胃苏冲剂三联疗法治疗消化性溃疡近期及远期疗效

目的观察胃苏冲剂三联疗法治疗消化性溃疡近、远期效果．方法经内镜确诊的53例消化性溃疡患者，其中GU7例，DU46例，男32例，女21例，年龄18岁～72岁．病程6mo～18a．临床表现为痞满36例，上腹疼51例，纳呆26例，嗳气35例，泛酸48例．应用胃苏冲剂（主要由紧苏梗、香附、陈皮、佛手等中药组成）、甲硝唑和羟氢苄青霉素三联治疗，并与对照组32例用麦滋林S颗粒、甲硝唑和羟氢苄青霉素三联疗法进行比较，胃苏冲剂或麦滋林S颗粒均3wk为一疗程，甲硝唑、羟氨苄青霉素均2wk为一疗程．疗程结束后复查内镜和尿素酶法测定Hp．结果经胃苏冲剂三联疗法治疗3wk后，总愈合率治疗组45／53例（81．1％），Hp根除率42／47例（89．3％），Hp根除率2／6（33．3％）；对照组27／32（84．3％），Hp根除者26／28（92．1％），未根除者1／4（25％）．两级总愈合率和Hp根除无明显差异（P＞0．05），两组内Hp根除的愈合率高于未根除者，差异有显著性（P＜0．05），追踪1a，治疗组已愈合43例，7例（16．2％）复发，其中Hp转阳的11例中7例（63．6％）复发，Hp阴性42例中仅5例（11．9％）复发，Hp阳性与阴性组复发率差异显著（P＜0．01），两组溃疡复发率差异不显著（P＞0．05）结论胃苏冲剂三联疗法治疗消化性溃疡有较好的近、远期     

cag A阳性幽门螺杆菌与老年胃十二指肠病的相关性

目的 探讨本地区老人幽门螺杆菌（Hp）tagA基因存在状况及其与老年胃十二指肠病的关系。方法 收集89例老年和96例青壮年慢性胃炎、消化性溃疡患菌及30例正常对照人群的血清标本及胃组织标本,应用血清学检验其Hp-cag A阳性菌株感染状况。结果 89例老年患者中慢性胃炎、胃溃疡、十二指肠溃疡的Hp-cag A基因的阳性率分别为73．5％（38／52）、81．3％（13／16）及85．7％（18／21）;96例青壮年患者中慢性胃炎、胃溃疡、十二指肠溃疡的Hp-cag A基因的阳性率分别为59．3％（32／54）、68．8％（11／16）及61．5％（16／26）;对照组Hp-cag A阳性病株感染率为33．3％,各疾病组间Hp-cag A阳件菌株感染率差异无显著性（P〉0．05）．仍均高于对照组（P〈0．05）;cag A阳性Hp菌株感染率老年组高于青壮年组（P〈0．05）。结论 本地区老年患者cag A阳性Hp菌株感染与上述3种胃十二指肠疚病的发生均密切相关．老年患者感染的Hp绝大多数为cag A阳性菌株。     

消化性溃疡与幽门螺杆菌的关系研究

目的探讨消化性溃疡与幽门螺杆菌的关系。方法研究对象为2007-2008年来我院消化科就诊并且经过胃镜确诊的患者人群。分为A、B两组,A组31例,均为消化性溃疡（胃、十二指肠溃疡）患者,B组28例,均为浅表性胃炎或正常人群,均经胃镜检查确诊。A、B两组人群在给予胃镜检查的同时取胃、十二指肠黏膜组织,置于Hp指示剂中以诊断是否感染Hp。结果A组Hp阳性25例,感染率80．6％,B组Hp阳性9例,感染率为32．1％,A、B两组Hp感染率比较,差异有显著性（P〈0．05）。结论消化性溃疡患者感染Hp明显高于正常人群,从而提出Hp感染是消化性溃疡产生的重要致病因素。     

