消化性溃疡患者非甾体类抗炎药服用史和幽门螺杆菌感染的协同致病性分析

目的了解服用非甾体类抗炎药(NSAIDs)和幽门螺杆菌(H.pylori)感染在消化性溃疡及合并上消化道出血发病中是否具有协同作用。方法应用病例对照研究,于1999年7月至2004年12月选取吉林大学中日联谊医院的803例消化性溃疡患者(其中208例溃疡合并上消化道出血者)与同一时期就诊的2061例非胃十二指肠疾病患者,进行NSAIDs服用史的调查和H.pylori感染的检测。结果服用NSAIDs合并H.pylori感染者患胃溃疡的OR值明显高于单纯服用NSAIDs者和单纯H.pylori感染者患胃溃疡的OR值之和;服用NSAIDs合并H.pylori感染的胃溃疡及十二指肠溃疡患者发生上消化道出血的OR值均低于单纯服用NSAIDs和单纯H.pylori感染的胃溃疡患者和十二指肠溃疡患者发生上消化道出血的OR值之和;与无溃疡未服NSAIDs者比较,偶尔服药者溃疡出血与短期服药者及长期服药者比较,差异无统计学意义。结论NSAIDs和H.pylori感染在胃溃疡的形成中具有协同作用;在溃疡合并上消化道出血的发病中无协同作用;溃疡合并上消化道出血与服用NSAIDs的时间长短无关。     

糖尿病合并消化性溃疡的临床特点分析

目的观察糖尿病合并消化性溃疡的临床特点,为临床诊治提供借鉴。方法选取该院2012年6月—2015年1月所收治的97例糖尿病合并消化性溃疡患者作为观察组,另在该院消化内科选取97例同时期单纯消化性溃疡患者作为对照组,比较两组患者恶心反酸、上腹疼痛、腹胀等不良反应的发生次数及频率、溃疡部位、幽门螺杆菌(H.pylori)感染发生率及治疗效果。结果观察组患者恶心反酸、上腹疼痛、腹胀情况、溃疡面积及幽门螺杆菌感染发生率均高于对照组,差异具有统计学意义(P0.05)。结论糖尿病合并消化性溃疡较单纯消化性溃疡面积更大,出血风险及H.pylori感染发生率更高,治疗难道更大。     

消化性溃疡发病相关因素探讨

背景消化性溃疡发病率呈逐年上升趋势,严重影响着患者的身心健康以及生命安全。目的分析消化性溃疡发病的相关因素,以期能够降低消化性溃疡发病率。方法随机选取2012年2月至2014年4月期间在我院治疗的218例消化性溃疡患者为观察组,选取同时期的189例慢性胃炎患者为对照组,回顾性分析两组患者的临床资料。结果单因素方差分析表明,消化性溃疡发病的相关危险因素包括吸烟、饮酒、幽门螺杆菌(H.pylori)感染、使用非甾体类抗炎药、合并有抑郁症、高血压、胆囊结石、反流性食管炎、痛风以及脑血管疾病。多因素方差分析结果表明,伴随有抑郁症、使用非甾体类抗炎药物、H.pylori感染、吸烟以及饮酒是消化性溃疡的独立危险因素。结论减少非甾体类抗炎药物使用、治疗H.pylori感染、戒烟戒酒以及保持心情愉悦可有效降低消化性溃疡发病率。     

非甾体类抗炎药物与幽门螺杆菌感染对消化性溃疡协同致病作用研究

目的研究非甾体类抗炎药物(NSAIDs)与幽门螺杆菌(H.pylori)感染对消化性溃疡协同致病作用。方法回顾性分析我院80例消化性溃疡患者临床资料,其中胃溃疡40例(A组)、十二指肠溃疡40例(B组),另选消化内科其他就诊非消化性溃疡患者50例作为对照(C组),比较三组NSAIDs使用情况、H.pylori感染率,比较H.pylori(-)/NSAIDs(-)、H.pylori(+)/NSAIDs(+)、H.pylori(-)/NSAIDs(+)、H.pylori(+)/NSAIDs(-)时三组分布例数。结果A组NSAIDs使用率显著高于B、C组(P0.05),B组H.pylori阳性率显著高于A、C组(P0.05)。H.pylori(+)/NSAIDs(+)、H.pylori(-)/NSAIDs(+)时A组占55.6%、50.0%高于另外两组,而H.pylori(+)/NSAIDs(-)时B组占比较高。H.pylori(+)/NSAIDs(+)是消化性溃疡的危险因素,OR值为20.013。结论NSAIDs与H.pylori均为十二指肠溃疡的危险因素,但两者并无协同作用,以H.pylori感染风险更高,而两因素在胃溃疡患者中具有显著协同作用,需引起临床重视。     

