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。     

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。     

幽门螺旋杆菌感染及非甾体抗炎药对消化性溃疡出血的影响研究

目的探讨服用非甾体抗炎药（NSAIDs）和幽门螺旋杆菌（H.pylori）感染与消化性溃疡出血的关系。方法选取我院2007年5月—2009年4月消化内科收治的消化性溃疡患者218例,均行内镜检查确诊为消化性溃疡（复合性溃疡除外）,同时行病理学检查以排除胃癌患者。对消化性溃疡并发出血的危险因素行单因素和多因素的分析。结果在单因素分析中,出血组与未出血组患者中年龄≥60岁的患者、有消化道出血史患者、有心脑血管病史者、有多个溃疡患者所占据的比例间比较差异均有统计学意义（P〈0.01）;进一步行多因素的分析发现,患者年龄≥60岁、患有消化性溃疡史、消化道出血史、心脑血管疾病史和单纯的H.pylori感染、单纯服用NSAIDs、H.pylori感染并同时服用NSAIDs为消化性溃疡并发出血的危险因素。结论幽门螺旋杆菌感染并未增加溃疡并发出血的危险性,但是当服用NSAIDs、年龄≥60岁、消化性溃疡或伴有出血病史、心脑血管疾病史等因素联合可以增加消化性溃疡出血的危险性。     

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

目的探讨消化性溃疡患者非甾体类抗炎药(NSAIDs)服用史和幽门螺杆菌(HP)感染的协同致病性。方法消化性溃疡患者155例(其中溃疡合并上消化道出血患者46例),再选取同期就诊的非胃十二指肠疾病患者91例为对照组。调查NSAIDs服用史,检测HP感染。结果服用NSAIDs合并HP感染患胃溃疡的OR值为18.87(95%CI为12.03~30.09),明显高于单纯HP感染和单独服用NSAIDs患胃溃疡的OR值之和;服用NSAIDs合并HP感染患十二值肠溃疡的OR值23.79(95%CI为13.21~38.51)明显低于单纯HP感染和单独服用NSAIDs患十二指肠溃疡的OR值之和;服用NSAIDs合并HP感染的胃溃疡和十二指肠溃疡合并上消化道出血的OR值分别为3.62(95%CI为1.01~17.98)和0.98(95%CI为0.28~7.89),均低于单纯HP感染和单独服用NSAIDs的胃溃疡和十二肠溃疡合并消化道出血的OR值之和;对照未服用NSAIDs者,偶尔服药与短期服药及长期服药溃疡出血者之间比较差异无统计学意义(P>0.05)。结论 NSAIDs和HP感染在消化性溃疡的发生中具有协同作用;在胃溃疡合并上消化道出血的发病中无协同作用;胃溃疡合并上消化道出血与服用NSAIDs时间长短无关。     

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。     

幽门螺杆菌相关性消化性溃疡与小肠细菌过度生长的关系

目的观察幽门螺杆菌(Helicobacter pylori,H.pylori)相关性消化性溃疡有无小肠细菌过度生长,以指导临床实践。方法对78例幽门螺杆菌相关性消化性溃疡组患者和健康对照组患者进行葡萄糖呼气试验。结果胃溃疡、十二指肠溃疡组小肠细菌过度生长(SIBO)阳性率分别为4.3%(2/46)、6.3%(2/32),胃溃疡组、十二指肠溃疡组、健康对照组在基础值及试餐后氢呼气浓度差异均无统计学意义(P>0.05)。结论幽门螺杆菌相关性消化性溃疡患者并未出现小肠细菌过度生长,只需进行根除H.pylori治疗。     

