Clinical characteristics of Helicobacter pylori-negative drug-negative peptic ulcer bleeding

AIM: To investigate the clinical characteristics and outcomes of idiopathic Helicobacter pylori (H. pylori)-negative and drug-negative] peptic ulcer bleeding (PUB).METHODS: A consecutive series of patients who experienced PUB between 2006 and 2012 was retrospectively analyzed. A total of 232 patients were enrolled in this study. The patients were divided into four groups according to the etiologies of PUB: idiopathic, H. pylori-associated, drug-induced and combined (H. pylori-associated and drug-induced) types. We compared the clinical characteristics and outcomes between the groups. When the silver stain or rapid urease tests were H. pylori-negative, we obtained an additional biopsy specimen by endoscopic re-examination and performed an H. pylori antibody test 6-8 wk after the initial endoscopic examination. For a diagnosis of idiopathic PUB, a negative result of an H. pylori antibody test was confirmed. In all cases, re-bleeding was confirmed by endoscopic examination. For the risk assessment, the Blatchford and the Rockall scores were calculated for all patients.RESULTS: For PUB, the frequency of H. pylori infection was 59.5% (138/232), whereas the frequency of idiopathic cases was 8.6% (20/232). When idiopathic PUB was compared to H. pylori-associated PUB, the idiopathic PUB group showed a higher rate of re-bleeding after initial hemostasis during the hospital stay (30% vs 7.4%, P = 0.02). When idiopathic PUB was compared to drug-induced PUB, the patients in the idiopathic PUB group showed a higher rate of re-bleeding after initial hemostasis upon admission (30% vs 2.7%, P < 0.01). When drug-induced PUB was compared to H. pylori-associated PUB, the patients in the drug-induced PUB were older (68.49 ± 14.76 years vs 47.83 ± 15.15 years, P < 0.01) and showed a higher proportion of gastric ulcer (77% vs 49%, P < 0.01). However, the Blatchford and the Rockall scores were not significantly different between the two groups. Among the patients who experienced drug-induced PUB, no significant differences were found with respect to clinical characteristics, irrespective of H. pylori infection.CONCLUSION: Idiopathic PUB has unique clinical characteristics such as re-bleeding after initial hemostasis upon admission. Therefore, these patients need to undergo close surveillance upon admission.     

Relationship between non-steroidal anti-inflammatory drug use and Helicobacter pylori infection in bleeding or uncomplicated peptic ulcers: A case-control study

BACKGROUND AND AIMS: Non-steroidal anti-inflammatory drug (NSAID) use has been closely associated with an increased risk of bleeding peptic ulcers, while the prevalence of Helicobacter pylori infection has been reported to be lower in bleeding ulcers than in non-bleeding ones. However, whether an interaction exists between NSAID use and H. pylori infection has not clearly been elucidated yet. The aims of this study were to determine the frequency of NSAID use and H. pylori infection, to predict risk factors in bleeding peptic ulcers and to determine whether NSAID use and H. pylori infection interact with each other. METHODS: Ninety-six patients with bleeding ulcer were included in the study. The control group consisted of 106 patients with non-bleeding ulcer. Data were analyzed by using the chi-squared test, Fisher's exact test and logistic regression analysis with or without interaction term (H. pylori by NSAID). RESULTS: Non-steroidal anti-inflammatory drug use was significantly more common in patients with bleeding ulcers than in controls (79.2 vs 38.7%, unadjusted odds ratio (OR): 6.02, 95% confidence interval (CI): 3.21-11.29). The frequency of the H. pylori infection was significantly lower in patients with bleeding ulcers than in controls (66.7 vs 89.6%, unadjusted OR: 0.23, 95% CI: 0.10-0.49). In the logistic regression analysis with the interaction term, male sex (adjusted OR: 3.70, 95% CI: 1.65-8.29), multiplicity of ulcers (adjusted OR: 4.10, 95% CI: 1.02-16.45) and NSAID use (adjusted OR: 33.87, 95% CI: 4.36-262.97) were independent risk factors for bleeding ulcers. There was a negative interaction between H. pylori and NSAID use (adjusted OR: 0.09, 95% CI: 0.01-0.83). CONCLUSIONS: The negative interaction between the two variables suggests that the presence of H. pylori is associated with a lower risk of bleeding in ulcer patients taking NSAIDs.     

