幽门螺杆菌在胃食管反流病中的作用

幽门螺杆菌（H．pylori）是慢性胃炎和消化性溃疡的主要致病因素之一,胃食管反流病（GERD）则是常见的消化道动力障碍性疾病。近年有关H．pylori与GERD关系的研究较多,但分歧较大,本文就H．pylori在GERD中的作用及抗H.pylori治疗对GERD的影响作一综述。胃内H．pylori对GERD的影响GERD的发生与胃食管交界处抗反流屏障［主要是食管下括约肌（LES）功能］异常、食管清除功能异常、食管上皮防御功能减弱、胃内压力升高和胃排空障碍等多种因素有关。LES功能受神经支配,其反射弧的传入神经起源于胃底,胃内因素可能通过刺激传入…     

慢性浅表性胃炎根治幽门螺杆菌与胃食管反流病的关系研究

幽门螺杆菌（Helieobaeter pylori，H．pylori）是慢性胃炎和消化性溃疡的主要致病因素之一，胃食管反流病（gastroesophageal reflux disease，GERD）则是常见的上消化道动力障碍性疾病。H．pylori与胃食管反流病的关系是近年来研究的热点，本文对120例慢性浅表性胃炎患者进行H．pylori根治治疗，观察GERD发病率的变化，现报告如下。     

根除幽门螺杆菌与胃食管反流病的关系研究

目的探讨根除幽门螺杆菌（H．pylori）与胃食管反流病（GERD）的关系。方法本研究采用食管内24hpH监测的方法，定量观察H．pylori阳性GERD患者根除H．pylori和单用兰索拉唑治疗3月后食管酸暴露的变化，以及H．pylori阳性慢性浅表性胃炎（CSG）根除H．pylori和姑息治疗3月后食管酸暴露的变化。RE组：反流性食管炎（RE）表现患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组采用丽珠唯三联＋兰索拉唑方案，对照组单用兰索拉唑。CSG组：慢性浅表性胃炎（CSG）患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组均采用丽珠唯三联方案，对照组不采用药物治疗。以上两组待H．pylori根除后，对比研究H．pylori根除组和对照组3月后食管24hpH监测参数。结果RE组：H．pylori根除和单用兰索拉唑治疗3月后两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。CSG组：H．pylori根除和姑息治疗3月两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。结论GERD患者根除幽门螺杆菌后食管酸暴露无明显改变，CSG患者根除幽门螺杆菌后食管酸暴露无明显改变，H．pylori感染可能与GERD的转归和发生无关。     

幽门螺杆菌感染与Barrett''''s食管

Barrett’s食管是慢性胃食管反流致食管下段鳞状上皮损伤后被柱状上皮所替代的一种病理改变，也是食管腺癌的癌前病变。幽门螺杆菌（Helicobacter pylori，H．pylori）是上消化道的重要致病菌，其感染可导致胃十二指肠溃疡、非贲门部胃癌及胃黏膜相关淋巴组织（mucosa-associated lymphoidtissue，MALT）淋巴瘤。近十年来，随着H．trylori人群感染率降低，消化性溃疡和胃窦、胃体部肿瘤发病率呈下降趋势，而胃食管反流疾病（gastro-oesophageal reflux disease，GERD）、Barrett’8食管、食管下段腺癌的发病率呈上升势头。因此，H．pylori感染在Barrett’s食管发病及其发展为食管腺癌中的作用，也受到越来越多的关注。     

胃食管反流病与幽门螺杆菌及胃排空关系的研究

目的探讨幽门螺杆菌(H.pylori)与胃食管反流病(GERD)的关系,以及H.pylori对GERD患者胃动力的影响。方法按中华医学会的GERD诊断标准,确诊GERD患者200例,进行胃镜、胃排空时间及H.pylori检查,依据洛杉矶分级将反流性食管炎(RE)分为A、B、C、D四级,200例无消化道症状的健康体检者作为对照组,进行H.pylori检查。结果 GERD组的感染率明显低于对照组(P<0.05),反流性食管炎(RE)的炎症程度与H.pylori的感染率呈负相关,GERD患者中H.pylori阳性组和H.pylori阴性组间胃排空情况无统计学差异(P>0.05)。结论 H.pylori可能对GERD有潜在的保护作用;RE炎症程度越重,H.pylori感染率越低;H.pylori不影响GERD患者的胃动力。     

