepared. Paired catalase controls wereincluded in all tests. Twenty-eight clinical isolates of H. pylori were tested. Growth wasdetermined on the basis of a plus/minus grading score.All of the solutions containing either fructose,glucose, glucose and fructose combinations, or honey were equally effective in inhibiting the growthof H. pylori. All of the isolates were inhibited bysolutions containing 15% (w/v) carbohydrate. Honeysolutions, with or without catalase, inhibited 24/28 isolates at a concentration of 10%, and 28/28isolates at a concentration of 15%. In conclusion,regional differences in honey activity against H. pyloriwere not detected, nor was the effect of killing related to the presence of hydrogen peroxide inthe honey samples. Osmotic effects were shown to be themost important parameter for killing H. pylori as allcarbohydrate solutions 15% (v/v) inhibited 100% of the H. pylori.     

Helicobacterpylori in Dental Plaque (A Comparison of Different PCR Primer Sets)

This study was designed to compare differentprimer sets for PCR analysis of H. pylori in the sameseries of 40 dental plaque samples. Three pairs ofprimers, HPU1/HPU2, HP1/HP2, and EHC-U/EHC-L, directed to the urease A gene, 16S rRNA gene, or 860-bpDNA of H. pylori, respectively, were used. Our resultsdemonstrate that EHC-L/EHC-U were more specific andsensitive for H. pylori added to saliva or dental plaque than HPU1/HPU2 and HP1/HP2. Thedetection rates for H. pylori DNA in dental plaquesamples from randomly selected adult patients from theDental Clinic of the University of Ulm were 26.5% (9/34) for HPU1/HPU2, 78.9% (30/38) for HP1/HP2, and100% (40/40) for EHC-U/EHC-L (P < 0.001). Nested PCRusing primers directed to the 860-bp DNA of H. pylorifurther confirmed the presence of H. pylori DNA (40/40) in all these samples. Our resultsindicate that primers EHC-U/EHC-L are to be recommendedfor PCR detection of H. pylori in the oralcavity.     

清热理气方对螺杆菌感染性胃炎的作用

为检验清热理气方（蒲公英６０ｇ,黄连１０ｇ,黄芩１０ｇ,枳壳１０ｇ,佛手１２ｇ,炙甘草６ｇ）对实验性猫胃螺杆菌胃炎的治疗作用。采用复制Ｂａｌｂ／ｃ猫有螺杆菌胃炎模型,以清热理气方大,中,小剂量９分别为２６．６ｇ／ｋｇ,１３．３ｇ／ｋｇ,６．６５ｇ／ｋｇ）给药,以三联疗法（灭滴灵２．６ｍｇ,四环素１．３ｍｇ,丽珠得乐１．３ｍｇ）为阳笥对照组,以生理气方作用不如三联疗法,给药４周,末次给药４周后观察结