Membrane-bound mucins and mucin terminal glycans expression in idiopathic or Helicobacter pylori,NSAID associated peptic ulcers

AIM: To determine the expression of membrane-bound mucins and glycan side chain sialic acids in Helicobacter pylori (H. pylori)-associated, non-steroidal inflammatory drug (NSAID)-associated and idiopathic-gastric ulcers.METHODS: We studied a cohort of randomly selected patients with H. pylori (group 1, n = 30), NSAID (group 2, n = 18), combined H. pylori and NSAID associated gastric ulcers (group 3, n = 24), and patients with idiopathic gastric ulcers (group 4, n = 20). Immunohistochemistry for MUC1, MUC4, MUC17, and staining for Erythrina cristagalli agglutinin and Sambucus nigra agglutinin (SNA) lectins was performed on sections from the ulcer margins.RESULTS: Staining intensity of MUC17 was higher in H. pylori ulcers (group 1) than in idiopathic ulcers (group 4), 11.05 ± 3.67 vs 6.93 ± 4.00 for foveola cells, and 10.29 ± 4.67 vs 8.00 ± 3.48 for gland cells, respectively (P < 0.0001). In contrast, MUC1 expression was higher in group 4 compared group 1, 9.89 ± 4.17 vs 2.93 ± 5.13 in foveola cells and 7.63 ± 4.60 vs 2.57± 4.50 for glands, respectively (P < 0.0001). SNA lectin staining was increased in group 4, in parallel to elevated MUC1 expression, indicating more abundant α2-6 sialylation in that group.CONCLUSION: Cytoplasmic MUC17 staining was significantly decreased in the cases with idiopathic ulcer. The opposite was observed for both MUC1 and SNA lectin. This observation may reflect important pathogenic mechanisms, since different mucins with altered sialylation patterns may differ in their protection efficiency against acid and pepsin.     

Helicobacter pylori and perforated peptic ulcer. Prevalence of the infection and role of non-steroidal anti-inflammatory drugs

AIMS: To study the prevalence of Helicobacter pylori infection in patients with perforated peptic ulcer, to compare it with the prevalence in patients with uncomplicated ulcer, and to assess the role of non-steroidal anti-inflammatory drugs in this prevalence. METHODS: Consecutive patients with perforated peptic ulcer were included in this retrospective study. As a control group, patients undergoing elective outpatient evaluation for the investigation of dyspepsia during the same time period and found to have a peptic ulcer at endoscopy were included. A 13C-urea breath test was carried out in all patients to diagnose H. pylori infection. RESULTS: Sixteen patients with perforated peptic ulcer and 160 with non-complicated peptic ulcer were included. Sixty-two percent of the patients with perforated peptic ulcer were infected by H. pylori, while the microorganism was detected in 87% of the patients without this complication (P = 0.01). Non-steroidal anti-inflammatory drugs intake was more frequent (P = 0.012) in patients with perforated peptic ulcers (56%) than in those without perforation (26%). H. pylori prevalence in perforated peptic ulcers was of 44% in patients with non-steroidal anti-inflammatory drugs intake, but this figure increased up to 86% when only patients not taking non-steroidal anti-inflammatory drugs were considered (P = 0.09). In the multivariate analysis, non-steroidal anti-inflammatory drugs intake was the only variable that correlated with peptic ulcer perforation [odds ratio, 3.6 (95% confidence interval, 1.3-10); P = 0.016]. CONCLUSION: The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is, overall, of only about 60%, which contrasts with the 90-100% figure usually reported in non-complicated ulcer disease. However, the most important factor associated with H. pylori-negative perforated peptic ulcer is non-steroidal anti-inflammatory drugs use, and if this factor is excluded, prevalence of infection is almost 90%, similar to that found in patients with non-perforating ulcer disease.     