口腔唾液幽门螺杆菌与功能性消化不良

目的探讨口腔唾液中Hp与功能性消化不良（FD）的关系，为Hp感染防治提供依据．方法87例FD患者内镜检查前用一次性容器收集唾液标本，内镜检查时取幽门前区粘膜活检标本作革兰染色光镜检查和快速尿素酶试验．唾液Hp检测采用美国MJ公司PTC-100扩增仪和上海复星生物有限公司Hp-PCR试剂盒．结果87例FD患者胃粘膜革兰染色和快速尿素酶试验均阳性45例（51．7％），阴性42例（48．3％）．阳性患者唾液Hp-PCR阳性18例（40％），阴性患者无一例唾液Hp-PCR阳性．FD不同临床类型唾液Hp-PCR阳性检出率依次为胃食管反流型32．5％（13／40），溃疡型17．6％（3／17），动力紊乱型6.7％（2／30），经统计学处理唾液Hp检出率胃食管及流型与溃疡型无显著差异（P＞0．05），与动力紊乱型差异显著（P＜0．01）．结论①FD患者口腔唾液中检出Hp，证明Hp可通过胃食管反流入口腔，且随时可能将Hp重新吞入，引起胃粘膜再感染和损伤．因此，根除Hp除选择敏感药物外，必须同时治疗消化不良，尤其是控制胃食管及流症状，否则Hp感染者就难以得到根治．②唾液中检出Hp，进一步证实Hp可通过唾液或口-口接触传播．由此可见，控制胃食管反流症状，保持口腔清洁卫生，改变国人的共餐饮食传统习惯，对阻止Hp人-人传播具有重要现实意义．     

CagA基因菌株Hp与胃、十二指肠疾病

目的通过检测胃、十二指肠疾病患者的幽门螺杆菌（Hp和CagA-Hp-IgG（细胞毒素相关蛋白抗体），探讨CagA基因菌株Hp与胃、十二指肠疾病的相关性。方法206例因胃肠症状在门诊、住院就诊者，男143例，女63例，年龄18岁～76岁．在内镜检查同时取胃粘膜组织4块，十二指肠溃疡者取距幽门1cm～2cm大弯侧，胃溃疡取溃疡边缘处，胃炎取炎症区．2块进病理检查，2块分别用尿素酶快速试验及用PCR法检测Hp，同时抽取静脉血3mL作CagA-Hp-IgG抗体检测．结果用尿素酶快速试验及PCR法检出Hp阳性者180例，男性感染率91％，女性78％，二者差异显著（P＜0．005），各年龄组构成无明显差异．两种检测方法的检出率无明显差异（P＞0．05）．检出CagA-Hp-IgG阳性者95例，在Hp感染组中阳性率89／180（50％），非感染组阳性率6／26（23％），二者差异显著（P＜0．05）．感染组CagA阳性者中，十二指肠球部溃疡44／55（80％），胃溃疡21／34（61％），慢性胃炎24／91（26％），三者差异明显（P＜0．025）．病理结果为轻、中、重度炎症CafA-Hp阳性率分别为25％，56％，70％，三者差异显著（P＜0．005）．结论CagA基因菌株Hp较CagA阴性菌株Hp具有更强的导致炎症的作用．CagA基因Hp是十二指肠球部溃疡、胃溃疡的重要发病因素．     

幽门螺杆菌与胃癌的关系

目的为了探索幽门螺杆菌（Hp）与胃癌及其病理类型的关系．方法对住院的经内镜及病理证实的23例胃癌，21例慢性浅表性胃炎及26例十二指肠溃疡患者进行冒窦粘膜Hp检测（采用快速尿素酶试验）及血清Hp-IgG抗体测定（采用ELISA法）．结果Hp在慢性浅表性胃炎、十二指肠溃疡、中晚期胃癌的检出率分别为52．4％，88．5％及78．3％．Hp在十二指肠溃疡及慢性浅表性胃炎的感染率具有明显差异（P＜0．01），而Hp在中晚期胃癌及慢性浅表性胃炎的感染率无差异（P＞0．05）．胃腺癌的Hp检出率高于印戒细胞癌的Hp检出率（P＜0．05）．结论①Hp与中晚期胃癌无明显相关性．②胃腺癌患者的Hp检出率较胃印戒细胞癌者的高．     

