幽门螺杆菌感染与反流性食管炎的关系

目的探讨幽门螺杆菌（Hp）感染与反流性食管炎（RE）的关系。方法对在本院消化科就诊的患者行内镜下快速尿素酶测定却感染，观察比较却阴性组、却阳性组RE的发病率。对却阳性组中经胃镜及病理切片证实为消化性溃疡的患者，进行却根除治疗，3个月后复查胃镜比较抗却治疗前后RE发病率的变化。结果却阳性组RE发病率为5．28％，却阴性组RE发病率为7．59％，二者差异有统计学意义（P〈0．05）。抗却治疗前后RE发病率分别为10．7％、35．7％，二者差异有统计学意义（P〈0．05）。结论①却不是RE的病因；②抗坳治疗会导致RE发病率的升高。     

幽门螺杆菌感染与反流性食管炎的关系分析

目的:探讨幽门螺杆菌(Hp)感染与反流性食管炎(RE)的相关性。方法:回顾性总结分析胃镜检查确诊反流性食管炎患者97例,同时选取104例慢性胃炎患者为对照。所有病例采用14C呼气试验检测Hp感染。结果:97例反流性食管炎患者中Hp感染率为45.4%,而对照组63.5%(P<0.01);REA、B、C级患者HP阳性率分别为59.4%、42.0%、26.7%,但差异无统计学意义(P>0.05)。结论:Hp感染可能是反流性食管炎的保护因素。     

反流性食管炎与幽门螺杆菌感染的关系

反流性食管炎 (RE)是由于胃、十二指肠内容物反流至食管 ,引起食管粘膜损害所致的病症。幽门螺杆菌 (Hp)在许多胃、十二指肠疾病的发病中起着重要的作用 ,但RE与Hp的关系尚不明确[1] 。本文对Hp感染与RE的关系进行了探讨 ,以了解Hp在RE发生中的作用。1　材料与方法1 1　病例选择　 2 0 0 0年 1月～ 2 0 0 2年 12月在我院内镜室行胃镜检查 ,诊断为RE并做了Hp检测的患者12 2例 ,其中男 95例 ,女 2 7例 ,年龄 17～ 72岁 ,平均4 7.3± 15 .7岁。以下情况不纳入分析 :(1)发现其他上消化道疾病者 ,如溃疡、肿瘤 ;(2 )复查的病例及曾经有抗H…     

幽门螺杆菌与反流性食管炎的关系

幽门螺杆菌 (Hp)是慢性胃炎和上消化道溃疡的主要致病因子 ,与胃癌和胃粘膜相关组织淋巴瘤关系密切 ,但Hp与反流性食管炎 (RE)的关系尚存在争议。我们对Hp与RE的关系进行研究以探讨Hp在RE发病中的作用。对象与方法1.对象 ;经胃镜检查选取 5 6例RE患者 ,男性 3 4例 ,女性2 2例 ,年龄 2 1～ 67岁。健康对照组 48例 ,男性 2 8例 ,女性 2 0例 ,年龄 18～ 70岁。2 .方法 :所有患者均行胃镜检查 ,RE按洛杉矶分类法分为4级 ,Ⅰ级 :病灶局限于食管粘膜皱襞 ,直径 <0 .5cm ;Ⅱ级 :病灶局限于食管粘膜皱襞 ,互不融合 ,但直径 >0 .5cm ;Ⅲ级 :病…     

反流性食管炎与幽门螺杆菌感染的关系

目的:研究反流性食管炎(reflux esophagitis,RE)患者幽门螺杆菌(H pylori)感染率,感染程度与定植部位及胃炎的活动度,并对比H pylori阳性与阴性的RE患者食管炎症的严重程度.方法:选取从2007-01/03在我科行胃镜检查证实的RE患者89例,按年龄,性别进行配对的方式随机抽取无反流对照组89例,对比两组H pylori感染率,感染部位,感染程度的差异,并比较RE组中H ylori阳性与阴性患者食管炎症的严重程度.结果:RE组与对照组H pylori感染率无统计学差异(P=0.137),但RE组H pylori感染程度较对照组轻(P胃体=0.024,P胃窦=0.000),且RE组胃体炎症严重程度较对照组轻(P=0.001);H pylori阳性与阴性的RE患者发生洛杉矶(LA)C级分别占8.3%和1 8.5%,D级分别占4.2%和12.3%,但食管炎症的轻重程度无显著性差异(P=0.353).结论:H pylori的感染程度及胃体胃炎的活动性与RE的形成有负相关性.     