食管裂孔疝、胃食管阀瓣与胃食管反流病

胃食管反流病（GERD）是指胃内容物反流入食管,引起不适症状和（或）并发症的一种疾病。GERD患病率国内为5．77％,而国外为7％-15％（亦有高达20％以上者）。近年研究显示,食管裂孔疝（HH）及胃食管阀瓣（GEFV）与GERD发生密切相关。现将HH、GEFV与GERD的关系综述如下。     

胃食管反流病患者酸反流与食管运动功能障碍的关系

背景：异常酸反流和食管运动功能障碍与胃食管反流病（GERD）密切相关。目的：研究GERD患者的食管运动和酸反流与食管黏膜损害的关系，以及两者之间的相关性。方法：选取有反酸、烧心、胸痛等典型胃食管反流症状的患者72例行上消化道内镜检查、食管测压和24hpH监测。根据pH〈4总时间百分比〈4．5％且DeMeester计分〈14．7的标准。将食管炎患者分为生理性酸反流组（pH^-组）和病理性酸反流组（pH^＋组）。结果：内镜下食管炎组24hpH监测各项指标较无食管炎组显著增高（P〈0．05），病理性酸反流的发生率显著高于无食管炎组（P〈0．01）。两组食管测压各项指标无显著差异，食管炎组pH^＋者的食管下括约肌压力（LESP）较pH^-者显著降低，食管体部蠕动波传导速度减慢，湿咽成功率减少（P〈0．05）。结论：GERD患者食管炎的发生与酸反流密切相关，有病理性酸反流的GERD患者易见食管运动功能障碍。     

胃食管反流病临床诊断路径探讨

背景：关于胃食管反流病（GERD）的临床诊断路径,目前尚未达成共识。目的：探讨简便易行、可靠的GERD临床诊断路径。方法：对初诊时有反酸、烧心等症状者行反流性疾病问卷（ROQ）调查,分值≥8者行13C-尿素呼气试验和胃镜检查．并予递减法抑酸治疗或在根除幽门螺杆菌（H．pylori）感染的基础上行递减法治疗。16周后复行RDQ调查,并随访6个月以上。结果：共118例患者符合纳入标准。RDQ分值≥12、可诊断为GERD者86例（72．9％）,RDQ均值为19．08分．烧心症状的频率和程度均高于其他症状。RDQ分值≥12者内镜诊断为反流性食管炎（RE）且H．pylori阳性的概率为57．O％（49／86）．RDQ分值〈12者内镜下无RE表现且HpyNn阴性的可能性为37．5％（12,32）。RDQ分值≥12者16周递减法抑酸治疗的有效率为95．3％（82／86）,随访过程中31．4％（27／86）的患者仍需间断服用H2受体拈抗剂。结论：以RDQ量表初诊GERD有一定可行性,如与内镜检查和H．pylori检测联合应用,对GERD的处理更具指导意义。     

胃食管反流病与幽门螺杆菌感染的关系研究

目的:探讨胃食管反流病(GERD)与幽门螺杆菌感染(H.pylori)的关系。方法:将内镜检查确诊的112例GERD患者,按H.pylori检测结果分为H.pylori( )组和H.pylori(-)组,以内镜下食管炎的分级进行严重度比较。H.pylori( )组H.pylori根除后与H.pylori(-)组在半年、1年后进行复发率的比较。结果:H.pylori( )组和H.pylori(-)组GERD重度检出率分别为36.8%(7/19)和63.2%(12/19),差异有显著性。H.pylori( )GERD患者H.pylori根除后半年、1年食管炎总复发率为70.5%与H.pylori(-)组GERD47.0%比较差异有显著性。结论:H.pylori(-)者GERD重,H.pylori( )GERD患者H.pylori根除后1年食管炎复发率较高,H.pylori对GERD可能有保护作用。     