肝硬化失代偿期并发自发性细菌性腹膜炎的危险因素分析

目的：探讨肝硬化失代偿期并发自发性细菌性腹膜炎(SBP)危险因素,提高早期诊断率.方法：我院近2年住院的肝硬化失代偿期患者共163例.对性别、年龄、肝性脑病、消化道出血、饮酒史、血清胆红素水平、血清蛋白水平、转氨酶、腹水白蛋白含量、肝硬化病因、既往SBP史、腹外感染灶及有无脾功能亢进等因素,用Logistic回归分析.结果：性别、年龄、肝性脑病、消化道出血、饮酒、病因是否为乙肝、及脾功能亢进等因素与肝硬化失代偿期并发SBP无相关性(P＞0.05)；而血清胆红素(OR=7.461,P＜0.01)、蛋白(总蛋白：OR=2.455,P＜0.05；白蛋白：OR=22.696,P＜0.01)、及转氨酶水平(ALT：OR=2.067,P＜0.05；AST：OR= 3.370,P＜0.01),腹水白蛋白水平(OR=36.692,P＜0.01),既往SBP史(OR=14.359,P＜0.01)以及腹外感染灶(OR=3.633,P＜0.05)等因素与肝硬化失代偿期并发SBP有相关性结论：血清胆红素,白蛋白,AST,腹水白蛋白,以及既往有SBP发病史是肝硬化失代偿期并发SBP的高危因素.血清总蛋白、ALT和有腹外感染灶是失代偿期肝硬化并发SBP的危险因素.     

AIDS与肝病患者胃镜活检组织幽门螺杆菌感染和消化性溃疡发现率的临床比较研究

目的探讨艾滋病、肝病和普通人群上中腹不适的患者胃幽门螺旋杆菌（H.pylori）感染发生率的异同,以发现H.pylori感染在诱发艾滋病患者和肝病患者消化性溃疡过程中作用的异同。方法艾滋病组患者46例,肝病组患者668例,非艾滋病非肝病普通人群对照组226例,均有上腹不适,行胃镜检查,活检组织分别进行快速尿素酶和Warthin-Starry银染检测H.pylori感染,同时记录内镜下发现的病变。结果肝病患者H.pylori感染率（36.08%）低于艾滋病患者（43.48%）和普通人群对照组（59.73%）（P〈0.05）,艾滋病患者H.pylori感染低于普通人群对照组患者（P〈0.05）;肝病伴发消化性溃疡患者的H.pylori感染率（45.22%）低于普通人群消化性溃疡患者的H.pylori感染率（80.49%）（P〈0.05）,艾滋病伴发消化性溃疡的H.pylori感染率（50.00%）与普通人群无差异（P〉0.05）。结论 H.pylori肝病患者消化性溃疡的发生与H.pylori感染的关系,不像普通人群消化性溃疡的发生与H.pylori感染的关系密切;而艾滋病患者中H.pylori感染率即使低于普通人群,H.pylori感染仍是促进艾滋病患者发生消化性溃疡的重要因素。     

糖尿病合并幽门螺杆菌感染的耐药分析

目的探讨糖尿病合并幽门螺杆菌(H.pylori)感染者的耐药性。方法对来我院诊治的80例H.pylori性消化性溃疡患者资料进行分析,实验组40例为消化性溃疡合并糖尿病患者,而对照组为单一消化性溃疡患者40例,对H.pylori培养并进行耐药性实验,比较两组患者H.pylori耐药。结果实验组40例株H.pylori培养成功率为90%,高于对照组(培养成功率为72.5%)(P<0.05);实验组21株对克拉霉素耐药,耐药率为52.5%;17株对阿莫西林耐药,耐药率为42.5%;19株对左氧氟沙星耐药,耐药率为47.5%,高于对照组(30%、12.5%、15%)(P<0.05)。结论合并糖尿病组H.pylori耐药率要高于普通的消化性溃疡患者,治疗时要加强患者耐药性实验,合理使用抗生素,降低药物耐药性。     

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.     