内镜检查幽门螺杆菌的检测943例分析

目的探讨幽门螺杆菌（Hp）在内镜检查中的感染率．方法对有消化道症状而做内镜检查的患者943例，男692例，女251例，年龄21岁～89岁，平均45．6岁．常规检查内镜，在胃窦部及病变处取材，分别进行快速尿素酶及组织学诊断．结果943例病例中Hp阳性563例占59．7％，慢性胃炎479例，Hp阳性241例占50．3％，轻度炎症Hp阳性率为14．7％，中、重度炎症Hp阳性率为69．9％，轻与中、重度炎症比较差异显著（P＜0．01），说明炎症愈重，Hp感染率愈高．消化性溃疡336例，Hp阳性276例占82．1％．胃溃疡Hp阳性率为80．4％，十二指肠溃疡Hp阳性率为87．6％．溃疡部位及分期与Hp阳性率无显著差异（P＞0．05），所有病例均有不同程度的胃窦部炎症，消化性溃疡伴胃粘膜中，重症炎症Hp阳性率为94．8％，说明Hp相关性胃炎与消化性溃疡有密切关系残胃27例，Hp阳性11例占40．7％，息肉26例，Hp阳性10例占38．5％，胃癌75例，Hp阳性25例占33．3％．结论Hp阳性率以消化性溃疡，慢性胃炎最高，其次是残胃和息肉，胃癌最低．     

幽门螺杆菌感染与胃癌的相关性研究

目的：为了研究幽门螺杆菌（Hp）感染与胃癌及肠化类型的关系。方法：对胃癌高发区1333例普查人群的胃活检组织和30例胃癌手术标本病理切片做Warthin－starry染色，对慢性萎缩胃炎伴肠化生、慢性浅表胃炎伴肠化生、癌旁肠化生用粘液组化方法染色分型。结果：Hp感染与十二指肠球部溃疡高度相关，与胃溃疡、慢性浅表活动性胃炎、早期胃癌显著相关，与单纯萎缩性胃炎、萎缩胃炎伴肠化生、胃增生性息肉亦相关（P均＜0．05）；进展期胃癌的Hp感染率与慢性非活动性胃炎相比较，差异无显著性（P＞0．05）；各型胃癌中以腺癌Hp检出率高（75．4％），与粘液细胞癌Hp检出率（30％）相比较，差异有非常显著性（P＜0．01）。各型肠化生之间的Hp检出率比较，差异无显著性（P均＞0．05）。结论：Hp感染与胃癌有相关性。     

舒威、阿莫西林、痢特灵治疗幽门螺杆菌阳性消化性溃疡的疗效

目的 探索幽门螺杆菌（Hp）阳性感染的理想治疗方案。方法 随机将84例幽门螺杆菌阳性十二指肠溃疡病人分为治疗组和对照组，即舒威（枸橼酸铋雷尼替丁）、阿莫西林、痢特灵三联组（n=42），丽珠胃三联组（n=42），进行为期7d的临床治疗观察，疗程结束后1个月复查。结果 舒威三联组与丽珠胃三联组溃疡治愈率分别85．72％和88．1％，Hp根除率分别为90．4％和92.8％，统计学差异无显著性（P〉0．05）。结论 舒威三联组疗效好、费用低，是消化性溃疡最经济的治疗方案。     

幽门螺杆菌阳性的十二指肠溃疡治疗

目的观察硫糖铝、雷尼替丁、阿莫西林联合治疗幽门螺杆菌（Hp）阳性的十二指肠球部溃疡效果和Hp的根除率，并探讨硫糖铝对治疗Hp感染有无协同作用．方法82例Hp阳性的十二指肠球部溃疡患者随机分成治疗组和对照组，每组各41例．两组在性别、年龄、溃疡病变程度等方面均具有可比性．治疗组服硫糖铝1．0，3次／d；雷尼替丁0．15，2次／d；阿莫西林0.5，3次／d．对照组服雷尼替丁0．15，2次／d；阿莫西林0．5，3次／d．治疗组和对照组均服药2wk停药．在治疗期间记录症状改变和药物不良反应停药后1mo复查内镜观察溃疡愈合和Hp根除情况．结果治疗组溃疡愈合率和Hp根除率分别为92％和87％；对照组溃疡愈合率和Hp根除率分别为59％和54％．治疗组溃疡愈合率和Hp根除率均明显高于对照组，有显著性差异（P＜0．05）．结论硫糖铝、雷尼替丁、阿莫西林联合治疗Hp阳性的十二指肠球部溃疡有较理想的溃疡愈合率和Hp根除率．硫糖铝不仅具有粘膜保护作用，而且对Hp感染有协同治疗作用．     