莫沙必利治疗胃食管反流病的随机、双盲、安慰剂交叉对照研究

目前对促胃肠动力药莫沙必利改善中国汉族胃食管反流病（GERD）患者胃食管反流症状和食管运动障碍的作用尚缺乏系统观察。目的：观察莫沙必利对中国汉族人群中GERD患者的治疗作用。方法：采用随机、双盲、安慰剂交叉对照研究设计，选取有典型胃食管反流症状的GERD患者23例行胃食管反流症状评估、食管测压以及24h食管DH和胆红素联合监测，对比研究莫沙必利和安慰剂各1周交叉治疗对胃食管反流症状的改善情况，以及对食管运动功能和胃食管反流事件的影响。结果：与安慰剂治疗相比，莫沙必利治疗可降低胃食管反流总症状积分，加快食管体部蠕动波传导速度，增加湿咽成功率，减少食管下端pH〈4总反流次数和长时间（≥5min）反流次数，降低pH〈4总时间百分比和DeMeester计分，降低食管下端胆汁反流总时间百分比，差异均有统计学意义（P〈0．05）。结论：莫沙必利治疗1周可有效改善本组中国汉族GERD患者的胃食管反流症状，部分改善食管运动障碍以及酸反流和胆汁反流．是治疗GERD安全、有效的药物。     

质子泵抑制剂的不良反应及其新型制剂

目前,质子泵抑制剂（PPIs）在治疗消化性溃疡（PU）、胃食管反流病（GERD）、幽门螺杆菌（H.pylori）感染、上消化道出血和其他酸相关疾病中占有重要地位。但由于PPIs半衰期短,代谢受细胞色素P450（CYP450）系统影响,导致其在临床应用中存在一定的缺陷和不足。目前,一些新型PPIs制剂正处于研发和临床试验中,可望在不远的将来进入临床应用。     

亚太地区胃食管反流病的特点

亚太地区胃食管反流病（GERD）的患病率呈升高态势。第六届上海国际胃肠病学会议上,来自亚洲、欧洲及澳洲的学者就亚太地区GERD的临床表现、流行病学和诊治现状进行了阐述,交流了中国大陆地区GERD的患病情况,如何处理GERD与幽门螺杆菌（H．pylori）感染、胃癌、消化性溃疡的共患病现象,以及在基于症状的GERD诊治中应当顾及到的问题等。     

Motion--Helicobacter pylori causes or worsens GERD: arguments against the motion.

Data from large epidemiological studies show that Helicobacter pylori is less prevalent in patients with gastroesophageal reflux disease (GERD) than in control subjects. The more virulent cagA-positive strains of the organism are also less commonly seen in patients with erosive esophagitis and in those with Barrett's esophagus than in those with less severe forms of GERD. Although the relationship between H pylori and gastric physiology is complex, the organism has little effect on acid secretion in most North American or Western European subjects, and has a net suppressive effect, especially in elderly subjects, in other parts of the world. Thus, the organism has a potential protective effect against GERD, which is exacerbated by gastric acidity. H pylori has no proven effect on other gastric factors that might provoke reflux, including delayed gastric emptying or inappropriate relaxation of the gastric fundus. Two well-designed interventional studies have found that eradication of H pylori either provoked GERD or had no effect. A third smaller study, which seemed to demonstrate that persistent infection was associated with GERD, was flawed, in that the two treatment groups were not comparable. The evidence thus does not support the idea that H pylori infection provokes or aggravates GERD.     

Tolerance to H2 receptor antagonist correlates well with the decline in efficacy against gastroesophageal reflux in patients with gastroesophageal reflux disease

BACKGROUND AND AIM: The attenuated antisecretory activity of H2 receptor antagonists (H2RA) during continuous administration is known as the tolerance phenomenon. The authors recently clarified that presence or absence of Helicobacter pylori infection influences the occurrence of the tolerance phenomenon. The aim of this study was to clarify whether tolerance to H2RA is correlated with attenuation of the inhibitory effect against gastroesophageal acid reflux in patients with gastroesophageal reflux disease (GERD). METHODS: Ten male patients with GERD symptoms and abnormal gastroesophageal reflux were investigated by pH monitoring on days 1 and 15 of continuous oral famotidine administration at 20 mg twice daily, and H. pylori infection was examined using the urea breath test. RESULTS: Intragastric and intraesophageal acidity were significantly decreased on the first day of famotidine administration, but then increased during the 15-day administration period in seven patients who were negative for H. pylori. In contrast, the efficacy of famotidine against gastric acid secretion and gastroesophageal acid reflux was not attenuated in three H. pylori-positive patients. The changes in GERD symptoms were correlated with the change in the degree of gastroesophageal reflux. CONCLUSION: The presence or absence of tolerance to H2RA during 15-day administration is correlated with the efficacy for inhibition of gastroesophageal acid reflux.     

GERD and H. pylori: is there a link?

