幽门螺杆菌感染与残胃病变关系的研究

目的：通过检测残胃黏膜幽门螺杆菌（Hp)感染，探讨Hp与残胃病变的关系，方法：对163例因溃疡病行胃大部切术后的残胃行胃镜，病理检查和Hp检测，以同期163例非残胃病变为对照组，进行Hp感染率的比较。结果：（1）残胃组与对照组Hp检出率分别为27．61％，62．14％（P＜0．01），（2）Billroth-I式，Billroth-Ⅱ式和Roux-en=-Y重建术残胃胆汁反流发生率分别为18．75％，61．2％和10．0％，前两者比较和后两者比较差异均有非常显著意义（P＜0．01），上述3种术式的Hp感染率分别为46．1％，29．4％，39．0％，前两者比较差异有显著意义（P＜0．05）。（3）术后6个月－5年，－10年，－20年，＞20年者Hp检出率分别为30．1％，24．3％，7．1％，0；前两个年限与后两个年限比较差异有非常显著意义（P＜0．01）。（4）不同年龄组Hp感染不尽相同，40岁以下组为55％，41－69岁组为42％，70岁以上组为26％，前两者与后者比较差异有显著意义（P＜0．05）。（5）残胃黏膜异型增生Hp感染率为57．1％，对照组异型增生Hp感染率为61．5％，两者比较差异无显著意义（P＞0．05），结论：Hp感染是残胃炎发生的重要病因。Billroth-Ⅱ式较Birroth-I式的胆汁反流率,颃是伴有胆汁反流者的Hp感染率却较低，胃大部切除术后年限越长，Hp感染率越低，年龄越大，Hp 感染越少，残胃黏膜异型增生是Hp感染及其它因素综合作用的结果，根治Hp有重要意义。     

2012~2014年邢台地区上消化道出血临床特征分析

【目的】探讨2012~2014年邢台地区上消化道出血（UGIH）的临床特征。【方法】回顾性分析2012~2014年本院消化科收治的243例UGIH患者临床资料,分析UGIH的二般资料、病因构成和影响因素。【结果】①一般资料：uGlH平均患病年龄（60．0±14．5）岁,高峰年龄为60～69岁,男女比例为2．2：1,男性发病年龄明显低于女性（P〈0．01）。②UGIH常见病因依次为：消化性溃疡、食管胃底静脉曲张、急性胃黏膜病变和胃癌。③临床特征：中、老年组女性所占比例显著高于青年组（P=0．019）;合并心脑血管疾病史者占36．2％,长期服用非类固醇类抗炎药（NSAIDs）和抗血栓药物者占42．8％,植入血管支架者占11．1％,合并HP感染占26．3％,有86．8％的患者存在不同程度贫血,有66．7％的患者存在失血相关症状,青年组症状发生率显著高于中、老年组（P=0．024）;青、中年组消化性溃疡所占比例均高于老年组（P=0．013）。④口服NSAIDs者消化性溃疡占66．0％,急性胃黏膜病变占18．1％,其中,急性胃黏膜病变所占比例高于无服药史的6．5％（P=0．006）。【结论】UGIH常见病因依次为消化性溃疡、食管胃底静脉曲张、急性胃黏膜病变和胃癌;UGIH患者以老年男性多见,但青年患者更易出现临床症状;口服NSAIDs增加急性胃黏膜病变所致的UGIH。     

糖尿病合并消化性溃疡62例临床分析

目的探讨糖尿病（diabetes mellins,DM）合并消化性溃疡（peptic alcer,PU）与非糖尿病性消化性溃疡的胃镜特点、临床症状、幽门螺杆菌（Hp）感染率及根除率的区别。方法 DM合并PU 62例为观察组;同期非糖尿病性PU 74例为对照组。两组均行胃镜及Hp检查,分析其胃镜特点、Hp感染率、临床症状。Hp阳性者予以常规三联疗法（泮托拉唑40 mg bid,阿莫西林1000 mg bid,克拉霉素500 mg bid）,4周后复查14C-尿素呼气试验,比较两组Hp根除率差异。结果两组胃镜特点、临床症状、Hp感染率及Hp根除率差异均有统计学意义（P〈0.05）。结论 DM合并PU患者临床症状、溃疡发生部位与非糖尿病性消化性溃疡患者均有所区别,对糖尿病患者可常规做胃镜检查,并对Hp感染患者适当延长治疗时间,以提高Hp根除率。     