消化性溃疡患者血管活性肠肽与十二指肠胃反流和幽门螺杆菌感染关系的研究

背景：消化性溃疡（PU）和十二指肠胃反流（DGR）患者的血浆血管活性肠肽（VIP）含量常高于正常水平，而幽门螺杆菌（H.pylori)感染可能参与PU的发病。目的：探讨PU患者的VIP和DGR和H.pylori感染的关系。方法：采用放射免疫测定（RIA）检测34例胃溃疡（GU）患者、42例十二指肠球部溃疡（DU）患者和30例健康人的血浆VIP含量；放射性核素^99mTc-EHIDA显像法测定DGR；双抗体夹心酶联免疫吸附测定（ELISA）检测血清H.pylori IgG抗体，Giemsa染色检测胃黏膜H.pylori。结果：GU组的血浆VIP含量显著高于DU组和正常对照组（P＜0．01）；DGR阳性率亦显著高于DU组（P＜0．05）。DGR阳性组的血浆VIP含量显著高于DGR阴性组（P＜0．01）。H.pyori阳性组的血浆VIP含量显著低于H.pylori阴性组（P＜0．05）。结论：PU患者血浆VIP含量升高可能是DGR发生的重要因素之一。     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM： To compare the prevalence of H pylori infection, peptic ulcer, cytomegalovirus （CNV） infection and Candida esophagitis in human immunodeficiency virus （HIV）- positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.
METHODS： A total of 151 patients （122 HIV-positive and 29 HIV-negative） with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of Hpylori infection, CMV, candida esophagitis and histologic chronic gastritis.
RESULTS： The prevalence of Hpylori was less common in HIV-positive patients （22.1%） than in HIV-negative controls （44.8%; P 〈 0.05）, and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer （20.7% vs 4.1%; P 〈 0.01）, but a higher prevalence of chronic atrophy gastritis （6.9% vs 24.6%; P 〈 0.05）, Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis （P 〈 0.05）. In HIV-positive patients, chronic active gastritis was not significantly different between those with Hpylori infection and those without.
CONCLUSION： The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to Hpylori infection.     

A low prevalence of H pylori and endoscopic findings in HTV-positive Chinese patients with gastrointestinal symptoms

AIM: To compare the prevalence of H pylori infection,peptic ulcer, cytomegalovirus (CMV) infection and Candida esophagitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.METHODS: A total of 151 patients (122 HIV-positive and 29 HIV-negative) with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of H pylori infection,CMV, candida esophagitis and histologic chronic gastritis.RESULTS: The prevalence of H pylori was less common in HIV-positive patients (22.1%) than in HIV-negative controls (44.8%; P ＜ 0.05), and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer (20.7% vs 4.1%; P ＜ 0.01), but a higher prevalence of chronic atrophy gastritis (6.9% vs 24.6%; P ＜ 0.05), Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis (P＜0.05). In HIV-positive patients, chronic active gastritis was not significantly different between those with H pylori infection and those without.CONCLUSION: The lower prevalence of H pylori infection and peptic ulcer in HTV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer.The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to H pylori infection.     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM: To compare the prevalence of H pylori infection,peptic ulcer,cytomegalovirus (CMV) infection and Candida esophagitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients,and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections. METHODS: A total of 151 patients (122 HIV-positive and 29 HIV-negative) with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of H pylori infection,CMV,candida esophagitis and histologic chronic gastritis. RESULTS: The prevalence of H pylori was less common in HIV-positive patients (22.1%) than in HIV-negative controls (44.8%; P < 0.05),and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group,HIV-positive patients had a lower incidence of peptic ulcer (20.7% vs 4.1%; P < 0.01),but a higher prevalence of chronic atrophy gastritis (6.9% vs 24.6%; P < 0.05),Candida esophagitis and CMV infection. Unlike HIV-negative group,H pylori infection had a close relationship to chronic active gastritis (P < 0.05). In HIV-positive patients,chronic active gastritis was not significantly different between those with H pylori infection and those without. CONCLUSION: The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to H pylori infection.     

Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori gastritis

OBJECTIVE: Helicobacter pylori and duodenogastric reflux (DGR) are both associated with chronic gastritis, peptic ulcer and gastric cancer. The nature of their interrelationship remains unclear. H. pylori eradication has also been reported to result in new or worsening acid gastro-oesophageal reflux (GOR). The aim of this study was to investigate the relationship between GOR, DGR and H. pylori infection. METHOD: 25 patients with H. pylori gastritis underwent ambulatory 24-hour oesophageal and gastric pHmetry and gastric bilirubin monitoring before and 12 weeks after H. pylori eradication, confirmed by 14C urea breath testing (UBT). Ten healthy subjects served as a control group. RESULTS: There were no differences between patient and control groups for gastric alkaline exposure or gastric bilirubin exposure (P> 0.25 in all categories). Oesophageal acid reflux was higher in the study group (P< 0.02). No differences were detected in oesophageal acid reflux, gastric alkaline exposure, or gastric bilirubin exposure (P = 0.35, 0.18 and 0.11, respectively) before and after eradication. CONCLUSIONS: Acid GOR is not increased by H. pylori eradication. DGR in patients with H. pylori gastritis is similar to that in healthy, non-infected subjects. H. pylori eradication produces no change in GOR or DGR. In patients with chronic gastritis, H. pylori infection and DGR appear to be independent of each other.     

原发性十二指肠胃反流程度与胃黏膜炎性反应关系的研究

目的 分析原发性病理性十二指肠胃反流(DGR)患者胃黏膜病变、幽门螺杆菌(Hp)感染及胆汁反流变化以及相互间的关系.方法 对58例原发性病理性DGR患者进行24 h胃内胆汁监测,以反流时间百分23.60%为界,将患者分为高反流组(29例)和低反流组(29例).并行胃镜检查及胃黏膜活检.分析原发性病理性DGR患者胃黏膜炎性反应、Hp感染、胆汁反流间的关系.结果 高反流组及低反流组的Hp阳性率分别为20.7%(6/29)和48.3%(14/29),差异有统计学意义(P＜0.05).高反流组胃窦和胃角部黏膜肠上皮化生检出率高于低反流组(P＜0.05).胃窦、胃角部黏膜新悉尼系统病理积分Hp阳性组高于Hp阴性组(P＜0.05),高反流组高于低反流组(P＜0.05).Hp阳性组胆红素吸收值≥0.25的时间百分比低于Hp阴性组(P＜0.05),HP阳性组短时间反流频率、长时间反流频率、最长反流时间、吸收值最大值、平均值和中位值与Hp阴性组间差异无统计学意义(P＞0.05).Hp阳性组和阴性组胆红素吸收值≥0.25的时间百分比与胃窦、胃角部黏膜新悉尼系统病理积分均呈正相关(P＜0.05).结论 原发性病理性DGR导致胃窦黏膜损伤的主要因素可能为胆汁反流,胆汁反流可抑制HP在胃内定植,Hp感染可能与胆汁反流协同作用导致胃黏膜损伤.     

The role of cagA Helicobacter pylori strains in gastro-oesophageal reflux disease

BACKGROUND AND AIMS: The role of Helicobacter pylori infection in gastro-oesophageal reflux disease is controversial. The aim of this study was to evaluate the prevalence of colonization by cagA-positive and cagA-negative H. pylori strains in the spectrum of gastro-oesophageal reflux disease. METHODS: A total of 108 patients (50 male/58 female; mean age, 50.3 years) with dyspepsia and peptic ulcer or erosive gastritis/duodenitis were categorized into patients without reflux and patients with reflux oesophagitis graded from I to IV. All patients underwent upper endoscopy with biopsies of the antrum. H. pylori was detected by histology, urease test and polymerase chain reaction. The cagA status was diagnosed in the gastric biopsy by polymerase chain reaction. RESULTS: The overall prevalence of H. pylori colonization in patients with reflux was 68.6% and was 70.2% in those without oesophageal disease (P = 0.862). Colonization by cagA-positive strains was also not statistically different between the two groups (31.4% versus 40.4%, P = 0.332). However, patients with grades II-IV reflux oesophagitis were less colonized by the bacterium (36.4%) than patients with grade I oesophagitis (77.5%) (P = 0.009). H. pylori cagA-positive strains were also less likely to colonize the stomach of patients with grades II-IV oesophagitis (0%), than grade I reflux oesophagitis (40%) patients and controls (40.4%). CONCLUSIONS: Infection of the stomach by H. pylori and especially by H. pylori cagA strains may play a protective role against the development of the most severe forms of gastro-oesophageal reflux disease.     