2型糖尿病合并消化性溃疡的临床特征

目的:探讨2型糖尿病合并消化性溃疡患者的临床特征.方法:比较天津市南开区中医医院收治的116例2型糖尿病合并消化性溃疡患者(实验组)和110例非糖尿病消化性溃疡患者(对照组)的临床资料,分析两组患者消化性溃疡发生部位、最大直径、治疗效果、幽门螺杆菌(Helicobacter pylori,H.pylori)根除率以及并发症发生情况上的差异性.结果:实验组患者胃溃疡发生率显著高于对照组(50.00%vs 36.36%),十二指肠溃疡发生率显著低于对照组(31.03%vs 50.91%),差异具有统计学意义(P<0.05);实验组患者消化性溃疡最大直径>10.0 mm者所占比例显著高于对照组(31.90%vs 25.45%),差异具有统计学意义(P<0.05);实验组患者愈合率和H.pylori根除率均显著低于对照组(28.45%vs40.91%、45.33%vs 71.43%),差异具有统计学意义(P<0.05);实验组患者贫血发生率显著高于对照组(76.72%vs 59.09%),差异具有统计学意义(P<0.05).结论:2型糖尿病患者消化性溃疡发病部位主要为胃部,病灶直径较大较深,出血风险更高,临床治疗难度更大,愈合和H.pylori根除效果较单纯消化性溃疡者差.     

慢性乙型肝炎及乙肝肝硬化合并消化性溃疡患者幽门螺杆菌感染状况

目的 探讨幽门螺杆菌(HP)感染与慢性乙型肝炎及乙肝肝硬化合并消化性溃疡的相关性及HP分型诊断的临床意义.方法 胃镜检查并应用免疫印迹法检测HP抗体,对慢性乙型肝炎消化性溃疡患者及乙肝肝硬化消化性溃疡患者HP感染情况进行分析,并对HP感染进行分型诊断.结果 慢性乙型肝炎消化性溃疡中年组和老年组HP感染率分别为73.73%和69.69%,HP感染总阳性率72.72%;乙肝肝硬化消化性溃疡中年组和老年组HP感染率分别为76.59%和81.81%,HP感染总阳性率77.58%.慢性乙型肝炎消化性溃疡组中胃溃疡10例,HP阳性率32.25%,十二指肠溃疡86例,HP阳性率85.14%;乙肝肝硬化消化性溃疡组中胃溃疡3例,HP阳性率27.27%,十二指肠溃疡42例,HP阳性率89.36%.结论 慢性乙型肝炎及乙肝肝硬化消化性溃疡与HP感染有明显相关性;其中HP抗体分型发现HPⅠ型菌株比Ⅱ型菌株更有可能增加慢性乙肝及乙肝肝硬化消化性溃疡的发生风险.     

幽门螺杆菌阴性消化性溃疡的病例对照研究

背景：幽门螺杆菌（H．pylori）感染是消化性溃疡（PU）的重要病因，但H．pyZori阴性溃疡在PU中仍占有一定比例。目的：分析总结H．pyfori阴性PU的临床特点。方法：回顾性分析2004年1月-2007年3月北京大学第三医院住院PU患者的病例资料。从H．pylori阳性患者中以l：l的比例为H．pylori阴性组随机选取性别相同、年龄相近的对照，分析比较两组临床特点。结果：共纳入480例PU患者，男女比例为3．62：1；HpyZori阴性120例，阳性360例，阴性患者中位年龄显著高于阳性患者（P〈0．001）。病例对照研究显示，Hpylori阴性组首发症状存在腹痛者显著少于对照组，有恶心、呕吐症状以及有PU史和非甾体抗炎药（NSAIDs）服用史者显著多于对照组（P〈0．05）。H．pyZori阴性组胃溃疡显著多于对照组，十二指肠溃疡显著少于对照组（P〈0．05）；内镜下慢性非萎缩性胃炎显著少于对照组，息肉显著多于对照组（P〈0．05）：组织学上胃黏膜炎症、炎症程度和活动性显著轻于对照组，淋巴组织增生和肠化生显著少于对照组（P〈0．05）。结论：H．pyfo矗阴性PU占本组PU总数的25．O％，患者年龄相对较大，临床多表现为无痛性溃疡，多有PU史和NSAIDs服用史。溃疡多发生于胃部，黏膜炎症程度较轻，活动性炎症少见。     

Prevalence of Peptic Ulcer in Dyspeptic Patients and the Influence of Age,Sex, and <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection

We investigated the prevalence of peptic ulcer in dyspeptic patients in China to analyze the influence of age, sex, and Helicobacter pylori (H. pylori) infection. The results showed that the prevalence of gastric and duodenal ulcer increased with age. In patients under 60 years old, the prevalence of duodenal and gastric ulcers in females was markedly lower than that in males, especially the prevalence of duodenal ulcer. The prevalence of duodenal ulcer and gastric ulcer in H. pylori-infected patients was markedly higher than in patients without H. pylori infection. In the patients under 60 years old, sex differences were still seen in both H. pylori-positive and H. pylori-negative patients. The prevalence of gastric and duodenal ulcers was markedly increased with age in both H. pylori-positive and H. pylori-negative patients. Multivariate logistic regression analysis showed that age, male sex, and H. pylori infection were three independent risk factors for gastric and duodenal ulcers.     