肝硬化门静脉高压性胃病患者幽门螺杆菌感染的临床研究

目的探讨肝硬化门静脉高压性胃病患者幽门螺杆菌（Helicobacterpylori,Hp）感染的临床特点。方法对2000年1月-2010年12月收治的51例确诊肝硬化并已行胃镜检查、Hp快速尿素酶试验的住院患者的Hp感染状况及相关因素进行回顾性研究。结果肝硬化门静脉高压性胃病患者Hp感染率为：4l.2％;Hp感染与年龄无关（P〉0．05）;Hp感染率随食管静脉曲张加重、肝功能恶化而降低（P〈O．05）;而与门静脉高压性胃病的发生（包括胃黏膜糜烂及溃疡）无关（P〈O．01）。结论肝硬化门静脉高压性胃病的发生与Hp感染无关。对有Hp感染的肝硬化门静脉高压性胃病患者无需常规行Hp根除治疗。     

雷尼替丁、硫糖铝、呋喃唑酮治疗消化性溃疡66例疗效观察

1997年1月-1998年1月，收治66例幽门螺杆菌（Hp）阳性的消化性溃疡患者，采用不同药物治疗进行临床观察，以探讨治疗消化性溃疡的有效方法。1临床资料1．1病例选择符合下列条件：①年龄18－60岁；②中上腹部胀痛、烧灼感、隐病或空腹痛1月以上；③胃镜证实胃、十二指肠溃疡，溃疡直径≥5mm，深度清晰可见；④Hp检测阳性；⑤以下患者除外：妊娠、哺乳妇女，合并幽门狭窄、胃癌、活动性出血、服用非皮质类固醇抗炎药和已抗Hp治疗者。66例随机分为AB两组。A组：33例，男29例，女4例；年龄20－54岁，平均39．8岁。胃溃疡5例，十二指肠溃疡24…     

三联疗法治疗十二指肠溃疡临床分析

目的观察应用三联疗法对幽门螺杆菌（Hp）相关性十二指肠溃疡（Du）的愈合和复发的影响。方法对胃镜确诊的两组Du患者分别用两种方法治疗4周后作胃镜检查，观察溃疡的愈合和Hp清除情况；1年后再次复查两组溃疡的复发率和再感染率。结果雷贝拉唑、甲硝唑、羟氨苄青霉素组成的三联疗法治疗4w后Du的愈合与雷贝拉唑组差异无统计学意义（P〉0．05），但Hp的根除率差异有统计学意义（P〈0．01）；1年后分别进行胃镜复查，雷贝拉唑组的溃疡复发与Hp的再感染明显高于三联疗法组。结论三联疗法治疗Hp相关性Du的治愈率和根除率高，不易复发，临床上值得进一步推广。     

残胃患者泌酸功能的检测分析

目的：研究胃远端部分切除术后患者泌酸功能及其与黏膜病理改变、胆汁反流和幽门螺杆菌（Hp）感染的相关性。方法：采用24hpH监测仪测定51例残胃患者空腹胃内pH值，根据24h胃内平均pH值分为低泌酸组（pH≥3）和正常泌酸组（pH〈3）。胃镜观察残胃黏膜以及Hp检测。结果：低泌酸组患者35例，其中29例黏膜呈重度萎缩；正常泌酸组16例，其中4例呈重度黏膜炎症（P=0．006）。胆汁反流率在低泌酸组和正常泌酸组分别为37．4％和18．7％（P=0．014）。两组间Hp感染率无明显差异。62．7％的患者胃酸分泌减少，但却接受抑酸药物治疗。结论：24h动态胃pH监测可有效评价残胃患者胃黏膜泌酸功能。胆汁反流和残胃炎程度与黏膜泌酸功能有明显相关性。约1／3残胃患者保持正常冒酸分泌功能，临床卜有大量患者接詈了不必要的抑酪治疗．     