幽门螺杆菌与胃食管反流病

胃内幽门螺杆菌（Ｈｐ）感染与胃炎，消化性溃疡甚至胃癌的发生密切相关，近年发现Ｈｐ亦可存在于食管的化生柱状上皮中，研究Ｈｐ感染与胃食管反充病及其并发症（Ｂａｒｒｅｔｔ食管及食管腺癌）的发生，发展之间的关系对胃食反流病的合理治疗有重要的意义。     

幽门螺杆菌和反流性食管炎关系初探

近年来国外对幽门螺杆菌(Hp)和胃食管反流病     

反流性食管炎与幽门螺杆菌感染

反流性食管炎是由于胃、十二指肠内容物反流至食管,引起食管粘膜损害。酸性胃内容物反流至食管是产生反流性食管炎的重要机制。近年的研究发现反流性食管炎患者幽门螺杆菌（Ｈ ．ｐｙｌｏｒｉ）感染的发生率较低,其原因尚未完全阐明。本研究旨在探讨反流性食管炎与Ｈ．ｐｙｌｏｒｉ之间的关系。 材料与方法 一、样本资料 １９９９年１月～２０００年６月就诊于上海第二医科大学附属仁济医院内镜中心胃镜检查者,排除其他上消化道病变（消化性溃疡、糜烂性胃炎、上消化道肿瘤等）,发现反流性食管炎患者３８５例,男２４７例,女１３８例,…     

幽门螺杆菌与胃食管反流病

胃内幽门螺杆菌(Hp)感染与胃炎、消化性溃疡甚至胃癌的发生密切相关。近年发现Hp亦可存在于食管的化生柱状上皮中。研究Hp感染与胃食管反流病及其并发症(Barrett食管及食管腺癌)的发生、发展之间的关系对胃食管反流病的合理治疗有重要的意义。     

Male sex, hiatus hernia, and Helicobacter pylori infection associated with asymptomatic erosive esophagitis

Background and Aims: Asymptomatic erosive esophagitis (AEE) is an easily forgotten subgroup of gastroesophageal reflux disease due to its lack of warning symptoms, despite having the risk of developing complications, such as bleeding, stricture, or even esophageal adenocarcinoma. Methods: A total of 2843 potentially eligible patients were screened at the health management center of Buddhist Tzu Chi General Hospital. A total of 1001 patients responded to the survey and gave informed consent; 998 patients who completed the reflux disease diagnostic questionnaire were enrolled. Of them, 594 patients who had no reflux symptoms were included for final analysis. The presence and severity of erosive esophagitis was graded according to the Los Angeles classification. Active infection of Helicobacter pylori (H. pylori) was determined by the Campylo‐like organism (CLO) test during endoscopies. Results: A total of 14.5% (86/594) of asymptomatic patients had endoscopic findings of erosive esophagitis. In the univariate analysis, male sex and hiatus hernia were significantly associated with AEE. Positive CLO tests had a trend association. Based on the multivariate analysis, male sex (odds ratio [OR]: 2.32, 95% confidence interval [CI]: 1.35–3.98), hiatus hernia (OR: 4.48, 95% CI: 2.35–89.17), and positive CLO test (OR: 0.57, 95% CI: 0.34–0.95) were associated with AEE, as compared to the healthy controls. Conclusions: AEE is not a rare condition, and constitutes 14.5% of the asymptomatic population. Male sex, hiatus hernia, and H. pylori infection are factors associated with AEE. These findings are not only helpful in identifying such asymptomatic patients, but also provide information to improve understanding of the relationship between H. pylori infection, reflux symptoms, and erosive esophagitis.     