The incidence of gastroesophageal reflux disease (GERD) and esophageal adenocarcinoma have increased in recent years as the incidence of peptic ulcer disease and distal gastric cancer have declined. Given the simultaneous decline in Helicobacter pylori infection, it is tempting to propose a relationship between H. pylori infection and these opposing time trends. Although H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from developing GERD and its complications. The most likely mechanism in which H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.     

The possible role of Helicobacter pylori in GERD

A variety of abnormalities contribute to the development of gastroesophageal reflux disease (GERD) including transient lower esophageal sphincter relaxation, low esophageal sphincter pressure, presence of a hiatal hernia, diminished esophageal clearance of refluxed gastric contents, and alterations in esophageal mucosal resistance. Helicobacter pylori infection clearly plays a role in the pathogenesis of peptic ulcer disease and mucosa associated lymphoma of the stomach and is a definite risk factor for distal gastric cancer. The role of H. pylori infection in GERD remains controversial and incompletely understood. Although H. pylori infection does not cause reflux disease, circumstantial evidence suggests that it may protect against the development of GERD and its complications in some patients. The most likely mechanism whereby H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.     

Helicobacter pylori and gastroesophageal reflux disease.

OBJECTIVES: 1. To determine the prevalence of Helicobacter pylori (H. pylori) infection in patients with gastroesophageal reflux disease (GERD), and to compare it with that in a control group. 2. To study the percentage of H. pylori-positive GERD patients according to different grades of esophagitis. MATERIAL AND METHODS: H. pylori prevalence by serological tests was compared among 692 patients with GERD and 200 healthy volunteer controls. Subsequently, the percentage of H. pylori was analyzed in the different grades of esophagitis, according to the Savary-Miller classification. RESULTS: no differences between the GERD group and control group were detected regarding age (50.5+/-14.7 vs 50.7+/-16.4 years, ns) and sex (63 vs 66% of men, ns); on the other hand the prevalence of H. pylori was 40% in the GERD group facing 66% in the control group, p <0.01. There were no differences in H. pylori prevalence according to the different grades of esophagitis, but logistical regression analysis showed that the absence of H. pylori infection was associated with the presence of grade IV esophagitis. CONCLUSIONS: the prevalence of H. pylori infection in GERD patients is lower than that of the general population, and its absence is associated with more severe grades of the disease. These results indicate that H. pylori plays a protective role against GERD.     

胃食管反流病与幽门螺杆菌感染的关系探讨

为了探讨胃食管反流病(GERD)与幽门螺杆菌(Helicobacter pylori, H.pylori)感染的关系,我们将经过电子胃镜确诊的GERD患者115例及对照组轻度慢性浅表性胃炎患者90例予活检胃窦组织快速尿素酶法及14C呼气试验法进行H.pylori检测,对比两组H.pylori感染情况.结果 显示:115例GERD组H.pylori感染率为37.39%,90例对照组H.pylori感染率为62.22%,GERD组H.pylori感染率明显低于对照组,有显著性差异(P＜0.01).     

中国华东地区人群胃癌癌前病变发病相关危险因素分析

目的探讨各种危险因素与中国华东地区人群胃癌癌前病变发病风险的关系,为胃癌癌前病变的个体化预防提供科学依据。方法收集中国华东地区胃癌癌前病变501例,浅表性胃炎523例;对两组多种危险因素进行描述性对比分析。结果与浅表性胃炎组比较,胃癌癌前病变组中的H.pylori感染、食管癌家族史、胃癌家族史、慢性萎缩性胃炎家族史、家族性腺瘤性息肉病、慢性萎缩性胃炎个人史、胃溃疡个人史、阿司匹林等非甾体抗炎药的使用、胃食管反流病、饮酒、亚硝基化合物饮食、不吃早餐三餐不定时、经常食用烟熏炙烤肉类食品、经常食用煎炸食品、经常食用辛辣食品、焦虑及抑郁的构成比,差异有统计学意义(P0.05)。与胃癌癌前病变相关的危险因素分析依次是慢性萎缩性胃炎个人史、家族性腺瘤性息肉病、胃癌家族史、阿司匹林等非甾体抗炎药的使用、经常食用辛辣食品、H.pylori感染、家族食管癌史、饮酒、焦虑、胃溃疡个人史、胃食管反流病、慢性萎缩性胃炎家族史。结论对于中国华东地区来说,慢性萎缩性胃炎个人史是胃癌癌前病变最突出的危险因素,其次为家族性腺瘤性息肉病和胃癌家族史。