老年消化性溃疡的临床特征分析

【目的】探讨老年消化性溃疡患者的临床表现及胃镜特点。【方法】将428例内镜确诊为消化性溃疡患者按年龄分为老年组和中青年组比较其临床特征。【结果】与中青年组相比较老年人消化性溃疡以胃溃疡多见，其所占比例分别为40．57％、12．19％。老年消化性溃疡组临床症状常不典型，与中青年组对比癌变的并发症发生率高（分别为6．60％和1．88％），且差异有显著性（P〈0．01），而出血、穿孔并发症的出现与中青年组比较也有显著差异（P〈0．01），幽门梗阻并发症的出现差异无显著性（P〉0．05）。【结论】及早进行内镜检查，有助于提高老年消化性溃疡的检出率，及早发现癌前病变，减少出血、穿孔、幽门梗阻等并发症的出现。     

上消化道出血病因及发病趋势分析

目的：探讨近10年来上消化道出血（upper gastrointestinal bleeding，UGB）的病因构成、发病趋势及与几个相关因素的关系。方法：对我院1993、1998和2003年间经内镜检查的UGB住院病人的临床资料进行统计分析。结果：（1）共检出UGB 2347例，1993年580例、1998年646例、2003年1121例。（2）消化性溃疡、急性胃粘膜病变、胃癌为UGB常见病因，分别占27．8％、21．1％、9．4％。（3）1993、1998和2003年三个年份中，急性胃粘膜病变分别占该年份UGB的24．3％、23．8％、17．9％；胃溃疡分别占8．3％、7．3％、4．5％；胃癌分别占6．0％、7．7％、12．0％；十二指肠溃疡分别占13．1％、19．8％、27．0％。（4）男性患者明显多于女性，男女之比为2．11：1。（5）随着年龄的增长，UGB的发病例数增加。（6）冬春两季的发病例数明显多于夏秋两季。结论：消化性溃疡是UGB的主要原因，其次是急性胃粘膜病变、胃癌。急性胃粘膜病变、胃溃疡的发病构成比呈下降趋势，差异有统计学意义（P〈0．01），胃癌、十二指肠溃疡的发病构成比呈上升趋势，差异有统计学意义（P=0．000）。UGB的病因分布与性别、年龄、季节、年代变化等因素相关。     

天津地区消化性溃疡的流行病学分析

目的：了解天津地区消化性溃疡的发病特点,以便有效预防其发生。方法：对2000年1月-2007年12月在天津市南开医院内科胃镜室就诊的12217例患者进行回顾性调查,了解胃溃疡及十二指肠溃疡（DU）患者的胃镜检出率、幽门螺杆菌（Hp）感染率、发病年龄、性别构成比、发病季节等。结果：12217例患者中共检出消化性溃疡2081例,总检出率为17.03%,其中DU1748例,检出率为14.31%,胃溃疡333例,检出率为2.72%。DU患者明显多于胃溃疡患者,DU：胃溃疡=5.25：1。2081例消化性溃疡患者中Hp阳性者1085例,总Hp感染率为52.14%。其中2000-2005年的Hp感染率为58.99%,2006-2007年的Hp感染率为41.81%,两组比较差异有统计学意义（P〈0.01）。DU患者Hp感染率为53.78%,胃溃疡患者Hp感染率为43.54%,两组比较差异有统计学意义（P〈0.01）。2081例消化性溃疡患者中男1471例,女610例,男：女=2.41：1。其中DU患者中男1231例,女517例,男：女=2.38：1。胃溃疡患者中男240例,女93例,男：女=2.58：1,两组比较差异无统计学意义（P（0.05）。DU患者年龄（50±15）岁,胃溃疡患者年龄（55±14）岁。2组患者40～59岁年龄组占总人数的49.3%。消化性溃疡以11-12月及3-4月高发,5-8月发病率较低,尤其6月份发病率最低,仅占6.15%。结论：天津地区DU患者多于胃溃疡患者,男性患者仍是消化性溃疡的主要患病人群,应对老年及女性患者、Hp阴性患者给予足够重视。     

Position of NSAIDs in causal factors of peptic ulcer

The cause of peptic ulcer is classified into five categories; infectious, drug-induced, hyperacidic, secondary, and idiopathic. Among these factors, H. pylori infection and non-steroidal anti-inflammatory drugs including aspirin (NSAIDs) are most important for development of gastroduodenal ulcer. More than 95 percent of gastroduodenal ulcers are associated with H. pylori or NSAIDs. Therefore, the frequency of non-H. pylori non-NSAIDs ulcer is very low. NSAIDs have the effect to inhibit synthesis of cyclooxygenase-1 (COX 1) and COX-2. This inhibitory action induces analgesic and anti-inflammatory effects. On the other hand, inhibitory action for COX-1 reduces the production of prostaglandin that is related to protective effect for gastrointestinal mucosa. Its mechanism is able to induce gastroduodenal ulcer. Since the elderly population in Japan is rising, the number of patients who need NSAIDs treatment is expected to increase in near future.     