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.     

北京地区消化性溃疡流行病学分析

目的:了解北京地区消化性溃疡(pepticulcer,PU)的发病特点及变化情况,以及幽门螺杆菌(Helicobacter pylori)与PU的关系,以便为PU的防治工作提供理论依据.方法:研究对象为1999-01-01/12-31在北京29家不同等级医院接受胃镜检查的患者.对其中经内镜下分期诊断为PU活动期及愈合期的患者采用问卷方式进行调查,调查内容主要包括PU患者的性别、年龄、血型、职业、生活习惯、服药情况以及H pylori感染情况.快速尿素酶试验、病理染色、~(13)C-尿素呼气试验和细菌培养检测H pylori感染,其中任一项检测阳性判断为H pylori感染.结果:采用回顾性研究方法,29家医院共有58546例北京地区患者接受了胃镜检查,PU检出率为13.83%.本次调查总共回收调查表3182份,DU:GU为2.81:1.PU检出率以40-60岁患者中检出率(41.2%)最高,GU比DU者平均年龄大6.4岁.不同血型构成比之间有显著性差异(P=0.006),其中以O型血最多,吸烟者明显高于非吸烟者(P=0.012).在1999年有2992例PU患者接受了H pylori感染检测,感染率为54.9%,不同类型PU间H pylori感染率无显著性差异(P=0.72).2042例患者在首次诊断PU时接受了H pylori感染检测,其中1660例(81.3%)H pylori检测阳性.经Logistic回归分析显示PU的复发主要与不规范治疗及H pylori感染密切相关结论:北京地区PU检出率呈下降趋势,患者首次诊断PU时H pylori感染率明显高于自然人群感染率,但1999年度H pylori感染的检出率较低.年龄、O型血、吸烟和H pylori感染是PU发病的危险因素,PU的复发主要与不规范治疗及H pylori感染密切相关.     

Low prevalence of Helicobacter pylori but high prevalence of cytomegalovirus-associated peptic ulcer disease in AIDS patients: Comparative study of symptomatic subjects evaluated by endoscopy and CD4 counts

BACKGROUND AND AIMS: The role of Helicobacter pylori infection in gastroduodenal lesions might be different between the general population and AIDS patients. The aim of the present study was to compare the prevalence of H. pylori and cytomegalovirus (CMV) infection in AIDS patients and HIV-negative controls. The impact of CD4 lymphocyte counts on H. pylori and CMV infection in the same subjects was also assessed. METHODS: One hundred and fifty-six patients (52 HIV-positive, 104 HIV-negative) with gastrointestinal symptoms were evaluated with upper gastrointestinal endoscopy and biopsy. Comparison of the prevalence of H. pylori and CMV infection was made by dividing AIDS patients into two groups: those with CD4 counts >100/mm3 and those with CD4 counts <100/mm3, and ulcer and non-ulcer patients. RESULTS: In comparison with HIV-negative controls, AIDS patients had a lower prevalence of H. pylori infection (P < 0.0001) but a higher prevalence of CMV infection (P < 0.0001). Cytomegalovirus infection was frequently found in AIDS patients with CD4 count <100/mm3, in comparison with those with a CD4 count >100/mm3. In AIDS patients, CMV was more frequently detected in subjects with peptic ulcers (P = 0.0125). Conversely, the prevalence of H. pylori infection in AIDS patients was not different between those with and without peptic ulcers. CONCLUSIONS: The low prevalence of H. pylori infection and peptic ulcer in AIDS patients suggests a different role of H. pylori infection in peptic ulcer or even a different mechanism of peptic ulcerogenesis in HIV-positive subjects. Cytomegalovirus, rather than H. pylori, may be the main causative pathogen of peptic ulcers in AIDS patients.