Has Helicobacter pylori eradication for peptic ulcer been overrated?

Discovery of Helicobacter pylori has changed the life cycle of peptic ulcer disease (PUD). However, PUD does not completely disappear after elimination of H. pylori. Some ulcers recur even after successful eradication of H. pylori in non-users of non-steroidal anti-inflammatory drug (NSAID). In addition, the incidence of H. pylori-negative, non-NSAID PUD (idiopathic PUD) is reported to increase with time. Moreover, H. pylori-positive ulcers are not always H. pylori-induced ulcers because there are two paradoxes of the H. pylori myth: the existence of H. pylori-positive non-recurring ulcer and recurring ulcer after cure of H. pylori infection. Taken together, H. pylori is not the only cause of peptic ulcer disease. Therefore, it is still necessary to seriously consider the pathophysiology and the management of the ulcers, which may exist after elimination of H. pylori.     

Helicobacter pylori infection and the prevention of peptic ulcer with proton pump inhibitors in elderly subjects taking low-dose aspirin

INTRODUCTION: The role of Helicobacter pylori infection on the risk of low-dose aspirin-related gastroduodenal damage and on the efficacy of the prevention therapy in elderly chronic users of low-dose aspirin is still controversial. AIM: To evaluate in symptomatic elderly chronic users of low-dose aspirin: (1) the association between H. pylori infection and the prevalence of upper gastrointestinal lesions; and (2) the effect of H. pylori infection on the efficacy of proton pump inhibitors in the prevention of aspirin-related gastroduodenal lesions. PATIENTS AND METHODS: Two hundred and forty-five symptomatic elderly who were taking aspirin 75-300 mg daily, at least during the last 3 months, were evaluated by endoscopy. A structured interview was carried out to evaluate gastrointestinal symptoms and the use of proton pump inhibitors. H. pylori infection was diagnosed according to histology and the rapid urease test on gastric biopsies. RESULTS: One hundred and twelve patients were H. pylori-positive and 133 patients were H. pylori-negative. A significantly higher prevalence of peptic ulcers was observed in H. pylori-positive than in H. pylori-negative subjects (36.6% versus 15.8%, P = 0.0002). The use of proton pump inhibitors was associated with a significant decreased risk of peptic ulcer both in H. pylori-positive (absolute risk reduction, ARR = -36.2, 95% confidence interval: -51.2 to -21.3, P < 0.001) and H. pylori-negative patients (ARR = -12.6, 95% confidence interval: -23.9 to -1.2, P = 0.03). However, the number of patients who needed to be treated in order to gain a reduction of one peptic ulcer (number needed to treat, NnT) was lower in H. pylori-positive than in H. pylori-negative patients (NnT = 3 versus 8). CONCLUSIONS: In symptomatic elderly chronic users of low-dose aspirin, H. pylori infection may influence the prevalence of peptic ulcers and the cost-effectiveness of the proton pump inhibitor prevention therapy.     

幽门螺杆菌阴性消化性溃疡并发出血危险因素分析

幽门螺杆菌（H．pylori）是引起消化性溃疡（PU）的重要因素，而H．pylori阴性溃疡在PU中占有一定比例，其病因、临床表现和治疗有其特殊性。目的：分析H．pylori阴性PU并发出血的危险因素，为其预防和治疗提供可靠依据。方法：回顾性分析2004年1月～2007年3月在北京大学第三医院住院治疗的PU患者的病例资料，所有患者均经内镜检查确诊，并经病理学检查排除恶性病变，对其中H．pylori阴性患者行出血相关危险因素分析。结果：共有480例PU患者入选，其中H．pylori阴性120例（25．O％），男95例（79．2％），女25例（20．8％），中位年龄65（19-87）岁；并发出血者共95例（79.2％）。对可能与H．pylori阴性PU并发出血相关的因素行单因素分析，结果显示无腹痛（P=0．015）、溃疡形状为类圆形（P=O．027）、溃疡分期为活动期（P〈0．001）、无反流性食管炎（RE）（P〈0．001）、凝血酶原活动度〈80％（P=-0．034）有统计学意义：进一步行Logistic逐步回归分析，结果显示无腹痛、溃疡分期为活动期、无RE、溃疡最大直径〈20mm有统计学意义（P〈0．05）。结论：无腹痛、溃疡形状为类圆形、分期为活动期、无RE、凝血酶原活动度〈80％与H．pflori阴性PU发生出血相关。无腹痛、溃疡分期为活动期、无RE、溃疡最大直径〈20mm为H．pylori阴性PU发生出血的独立危险因素。     