Pathologic condition and prognosis of NSAids ulcer

Recently, H. pylori infection rate has decreased and non-steroidal anti-inflammatory drugs(NSAIDs including aspirin) induced ulcers have increased more and more with aging in Japan. Pathological and clinical conditions of NSAIDs ulcer are different from that of H. pylori-related peptic ulcer. In other words, main pathologic condition of NSAIDs ulcer is not only gastric acid secretion but also destruction of defense mechanisms of upper gastrointestinal mucosa, because NSAIDs inhibit both cyclooxygenase (COX)-1 and COX-2 which block production of prostaglandins, consequently resulting in impairing gastroduodenal protective factors. Moreover, it is not rare that NSAIDs ulcer has serious complications such as bleeding and/or perforation. These should be paid attention in NSAIDs users in routine practice.     

Trends in peptic ulcer pharmacotherapy

Considering the diseases of the stomach and duodenum, peptic ulcer has been the one with a significant clinical impact. The pathophysiology of peptic ulcer has centred on an imbalance between aggressive and protective factors. The discovery of Helicobacter pylori as a cause of peptic ulcer has changed our approach greatly towards this disease. Despite the decreasing frequency of H. pylori-induced peptic ulcers, peptic ulcer remains a major clinical problem partly because nonsteroidal anti-inflammatory drug (NSAID)-related ulcers and hospital admissions for ulcer complications associated with NSAIDs have increased in frequency. The interaction between H. pylori and NSAIDs is one of the most controversial issues in peptic ulcer. In this article, current concepts of peptic ulcer etiopathogenesis and the management of peptic ulcer according to the etiology were reviewed.     

Clinical features and diagnosis of non-steroidal anti-inflammatory drugs induced ulcers of the stomach

Helicobacter pylori (H. pylori) infection and non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin induce serious gastrointestinal ulcer and bleeding. Also both H. pylori infection and NSAIDs or aspirin use independently and significantly increase the risk of peptic ulcer and its complications. Interestingly, it has been reported that no evidence exists that reducing the dose or using modified release formulations such as enteric-coated of aspirin would reduce the incidence of ulcer bleeding. Selective COX-2 inhibitors use shows a low relative risk of ulcer bleeding than NSAIDs. However, when combined with aspirin, the differences between selective COX-2 inhibitors and NSAIDs tend to disappear. NSAIDs/aspirin dominantly develops multiple ulcers from the angulus to the antrum regardless of H. pylori infection. In contrast, the irregular shape of ulcer is more frequently detected in patients taking NSAIDs in comparison with H. pylori-associated ulcer, but the association was not seen in cases taking aspirin. This result indicates that the mechanism of ulcer formation may be different between NSAIDs and aspirin.     

Ulcers and gastritis

This article reviews recently published literature regarding ulcers and gastritis. Although endoscopy is the most useful procedure for diagnosis in the upper gastrointestinal tract, complications do occur, and procedure-related costs are significant. The appropriate indication for endoscopy has recently been debated. Helicobacter pylori is known to be an important pathogen involved in gastric and duodenal inflammation. Peptic ulcer disease and severe gastric mucosal injury are caused by virulent strains, and many reports have focused on CagA. Follow-up studies on surveillance endoscopy in patients with peptic ulcer or gastritis report that patients with atrophic gastritis and intestinal metaplasia are at significantly higher risk for gastric cancer. H. pylori eradication sometimes causes gastroduodenal erosion and reflux esophagitis, and the mechanisms involved have been revealed. Proton-pump inhibitors are useful in the treatment of ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs), reflux esophagitis, and for preventing rebleeding after endoscopic hemostasis, but the effect of long-term acid suppression on the gastric mucosa is still a matter of debate. H. pylori infection and NSAID intake are both risk factors for peptic ulcer disease, and are important aspects in this field.     