非甾体抗炎药应用及幽门螺杆菌感染对消化性溃疡出血的影响

消化性溃疡(peptic ulcer)是消化系统常见的疾病之一,其病因多种多样.消化性溃疡的主要并发症是合并出血.近年来,幽门螺杆菌(Helicobacter pylori, H.pylori)感染和非甾体抗炎药(non-steroidal anti-inflammatory drugs, NSAIDs)应用对溃疡出血的影响日益受到重视.本文总结了这两方面因素与溃疡出血的关系,提出了相应的治疗策略.     

Interaction between Helicobacter pylori infection,nonsteroidal anti-inflammatory drugs and/or low-dose aspirin use: Old question new insights

Previous reports clearly demonstrated that Helicobacter pylori (H. pylori) infection, nonsteroidal anti-inflammatory drugs (NSAID) or low dose aspirin (ASA) use significantly and independently increased the risk for the development of peptic ulcer disease. Today, the presence of H. pylori infection associated with low dose ASA and/or NSAID use in the same patient is becoming more frequent and therefore the potential interaction between these factors and the consequences of it has important implications. Whether NSAID intake in the presence of H. pylori infection may further increase the risk of peptic ulcer carried by the presence of only one risk factor is still a matter of debate. Studies on the interaction between the two risk factors yielded conflicting data and no consensus has been reached in the last years. In addition, the interaction between H. pylori infection and low-dose ASA remains even more controversial. In real clinical practice, we can find different clinical scenarios involving these three factors associated with the presence of different gastrointestinal and cardiovascular risk factors. These huge variety of possible combinations greatly hinder the decision making process of physicians.     

幽门螺杆菌感染、服用非甾体抗炎药与消化性溃疡的关系

目的 研究消化性溃疡患者由于幽门螺杆菌（H.pylori）感染或服用非甾体抗炎药（NSAIDs）的发生率.方法 选取湖北省武汉市武昌医院2010年3月-2012年7月诊治的152例消化性溃疡患者,将其作为治疗组,同时选取同一时间段到消化科就诊的234例非消化性溃疡患者,将其作为对照组.结果 胃溃疡组感染H.pylori的几率是对照组的2.308倍,十二指肠溃疡组是对照组的8.186倍;胃溃疡组服用NSAIDs的几率是对照组的6.072倍,十二指肠溃疡组是对照组的2.823倍;胃溃疡组同时感染H.pylori和服用NSAIDs的几率是对照组的14.972倍,十二指肠溃疡组是对照组的28.873倍.结论 H.pylori感染同时服用了NSAIDs患者增加消化性溃疡的发生危险性,两种因素同时存在可以起协同作用,增加消化性溃疡的发生几率.     

High Recurrence Rate of Idiopathic Peptic Ulcers in Long-Term Follow-up

Background/Aims

Our aim was to compare the long-term clinical outcomes of idiopathic peptic ulcer disease (IPUD) with those of Helicobacter pylori-positive and nonsteroidal anti-inflammatory drug (NSAID)-induced peptic ulcer disease (PUD).

Methods

Patients with endoscopically diagnosed PUD were retrospectively reviewed. According to their H. pylori-infection status and history of NSAIDs use, patients were categorized into three groups: H. pylori-positive PUD, NSAID-induced PUD, and IPUD. Clinical outcomes were analyzed, and the recurrence rate of PUD was compared among the three groups.

Results

A total of 238 patients were enrolled. Those with IPUD, NSAID-induced PUD, and H. pylori-positive PUD comprised of 56, 60, and 122 patients, respectively. The 5-year cumulative incidences of recurrent ulcers were 24.3% (95% confidence interval [CI], 11.6% to 37.0%) in IPUD, 10.9% (95% CI, 2.6% to 19.2%) in NSAID-induced PUD, and 3.8% (95% CI, 0.1% to 7.5%) in H. pylori-positive PUD (IPUD vs NSAID-induced PUD/H. pylori-positive PUD, p=0.43/p<0.001 by log-rank test). In the Cox-proportional hazards model, only IPUD remained as an independent risk factor associated with recurrent ulcers (hazard ratio, 5.97; 95% CI, 1.94 to 18.34; p=0.002).