老年非甾体抗炎药相关消化性溃疡的临床特征及影响因素

目的分析老年非甾体抗炎药(NSAIDs)相关消化性溃疡的临床特征及影响因素。方法回顾性分析323例消化性溃疡患者临床完整资料,据患者发生消化性溃疡前10 d是否服用NSAIDs分为NSAIDs组(n=122)、非NSAIDs组(n=201)。设计一般情况调查表,仔细查阅患者病历资料,详细记录两组基线资料、症状、胃镜检查特点及NSAIDs患者用药情况,分析NSAIDs相关消化性溃疡临床特征及影响老年NSAIDs相关消化性溃疡发生的相关因素。结果NSAIDs组年龄、心脑血管例数均明显高于非NSAIDs组,腹痛发生率明显低于非NSAIDs组,无临床症状比例明显高于非NSAIDs组,差异有统计学意义(P<0.05);NSAIDs组溃疡多发于胃部,非NSAIDs组胃溃疡多发于十二指肠部位,差异有统计学意义(P<0.05);NSAIDs组多发病灶占比高,非NSAIDs组单发病灶占比高,差异有统计学意义(P<0.05);NSAIDs组122例患者服用阿司匹林74例,服用消炎药10例,止痛药38例,服用不同非甾体抗炎药患者胃镜下溃疡形态、大小、数量比较,差异无统计学意义(P>0.05);经非条件多项Logistic回归分析证实,年龄、心脑血管疾病及幽门螺杆菌(Hp)感染均可能是诱发NSAIDs相关性消化性溃疡发生的影响因素(OR>1,P<0.05)。结论老年NSAIDs相关消化性溃疡发病年龄高于非NSAIDs相关消化性溃疡,且多合并心脑血管疾病,多发于胃部,而胃溃疡中多累及胃窦位置,无显著临床症状,胃镜检查下溃疡多发占比高,服用不同种类NSAIDs药物在溃疡大小、形态等方面无显著差异,年龄、心脑血管疾病及Hp感染均是老年NSAIDs相关消化性溃疡的危险因素。     

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。     

老年人上消化道出血与口服NSAIDs、Hp感染相互关系的探讨

目的 探讨老年人上消化道出血与服用NSAIDs、Hp感染之间的关系。方法 采用病例对照分析的方法对146例老年上消化道出血的病例组及非上消化道出血的对照组进行胃镜检查和Hp感染检测，并统计NSAIDs服用史。结果 老年人上消化道出血者（包括胃镜疡和十二指肠溃疡）服用NSAIDs较对照组明显增加；胃溃疡病例组Hp感染明显低于对照组；而十二指肠溃疡患者，两组之间Hp感染率无明显差异，Logistic回归分析结果证明，服用NSAIDs可以增加老年人（包括胃溃疡和十二指肠溃疡）上消化道出血的危险性；Hp感染与胃溃疡所致上消化道出血的危险性呈负相关，而与十二指肠溃疡所致上消化道出血无明显关系。偶尔服用NSAIDs同样可以增加老年人上消化道出血的危险性。结论 服用NSAIDs可增加老年人上消化道出血的危险性；Hp感染可减少胃溃疡上消化道出血的危险性，而与十二指肠溃疡关系不明显。服用NSAIDs与Hp感染是老年人上消化道出血的两个独立因素。     

消化性溃疡相关致病因素协同致病性分析

目的 了解消化性溃疡患者相关致病因素(主要是服用NSAIDs与Hp感染)的协同致病作用.方法 应用病例对照研究的方法 对200例消化性溃疡患者及52例溃疡合并上消化道出血者及同一时期就诊的206例非胃十二指肠疾病患者进行NSAIDs服用情况的调查和Hp感染的检测. 结果 服用NSAIDs合并Hp感染者患胃溃疡的OR值为19.11,明显高于单纯服用NSAIDs者(OR值5.93)和单纯Hp感染者(OR值5.74)患胃溃疡的OR值之和;服用NSAIDs合并Hp感染的胃溃疡发生上消化道出血的OR值为3.73,十二指肠溃疡患者发生上消化道出血的OR值为0.93,均低于单纯服用NSAIDs和单纯Hp感染的胃溃疡患者(OR值分别为3.9和0.56)和十二指肠溃疡患者(OR值分别为4.7和0.42)发生上消化道出血的OR值之和;与无溃疡未服NSAIDs者比较,间断服药者溃疡出血的OR值为3.99,短期服药者的OR值为2.89,长期服药者的OR值为3.39,三组比较无显著差异(P＞0.05).患十二指肠溃疡的老年患者为33/120(27.5%),与非老年组比较有非常显著性差异(P＜0.01). 结论 服用NSAIDs和Hp感染在胃溃疡的形成中存在协同作用;在溃疡合并上消化道出血的发病中并无协同作用;溃疡合并上消化道出血与服用NSAIDs的时间长短无关;年龄因素在十二指肠溃疡的发病过程中发挥重要作用.     