Pathogenesis of gastric and duodenal ulcer in the elderly

In the elderly, H. pylori infection and nonsteroidal anti-inflammatory drug(NSAID) use are most important risk factors for peptic ulcer disease. It is now recognized that, in patients with H. pylori infection, nonatrophic antral-predominant gastritis results in increased acid secretion, which is seen in duodenal ulcer patients, whereas corpus-predominant gastritis and pangastritis result in decreased acid secretion, that are seen in patients with proximal gastric ulcer and gastric cancer. These physiological changes are considered to be related to disease outcome. On the other hand, NSAIDs induced gastrointestinal toxicity is primarily due to the inhibition of mucosal prostaglandin synthesis in the gastric mucosa, which subsequently impairs the gastric cytoprotective factors. These two factors may independently, or even synergistically, cause the development of peptic ulcer disease in the elderly.     

Peptic ulcer and dyspepsia

Peptic ulcers are defects in the gastrointestinal mucosa that extend through the muscularis mucosae. They persist as a function of the acid or peptic activity in gastric juice. Twenty years ago, most ulcers were considered idiopathic; but a revolution in knowledge has occurred, so that it is now understood that the great majority of ulcers results from infection with Helicobacter pylori (HP) or use of nonsteroidal anti-inflammatory drugs (NSAIDs). Before this revolution, peptic ulcer disease was a common public health problem, responsible for considerable morbidity, some mortality, and high economic cost. Today, the overall prevalence of ulcers is falling, but complication rates remain relatively stable. These complex trends primarily reflect 3 factors: the rapid decline in the prevalence of HP in the population of developed countries, an increase in consumption of NSAIDs, and change in rates of smoking. Peptic ulcer prevalence is falling in younger individuals because of decreased prevalence of HP, whereas complications are rising in older subjects, largely as the result of increased NSAID use.     

NSAIDs相关性消化性溃疡出血与非NSAIDs消化性溃疡出血的临床对照研究

目的探讨非甾体类抗炎药(NSAIDs)相关性溃疡出血与非NSAIDs消化性溃疡出血的差异。方法通过临床对照研究,比较46例NSAIDs相关性溃疡出血与88例非NSAIDs消化性溃疡出血的临床资料。结果 NSAIDs组年龄显著高于非NSAIDs组,女性患者比率高于非NSAIDs组;NSAIDs组具有心脑血管和/或风湿免疫性疾病的患者多于非NSAIDs组,而既往具有消化性溃疡病史的患者低于非NSAIDs组;NSAIDs组上腹痛症状显著低于非NSAIDs组;NSAIDs组发病时血糖高于非NSAIDs组;NSAIDs组胃溃疡比率显著高于非NSAIDs组。以上差异均有统计学意义(P<0.05)。结论 NSAIDs相关性溃疡出血发病年龄、性别、临床表现及溃疡的发生部位与非NSAIDs溃疡患者均有差异,熟悉NSAIDs相关性溃疡出血的特点有利于临床诊治。     

Current state and measures of NSAIDs induced ulcer

In recent years, the incidence of Helicobacter pylori (H. pylori) infection has been decreasing and the incidence of peptic ulcer and bleeding ulcer induced by NSAIDs, especially low-dose aspirin (LDA), have been increasing. PPI and PG are useful for treatment and prevention of ulcers in patients receiving continuous administration of NSAIDs and/or LDA. H. pylori eradication is effective if performed before the start of NSAIDs administration, but a beneficial effect of H. pylori eradication performed during NSAIDs treatment cannot be expected. The incidence of ulcers is lower when administering COX-2-selective inhibitor than when administering non-selective NSAIDs, but attention must be given to cardiovascular events as side effects when administering COX-2-selective inhibitor.     

1382例上消化道出血病因及相关因素分析

目的：探讨上消化道出血（UGB）的病因及相关因素。方法：回顾性分析本院1994年1月－2003年12月1382例UGB住院病人的临床资料。结果：消化性溃疡、胃癌、急性胃粘膜病变（AGML）为UGB的常见病因．分别占33．o％,18．8％和17．6％;上消化道重度出血率以食管静脉曲张最高（50．0％）;冬春季节高于夏秋季节;男性发病高于女性;不同性别、年龄者出血病因不尽相同。结论：上消化道出血病人尽快行内镜检查确诊病因,以指导治疗。若能重视卫生宣教工作,可降低UGB发病率。