Conclusions

IPUD exhibited a higher recurrence rate than H. pylori-positive and NSAID-induced PUD in long-term follow-up and was an independent risk factor for ulcer recurrence.     

Role of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use in bleeding peptic ulcers in Japan

Background Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) are well-known major causes of peptic ulcers. This study aimed to characterize the features of bleeding peptic ulcers in Japan. Methods This prospective study evaluated 116 patients revealed to have bleeding peptic ulcers from January 2000 to December 2002. Results Eighty-eight of the 116 patients (75.9%) had H. pylori infection. Seventy (60.3%) patients were positive for H. pylori with no history of NSAID use (group A), and 18 (15.5%) were positive for H. pylori with a history of NSAID use (group B). Among the H. pylori-negative patients, 15 (12.9%) were associated with NSAID use (group C). Thirteen (11.2%) patients had no H. pylori infection or history of NSAID use (group D). Among the 33 patients with a history of NSAID use, 11 were on-demand NSAID users and 14 took daily low-dose aspirin. The patients in groups B and C were significantly older that those in groups A and D, and they more frequently had coexisting diseases compared with group A. In group D, 11 patients had atrophic changes revealed by endoscopic examination, suggesting a past H. pylori infection, and these atrophic changes remained at the time of bleeding. Many of the patients in group D had serious comorbidity. Compared with healthy control subjects, the concentrations of both phosphatidylcholine and phosphatidylethanolamine were significantly decreased in the antral gastric mucosa in all patient groups. Conclusions NSAID use contributed to bleeding ulcers in 28.4% of patients; thus, low-dose aspirin or on-demand NSAID use may cause bleeding ulcers. There were only two (1.7%) confirmed cases of H. pylori-negative, non-NSAID ulcers.     

幽门螺杆菌和非甾体抗炎药对胃上皮细胞增殖的影响

目的　从体外研究的角度探讨幽门螺杆菌 (Hp)和非甾体抗炎药 (NSAID)对胃上皮细胞增殖的影响及其相互作用。方法　胃癌细胞株AGS与Hp和 (或 )吲哚美辛、阿司匹林体外共培养 ,通过MTT比色法和WesternBlot法检测增殖细胞核抗原 (PCNA) ,观察Hp和NSAID对胃上皮细胞增殖的影响。结果　MTT比色法显示CagA阳性的标准Hp菌株NCTC116 37能明显促进胃上皮细胞增殖 ,吸光度 (A)值明显升高 (P <0 .0 5 ) ,而CagA阴性的标准Hp菌株NCTC12 90 8则未发现有促增殖作用 ,且Hp对上皮细胞生长的效应取决于Hp作用的密度 ,在低密度 (3.2× 10 4～ 4 .0× 10 6CFU/ml)时NCTC116 37促进胃上皮细胞生长 ,在高密度 (>2× 10 7CFU/ml)时则抑制其生长 (P <0 .0 5 )。吲哚美辛和阿司匹林均能抑制胃上皮细胞生长 (P <0 .0 5 ) ,并呈浓度依赖性。当Hp和NSAID共同作用于AGS细胞时 ,Hp的促生长作用被逆转 ,呈现出抑制细胞生长的效应 ,A值明显降低 (P <0 .0 5 )。PCNA的WesternBlot检测结果发现 ,Hp菌株NCTC116 37可明显促进细胞PCNA的表达 ,而吲哚美辛和阿司匹林则抑制其表达 ,当两者共同作用于AGS细胞时 ,PCNA的表达明显减弱。结论　Hp对胃上皮细胞的增殖效应与Hp的密度及菌株差异有关 ,CagA阳性的Hp易促进胃上皮细胞生长 ,NSAID可抑制其     

Long-term outcome of Helicobacter pylori-negative idiopathic bleeding ulcers: a prospective cohort study