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。     

非甾体类抗炎药相关性胃十二指肠黏膜损害临床调查分析

目的 探讨非甾体类抗炎药(NSAID)相关性胃十二指肠黏膜损害的发生情况及其危险因素.方法 收集心血管科与风湿免疫科门诊中184例长期服用NSAID的患者作为研究对象.记录患者的一般资料,对患者的消化不良症状进行评分,胃镜下行黏膜损伤评分,留取标本行幽门螺杆菌(Hp)检测,并行统计分析.结果 在184例长期服用NSAID患者中共发现消化性溃疡63例(34.2%),其中胃溃疡22例、十二指肠溃疡34例、复合性溃疡7例.在其余121例无溃疡患者中,57例胃黏膜存在3处或3处以上糜烂灶.Logistic多因素回归分析发现,Hp感染是长期服用NSAID人群发生消化性溃疡的重要危险因素(OR=13.86,95%CI:6.53～29.43).低剂量阿司匹林与其他NSAlD导致胃十二指肠黏膜损伤的发生率相似(OR=0.45,95%CI:0.16～1.28).结论 长期服用NSAID者胃十二指肠黏膜易受损,Hp感染是重要的危险因素.低剂量阿司匹林致胃肠道损伤的发生率与其他NSAID相似.     

Does the declining prevalence of Helicobacter pylori unmask patients with idiopathic peptic ulcer disease? Trends over an 8 year period

OBJECTIVES: Recent studies have suggested that the prevalence of Helicobacter pylori infection in patients with ulcer disease who were not using non-steroidal anti-inflammatory drugs (NSAIDs) has been overestimated. The decreasing prevalence of H. pylori could lead to a relative increase in the number of patients with this idiopathic peptic ulcer disease (IPUD). This study aimed to investigate the prevalence of IPUD and any possible trends. DESIGN AND METHODS: The reports of all upper gastro-intestinal endoscopies performed in a Dutch regional hospital over the period 1991 to 1998 were reviewed. If a gastric and/or duodenal ulcer had been diagnosed, data concerning possible H. pylori infection (culture, histology, rapid in-house urease test) were retrieved. If H. pylori tests were negative, hospital files were examined for possible use of NSAIDs or other rare causes of ulcer disease. When these were not found, stored biopsy specimens were tested for H. heilmanii by using the polymerase chain reaction technique. RESULTS: Ulcer disease was diagnosed in 405 patients who had undergone endoscopy (159 with gastric ulcer, 235 with duodenal ulcer, and 11 with both gastric and duodenal ulcer). H. pylori infection was found in 349 of these patients (86.2%). Thirty-three of the 56 H. pylori negative patients used NSAIDs and three patients had Crohn's disease, leaving 20 patients with IPUD (4.9%, 12 gastric ulcer and eight duodenal ulcer). Time trends over the study period showed a decrease of H. pylori associated peptic ulcer disease (P <0.002) and an increase of NSAID associated peptic ulcer disease (P <0.0005). The prevalence of IPUD remained stable (P=0.978). CONCLUSIONS: The prevalence of patients with H. pylori negative ulcer disease significantly decreased in our study population due to an increase in the number of patients with NSAID associated peptic ulcer disease. IPUD was rare and its prevalence did not increase over a period of 8 years.     

Peptic ulcer bleeding: interaction between non-steroidal anti-inflammatory drugs, Helicobacter pylori infection, and the ABO blood group system