胃肠外疾病患者幽门螺杆菌感染分析

目的检测幽门螺杆菌（Helicobacterpylori，H．pylori）在胃肠外疾病患者中的感染率及其分布特征，探讨其与胃肠外疾病发病的相关性，以期在疾病预防及临床治疗中发挥指导作用。方法对1530例特发性血小板减少性紫癜、糖尿病、结缔组织病、肝硬化、过敏性紫癜及其他胃肠外疾病患者进行14C-尿素呼气试验检测。结果1530例胃肠外疾病患者中有1140例14C-UBT结果阳性，感染率74．5％。特发性血小板减少性紫癜、糖尿病、结缔组织病、过敏性紫癜组H．pylori感染率均高于健康人（P〈0．05），肝硬化患者H．pylori感染率与健康人无明显差异。特发性血小板减少性紫癜、糖尿病、结缔组织病等合并慢性胃炎或消化性溃疡的病例H．pylori感染率较单纯慢性胃炎或消化性溃疡患者高（P〈0．05），而肝硬化及过敏性紫癜组则无明显差异。在特发性血小板减少性紫癜等胃肠外疾病患者中联合抗日．pylori治疗疗效优于单纯治疗原发病。结论H．pylori感染可能在消化道以外疾病的发生发展过程中起重要作用，但是否为相关胃肠外疾病发病的独立危险因素需要进一步证实。     

Attributable Risk of H. pylori in Peptic Ulcer Disease

Recent reports in the United States have found that fewer peptic ulcers are due to Helicobacter pylori than previously believed. The aim of this study is to determine if the declining prevalence of H. pylori infection in the general population can account for the apparent increase in the frequency of non-H. pylori ulcers. A total of 396 patients with peptic ulcer or ulcer scar were enrolled in this study. The pre-1950 population consisted of 149 patients with gastric ulcers and with 44 duodenal ulcers. The post-1950 population consisted of 96 patients with gastric ulcers and 107 with duodenal ulcers. The frequency of H. pylori-negative gastric ulcers was 5.4% in patients born before 1950 and 4.2% in patients born after 1950, and the frequency of H. pylori-negative duodenal ulcers was 0% and 1.9%, respectively. There are no statistical differences between the two populations in gastric and duodenal ulcers. H. pylori seropositivity was 74.9% in asymptomatic volunteers born before 1950 and 20.7% in those born after 1950 (P < 0.01) in the general population. The attributable risk of H. pylori infection in peptic ulcer diseases was not affected by the prevalence of H. pylori infection in the general population in Japan. This suggests that the apparent increase in frequency of non-H. pylori ulcers in the United States is not simply due to the declining prevalence of infection. Other explanations for non-H. pylori ulcers should be sought.     

幽门螺杆菌相关上消化道疾病与复发性阿弗他溃疡相关性研究

目的探讨幽门螺杆菌（Helicobacter pylori，H．pylori）相关上消化道疾病与复发性阿弗他溃疡（recurrent aphthousulcer，RAU）的关系。方法运用聚合酶链反应技术和尿素酶试验对150例上消化道疾病患者的唾液和胃黏膜中的H．pylori检测，结合RAU的流行病学调查进行统计比较，并分析口腔和胃内H．pylori感染的相互影响及对龋齿的影响。结果胃黏膜H．pylori阳性患者中RAU的发病率为50．94％（27／53），明显高于阴性组13、40％（13／97）（P〈0．001）；口腔中H．pylori阳性和阴性两组患者的龋失补指数中位数分别为3．0和1．0，差异具有统计学意义（P〈0．05）；口腔中H．pylori阳性患者中RAU的发病率为24．72％（22／89），与阴性组29．51％（18／61）比较无明显差异（P〉0．05）；口腔内H．pylori感染与胃内H．pylori感染未见明显相关性（P〉0．05）。结论H．pylori相关上消化道疾病与RAU密切相关；口腔内H．pylori感染与龋齿发生有相关性。     