BACKGROUND & AIMS: Helicobacter pylori-negative idiopathic ulcers are increasingly recognized. The secular trend and long-term outcome of this condition are unknown. METHODS: We prospectively studied consecutive patients with bleeding gastroduodenal ulcers from January to December 2000. The incidence and etiology of ulcers during this period were compared with that between September 1997 and August 1998. H. pylori-negative idiopathic ulcers were defined as negative tests for H. pylori, no exposure to analgesics within 4 weeks, and absence of other risk factors for ulcers. After the ulcers had healed, patients with H. pylori-negative idiopathic ulcers and patients with H. pylori ulcers who received eradication therapy were followed up for 12 months without anti-ulcer drugs. RESULTS: Six hundred thirty-eight patients had bleeding ulcers: 213 (33.4%) were H. pylori ulcers, and 120 (18.8%) were H. pylori-negative idiopathic ulcers (vs 480 [50.3%] H. pylori ulcers and 40 [4.2%] H. pylori-negative idiopathic ulcers in 1997-1998; P < .001). H. pylori-negative idiopathic ulcers accounted for 16.1% of patients who were admitted for bleeding and 42.4% of patients who bled while in the hospital (P < .0001); 28.3% of patients with H. pylori-negative idiopathic ulcers had histologic evidence of past H. pylori infection. The probability of recurrent ulcer complications in 12 months was 13.4% (95% CI: 7.3%-19.5%) in patients with H. pylori-negative idiopathic ulcers and 2.5% (95% CI: 0.4%-4.6%) in patients with H. pylori ulcers who received eradication therapy (P = .0002). CONCLUSIONS: The incidence of H. pylori-negative idiopathic bleeding ulcers is rising. These ulcers are prone to recurrent complications.     

Peptic ulcer bleeding: accessory risk factors and interactions with non-steroidal anti-inflammatory drugs

AIMS: To determine risk factors for peptic ulcer bleeding other than non-steroidal anti-inflammatory drugs (NSAIDs). Methods-Data on possible antecedent risk factors obtained in a large case control study of 1121 patients admitted to hospitals in Glasgow, Newcastle, Nottingham, Oxford, and Portsmouth with bleeding peptic ulcers were compared with the same information obtained in 989 population controls. Data were analysed by logistic regression with the calculation of odds ratios (OR) and 95% confidence intervals (CI). RESULTS: From a logistic regression model, oral anticoagulants (OR 7. 8; 95% CI 2.8-21.5), previous peptic ulcer (3.8; 2.6-4.9), treatment for heart failure (5.9; 2.3-13.1), oral corticosteroid use (2.7; 1. 3-4.5), treatment for diabetes (3.1; 1.2-4.3), and current smoking (1.6; 1.2-2.0) were all independent risk factors. No association was found with use of calcium channel antagonists. Odds ratios for concomitant NSAID usage were multiplicative with the exception of current smoking. CONCLUSIONS: Some 45% of admissions for peptic ulcer bleeding in England and Wales in those aged 60 or more are calculated to be attributable to, or associated with, these accessory risk factors, which, together with those associated with aspirin or other NSAID use will account for over 80% of predisposing factors to ulcer bleeding.     

非类固醇类抗炎药相关消化性溃疡的预防和治疗

非类固醇类抗炎药(NSAIDs)是消化性溃疡(PU)的主要病因.NSAIDs相关PU的发病率和并发症发生率较高.在应用NSAIDs时,可选用胃肠毒性较低的非选择性NSAIDs,并与质子泵抑制剂或米索前列醇合用;或单用选择性环氧合酶-2抑制剂(高危患者考虑加用质子泵抑制剂),可以降低NSAIDs相关PU的发病率.治疗NSAIDs相关PU最有效的方法是停用NSAIDs,然后应用组胺H2受体拮抗剂或质子泵抑制剂,以促进溃疡愈合;不能停用NSAIDs的患者,应同时应用质子泵抑制剂,以缓解症状、促进溃疡愈合和预防并发症发生.选择性环氧合酶-2抑制剂是否增加心、脑血管血栓形成的危险,有待进一步研究.新一代安全性较高的NSAIDs正在研制中.     