BACKGROUND: Helicobacter pylori infection is found in almost all patients with an uncomplicated ulcer. Non-steroidal anti-inflammatory drug (NSAID) use is the main risk factor for bleeding peptic ulcer. In the older literature ABO blood groups were mentioned as a risk factor. There is continuing uncertainty about the interaction between these risk factors and the development of peptic ulcer bleeding. We therefore determined the separate and combined effect of NSAIDs, H. pylori infection, and the ABO blood group system in patients with a bleeding peptic ulcer. METHODS: The prevalence of NSAID use, H. pylori infection, and blood group O was determined in 227 patients who were admitted with a bleeding gastric or duodenal ulcer between 1990 and 1997. These results were compared with the expected frequency of these risk factors in the Dutch population. RESULTS: NSAID use was reported in 48.2% of the patients with a bleeding peptic ulcer. The H. pylori prevalence was 62.0%, whereas blood group O was present in 49.3% of the patients. NSAID use was the strongest risk factor for hemorrhage caused by a peptic ulcer (relative risk, 8.4), whereas the relative risk associated with H. pylori infection and blood group O was 1.5 and 1.2, respectively. With univariate analysis NSAID use and H. pylori infection seemed to be separate risk factors and did not really potentiate each other's effect. Moreover, blood group O did not potentiate the strong effect of NSAIDs. CONCLUSION: H. pylori infection may add only a little to the important risk of NSAID use in the development of bleeding peptic ulcers.     

What consideration should be given to Helicobacter pylori in treating nonsteroidal anti-inflammatory drug ulcers?

Although Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) both cause peptic ulcers, they do so by different mechanisms so any interaction is not necessarily harmful. H. pylori has been shown to enhance gastric mucosal prostaglandin synthesis, while NSAIDs suppress it Pragmatically, there is no compelling evidence in favour of H. pylori eradication in all patients who take NSAIDs. As a broad generalisation, in therapeutic studies of NSAID users, those who have no ulcer at trial entry are more prone to ulcer development if they are H. pylori-positive. By contrast, in those who have ulcers at baseline, H. pylori-positive individuals are less likely to develop ulcers, particularly if taking acid-suppressive therapy. Trials of H. pylori eradication therapy tend to replicate this dichotomy. In one study of patients starting NSAIDs for the first time, with no ulcer history and no baseline ulcer, use of bismuth-based eradication therapy was associated with a lower incidence of gastric ulcer at 2 months. Conversely, in a study of patients with endoscopically proven ulcers and/or troublesome dyspepsia, proton pump inhibitor based eradication treatment had no effect on outcome (of acid suppression) over 6 months. H. pylori eradication has been associated with significantly slower healing of gastric ulcers compared with patients who did not undergo eradication. However, the effect of H. pylori eradication on healing of NSAID-associated duodenal ulcers does not appear to be so dramatic, and limited evidence suggests that it may be possible to prevent H. pylori-associated duodenal ulcer by eradicating the infection. An evidence-based approach to treatment would suggest that NSAID users should undergo H. pylori eradication therapy if they have a duodenal ulcer, whether or not they continue NSAIDs. Because COX-2 inhibitors appear not to be ulcerogenic, management of H. pylori in patients taking these drugs can be based upon the same risk assessment as in patients not taking anti-arthritis drugs. H. pylori eradication should not be used universally or in high-risk gastric ulcer patients who require management with acid suppression.     

Recurrence of Helicobacter pylori infection and the long-term outcome of peptic ulcer after successful eradication in Japan.

Recurrence of peptic ulcer after successful eradication of Helicobacter pylori is closely associated with reinfection. The aim of this study was to examine the recurrence of peptic ulcer and reinfection with H. pylori after successful eradication. To eradicate H. pylori infection, patients with active peptic ulcer disease were assigned to two treatment groups depending on the year of their enrollment (AM group and OAMR group). Patients in the AM group received 400 mg of cimetidine twice per day, 300 mg of amoxicillin three times per day, and 250 mg of metronidazole three times per day for 2 weeks. Patients in the OAMR group received 20 mg of omeprazole once per day, 500 mg of amoxicillin granules three times per day, 250 mg of metronidazole three times per day, and 150 mg of roxithromycin twice per day for 1 week. After endoscopy verified ulcer scarring and successful eradication of H. pylori infection, study patients were followed up monthly and did not undergo acid-suppressive therapy. Endoscopy was performed at 6-month intervals for the 1st year. After the 1st year, follow-up endoscopies were performed annually. In total, 107 patients with peptic ulcer (duodenal ulcer [DU], 65; gastric ulcer [GU], 42) were followed up for a mean period of approximately 2 years. Recurrence of infection occurred in 10 (9.3%) of 107 patients (AM group, 9; OAMR group, 1) after 210 patient-years of follow-up; the recurrence rate was 4.8% per patient-year. Recurrence of H. pylori infection was significantly higher in the AM group (23.1%) than in the OAMR group (1.5%). H. pylori infection recurred in two patients 6 months after eradication therapy, in seven 1 year after, and in one 2 years after. Thereafter, no further cases of H. pylori recurrence were observed. During follow-up periods, seven cases of ulcer recurrence were observed (DU, 4; GU, 3). The rate of peptic ulcer recurrence within 2 years after eradication therapy was significantly higher than that after more than 2 years. Four cases of ulcer recurrence (DU, 3; GU, 1) also had recurrence of H. pylori infection. One recurrent case of DU without reinfection was associated with nonsteroidal anti-inflammatory drugs. The remaining two cases of GU recurred without H. pylori reinfection. In conclusion, peptic ulcer recurrence rarely occurred (3 [2.9%] of 103) in patients cured of H. pylori infection. Reinfection after apparent successful eradication was rarely noted when a powerful therapeutic regimen in eradication was used. Therefore, to eradicate H. pylori, a highly effective therapeutic regimen should always be used.     