消化性溃疡与ABO血型、Lewis表型分布及幽门螺杆菌感染的相关性研究

目的探讨消化性溃疡（PU）与ABO血型、Lewis表型的分布及幽门螺杆菌（H．pylori）感染的关系。方法70例消化性溃疡患者为研究组,96例健康志愿者为对照组,比较ABO血型、Lewis表型分布和H．pylori感染的差异。结果PU组O型血者占52．9％,明显高于O型血在正常人群中的分布（31．3％,P〈0．05）;在非O型血患者中Lewis表型为Le（a＋b＋）者占51．5％,明显高于Le（a＋b＋）表型在对照组非O型血中的频率（9．1％,P〈0．001）。PU组不同ABO血型者H．pylori感染率比较无统计学差异（P〉0．05）;PU组Le（a-b＋）表型者H．pylori感染率为67．6％,明显高于其他Lewis表型（P〈0．05）。结论ABO血型中O型血者易患消化性溃疡,且非O型血Lewis表型为Le（a＋b＋）者也是消化性溃疡的高危人群。ABO血型间H．pylofi感染比较无显著性差异,Le（a-b＋）表型可能是H．pylori感染的一个危险因素。     

Impact of non-steroidal anti-inflammatory drug and aspirin use on the prevalence of dyspepsia and uncomplicated peptic ulcer disease

BACKGROUND: Non-steroidal anti-inflammatory drug and aspirin (here collectively called NSAIDs) use is the second most common aetiologic factor for peptic ulcer disease and a major factor for peptic ulcer complications. The role of NSAIDs in the pathogenesis of uncomplicated peptic ulcer is less well understood and the interaction between NSAIDs and Helicobacter pylori infection on ulcer development is controversial. The aim of the present study was to examine the role of NSAIDs in the occurrence and clinical features of uncomplicated peptic ulcer disease. METHODS: A total of 1091 consecutive patients referred for open-access upper gastrointestinal endoscopy by general practitioners (GPs) were enrolled. The use of NSAIDs was gathered from a structured questionnaire completed by the patients and from patient files by GPs. The exclusion criteria were previous H. pylori eradication and gastric surgery, as well as symptoms and/or signs suggestive of acute gastrointestinal bleeding. RESULTS: Of the whole study group (n = 1091), 76 (7%) patients had a peptic ulcer. Thirty patients had an NSAID-use-associated peptic ulcer and 46 patients a non-NSAID-use peptic ulcer. Of patients with chronic gastritis (n = 599), 71% were H. pylori-positive and 108 used NSAIDs. Of those with chronic gastritis, 23 had an NSAID-use-associated peptic ulcer and 38 a non-NSAID ulcer. Of patients with normal gastric histology (n = 492), 75 patients used NSAIDs, 7 had an NSAID ulcer and 8 a non-NSAID ulcer. The only independent risk factor for peptic ulcer in patients using NSAIDs was H. pylori infection (odds ratio (OR) 3.1, 95% confidence interval (CI) 1.3-7.3), whereas dyspepsia (OR 1.0, 95% CI 0.4-2.4), male sex (OR 1.4, 95% CI 0.6-3.4), age (OR 1.0 per decade, 95% CI 0.8-1.3) and anaemia (OR 2.9, 95% CI 0.9-8.7) were not risk factors. In patients not using NSAIDs, independent risk factors for peptic ulcer were dyspepsia (OR 4.3, 95% CI 2.1-8.8), male sex (OR 2.0, 95% CI 1.1-2.8), age (OR 1.2 per decade, 95% CI 1.0-1.5), anaemia (OR 6.2, 95% CI 2.6-14.9) and H. pylori infection (OR 7.5, 95% CI 3.4-16.6). When comparing patients using NSAIDs or not, the OR of patients on NSAIDs for peptic ulcer was 2.7 (95% CI 1.5-5.0) among patients with chronic H. pylori gastritis (n = 424) and 5.3 (95% CI 1.8-15.0) among patients with normal gastric mucosa (n = 492). CONCLUSIONS: The use of NSAIDs increases the risk of peptic ulcer 3- and 5-fold in H. pylori-positive and H. pylori-negative patients, respectively. Dyspepsia is a poor predictor of peptic ulcer among patients using NSAIDs, and serologic H. pylori testing and treatment for chronic NSAID users is recommended.