非甾体抗炎药相关性溃疡并出血的临床分析

目的 探讨非甾体抗炎药相关性溃疡并出血的临床及内镜特点。方法 对196例消化性溃疡并出血病人的临床资料进行回顾性分析，根据出血前1周内是否服用NSAIDs分为NSAIDs组(55例)和非NSAIDs组(141例)，并进行分析比较。结果 NSAIDs组与非NSAIDs组在年龄、溃疡类型、溃疡数目、临床症状及Hp感染等方面均有显著差异。结论 加强对非甾体抗炎药相关性溃疡并出血的认识，并采取相应措施，以减少非甾体抗炎药对胃肠道产生的毒副作用。     

Helicobacter pylori eradication in the management of patients with idiopathic thrombocytopenic purpura

PURPOSE: To investigate the relation between Helicobacter pylori infection and the clinical features of idiopathic thrombocytopenic purpura (ITP), and to examine the effects of H. pylori eradication on platelet counts. METHODS: A(13)C urea breath test for H. pylori infection was performed in a cohort of 137 consecutive patients with ITP. Patients who tested positive received standard eradication therapy if their platelet count was <50 x 10(9)/L or if they had symptoms of dyspepsia. RESULTS: H. pylori infection was detected in 64 patients (47%), and was not associated with dyspepsia or other clinical or laboratory features. Eradication therapy was successfully administered to 52 patients. Platelet responses were observed in 17 (33%) of these patients, which lasted for more than 1 year in 11 patients. Duration of ITP was shorter among responders than nonresponders. Only one response was observed among patients with severe thrombocytopenia (platelet count <30 x 10(9)/L). CONCLUSION: The prevalence of H. pylori infection in patients with ITP is similar to that found in the general population. Infection is not associated with distinctive features of the disease. H. pylori eradication may improve the platelet counts in adults in whom the ITP is of recent onset and in those with less severe degrees of thrombocytopenia, but was not effective in patients with chronic severe ITP.     

非甾体类抗炎剂致上消化道溃疡的临床特点

[目的]研究非甾体类抗炎剂（NSAIDs）相关胃、十二指肠溃疡的临床特点。[方法]统计2001年1月～2006年1月消化病专家门诊及住院患者的临床资料。根据胃镜检查前1周内有无服用NSAIDs史，将138例患者分为A（服NSAIDs，41例）、B（未服NSAIDs，97例）组，对2组患者的临床症状、胃镜、活检结果进行比较。[结果]饱胀、烧心、恶心、腹痛4项主症中前3项A组均高于B组，但腹痛B组高于A组（P〈0．05）。A组中胃溃疡（GID占80．5％（多发性为24．4％），十二指肠球部溃疡（DID为19．5％（多发性4．9％）；B组分别为48．5％（12．4％）、51．5％（11．3％）。活动性溃疡A组占63．4％，溃疡灶〈10mm占80．5％；B组分别为42．3％、62．9％，2组间比较P〈0．01。幽门螺杆菌检出率A组63．4％，B组81．3％，B组明显高于A组（P〈0．05）。[结论]提高临床医师对NSAIDs相关溃疡临床特点的认识，加强对必须服用NSAIDs者的防治及医学指导，尽量减少其不良反应。     

Helicobacter pylori-negative gastric mucosa-associated lymphoid tissue lymphomas: A review

Since Isaacson and Wright first reported on the extranodal marginal zone B-cell lymphoma of the stomach in 1983,following studies have clarified many aspects of this disease.We now know that the stomach is the most affected organ by this disease,and approximately90% of gastric mucosa-associated lymphoid tissue(MALT) lymphomas are related to Helicobacter pylori(H.pylori) infection.This implies that approximately 10% of gastric MALT lymphomas occur independent of H.pylori infection.The pathogenesis of these H.pylori-negative gastric MALT lymphomas remains unclear.To date,there have been several speculations.One possibility is that genetic alterations result in nuclear factor-kappa B(NF-κB) activation.Among these alterations,t(11;18)(q21;q21) is more frequently observed in H.pylori-negative gastric MALT lymphomas,and such translocation results in the synthesis of fusion protein API2-MALT1,which causes canonical and noncanonical NF-κB activation.Another possibility is infection with bacteria other than H.pylori.This could explain why H.pylori eradication therapy can cure some proportions of H.pylori-negative gastric MALT lymphoma patients,although the bacteria responsible for MALT lymphomagenesis are yet to be defined.Recent advances in endoscopy suggest magnifying endoscopy with narrow band imaging as a useful tool for both detecting gastric MALT lymphoma lesions and judging the response to treatment.A certain proportion of H.pylori-negative gastric MALT lymphoma patients respond to eradication therapy; hence,H.pylori eradication therapy could be considered as a first-line treatment for gastric MALT lymphomas regardless of their H.pylori infection status.     