Helicobacter pylori and risk of ulcer bleeding among users of nonsteroidal anti-inflammatory drugs: a case-control study.

BACKGROUND & AIMS: Peptic ulcer complications related to use of nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common serious adverse drug reactions. Whether Helicobacter pylori infection potentiates this gastrointestinal toxicity of NSAIDs is still unresolved. In this study, we investigated the role of H. pylori as a cause of bleeding peptic ulcer among NSAID users. METHODS: A case-control study of current users (n = 132) of NSAIDs (including acetylsalicylic acid), admitted because of bleeding peptic ulcer, was performed. Controls were 136 NSAID users without gastrointestinal complications. H. pylori was diagnosed by either increased levels of serum immunoglobulin G or by 13C-urea breath test. RESULTS: Fifty-eight (44%) case subjects had a bleeding gastric ulcer, 54 (41%) had a bleeding duodenal ulcer, 12 (9%) had both gastric and duodenal ulcers, and 8 (6%) had hemorrhagic gastritis. H. pylori was present in 75 (57%) cases compared with 59 (43%) controls. The adjusted odds ratio of bleeding peptic ulcer among NSAID users associated with H. pylori infection was 1.81 (95% confidence interval, 1.02-3.21). H. pylori accounted for approximately 24% of bleeding peptic ulcers among elderly NSAID users. CONCLUSIONS: NSAID users infected with H. pylori have an almost twofold increased risk of bleeding peptic ulcer compared with NSAID users without H. pylori.     

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。     

Non-Helicobacter pylori and non-NSAID peptic ulcer disease in the Japanese population

BACKGROUND: Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs) are recognized as the major causes of peptic ulcer disease. The status of H. pylori infection in the background population may influence the incidence of H. pylori-negative peptic ulcer disease. OBJECTIVE: To examine the incidence of H. pylori-negative peptic ulcer disease without intake of NSAIDs in Japan. PATIENTS: A total of 398 patients who had no eradication therapy for H. pylori prior to this study, including 246 patients with gastric ulcer (GU) and 152 patients with duodenal ulcer (DU), were enrolled. METHODS: H. pylori status was assessed by rapid urease tests, histological examinations (haematoxylin & eosin stain, Giemsa stain and/or immunostaining) and serum IgG antibody. Two biopsy specimens were taken from the antrum within 3 cm of the pyloric and two from the middle corpus of the stomach, along the greater curvature. Patients were asked a series of questions regarding risk factors, including the use of NSAIDs. The presence of gastritis, gastric atrophy and intestinal metaplasia was examined according to the updated Sydney system. RESULTS: Of the 246 patients with GU, 12 patients (4.9%) were considered to be H. pylori-negative. Of the 152 patients with DU, two patients (1.3%) were considered to be H. pylori-negative. Hence, a total of 14 patients were found to be H. pylori-negative. Nine of them were taking NSAIDs. Consequently, the frequency of H. pylori-negative ulcer without intake of NSAIDs was 1.3%. There was no significant difference in the frequencies of H. pylori-negative patients between the GU and DU groups. CONCLUSION: The incidence of H. pylori-negative peptic ulcer disease without intake of NSAIDs was very low in the Japanese population.