Helicobacter pylori eradication in West Asia:A review

The efficacy of first-and second-line Helicobacter pylori(H.pylori)eradication regimens varies considerably in West Asian countries,mainly due to the variable prevalence of resistant organisms.However,no review article has yet evaluated and compared the efficacy of different regimens among different countries of this region.Therefore,we conducted a review to select the best options and provide recommendations for H.pylori treatment in this geographic region.A search through PubMed was carried out to obtain relevant randomized clinical trials published in English language up to June2013.According to the results,among different therapeutic regimens used as the first-line protocols,10-d Bismuth-Furazolidone/Metronidazole quadruple therapy,14-d Clarithromycin-containing hybrid therapy and 14-d quadruple therapy including a proton pump inhibitor +Bismuth+Tetracycline(500 mg QID)+Metronidazole(500 mg TDS)seemed to be appropriate options.Among second-line therapeutic regimens,Bismuthbased quadruple therapies containing Tetracycline and Furazolidone/Metronidazole,triple therapy containing Amoxicillin and Gatifloxacin and Quadruple therapy including Bismuth+Azithromycin and Ofloxacin seemed to be effective options.Third-line therapies were not evaluated in West Asia;most guidelines,however,recommend choosing optimal eradication regimen according to the pattern of antibiotic susceptibility of H.pylori.Although we limited our investigation to H.pylori eradication regimens in West Asia,the clinical significance of the results goes beyond the countries situated in this geographic region.In fact,the results are transferrable to any region as long as the patterns of resistance are the same.     

Helicobacter pylori infection in bleeding peptic ulcer patients after non-steroidal antiinflammatory drug consumption

AIM:To establish the prevalence of Helicobacter pylori (H. pylori ) infection in patients with a bleeding peptic ulcer after consumption of non-steroidal antiinflamma- tory drugs (NSAIDs). METHODS:A very early upper endoscopy was performed to find the source of upper gastrointestinal bleeding and to take biopsy specimens for analysis of H. pylori infection by the rapid urease (CLO) test, histological examination, and bacterial culture. IgG anti-CagA were also sought. The gold standard for identifying H. pyl...     

Low prevalence of idiopathic peptic ulcer disease: An Italian endoscopic survey

Background

Peptic ulcer disease (PUD) represents a common condition, although its incidence is decreasing. Previous studies reported a high rate of idiopathic PUD prevalence.

Aim

To investigate prevalence, relative distribution of etiologic factors and prevalence of complication of PUD in an Italian endoscopic series.

Materials and methods

All gastroscopies performed in adult patients during 3 years were considered. Patients with PUD, with antral and corporal histology, were included in the study. Helicobacter pylori infection was assessed by histology. Idiopathic PUD was defined as an ulcer without evidence H. pylori infection or prior exposure to NSAIDs.

Results

300 patients with PUD out of 11,148 gastroscopies were included in our study accounting for a prevalence of 2.7%. H. pylori-associated PUD was diagnosed in 62.3%, NSAID/aspirin-associated PUD in 22%, H. pylori/NSAID/aspirin-associated PUD in 11.6%, and idiopathic PUD in the remaining 4% of cases. Regarding ulcer complications the logistic regression analysis identified the following significant risk factors for GI bleeding: NSAIDs and/or aspirin use, age >65 years and coexistent gastric and duodenal ulcers.

Conclusion

Our data found a low endoscopic prevalence of peptic ulcer. Both H. pylori infection and NSAIDs and/or aspirin use remain the main determinants and idiopathic ulcer prevalence is very low.