Helicobacter pylori eradication may induce de novo, but transient and mild, reflux esophagitis: Prospective endoscopic evaluation

Backgrounds and Aim:  The effect on reflux esophagitis of eradicating Helicobacter pylori is variable and not fully defined. We previously reported that in patients who have reflux esophagitis associated with duodenal ulcer, a significant improvement in the pre-existing reflux esophagitis occurred after H. pylori was eradicated. In the present study, we asked whether H. pylori eradication leads to de novo development of reflux esophagitis in peptic ulcer patients.
Methods:  Prospective post-eradication evaluations were conducted in 1195 H. pylori -positive patients with peptic ulcer diseases who were confirmed not to have reflux esophagitis by endoscopic examination before eradication therapy. After eradication therapy, endoscopy and a urea breath test were performed yearly.
Results:  A total of 1187 patients were followed for up to 10.0 years (a mean of 3.6 years). Reflux esophagitis developed in 279 of 1000 patients cured of infection and in 26 of 187 patients who had persistent infection ( P  < 0.0001, Fisher's exact test). The esophagitis was mild (Los Angeles grade A) in most patients, transient in approximately one-half, and rarely necessitated long-term medication for the condition. Cure of infection, alcohol consumption, younger age, and high body mass index were identified as significant factors for the risk of developing non-transient reflux esophagitis.
Conclusions:  Cure of H. pylori infection may increase the risk of developing reflux esophagitis in patients with peptic ulcer, but the esophagitis is mostly mild and transient, and long-term medication is rarely required. Thus, H. pylori eradication therapy need not be withheld for fear of provoking reflux esophagitis.     

Influence of Helicobacter pylori eradication on reflux esophagitis in Japanese patients

The relationship between Helicobacter pylori eradication and reflux esophagitis is controversial. We analyzed the development of reflux esophagitis and the change in the grade of pre-existing reflux esophagitis after eradication. Enrolled were 559 Japanese patients who received eradication therapy for H. pylori . The grade of reflux esophagitis by endoscopy before and after therapy was evaluated retrospectively. No esophagitis was present before eradication in 526 patients. H. pylori was and was not eradicated in 429 and 97, respectively. Reflux esophagitis developed in 40 of the eradication group and in three of the treatment failure group, with prevalence higher with successful eradication ( P  = 0.04). Successful eradication and hiatus hernia were significant risk factors for reflux esophagitis development. Twenty-seven of 33 patients with pre-existing reflux esophagitis had successful eradication and six treatment failure. The reflux esophagitis grade worsened in two (Los Angeles classification from A to B) and improved in 14 patients after eradication. With treatment failure, reflux esophagitis worsened in none and improved in three patients. There showed no significant change in the grade of pre-existing reflux esophagitis after H. pylori eradication but the sample size was too small to evaluate the difference. In conclusion, the eradication of H. pylori increases the prevalence of reflux esophagitis, and hiatus hernia was a significant risk factor for the development of reflux esophagitis.     

幽门螺杆菌与胃食管反流病

幽门螺杆菌（Helicobacter pylori，H．pylori）与胃食管反流病（gastroesophageal reflux disease，GERD）的关系各研究结果不尽一致，流行病学研究表明，在GERD中不仅Mpylori感染率较低，而且cagA的检出率也低，二者都与食管疾病严重程度呈负相关。亦有文献报告H．pylori感染与GERD发生无明显关系。H．pylori对食管保护作用机制可能与其能提高LES压力、降低胃内酸度和影响食管对酸的敏感性有关。有研究表明，H．pylori可以提高质子泵抑制剂的抑酸效果，亦有人认为H．pylori并不影响GERD疗效。因此H．pylori与GERD的关系仍需进一步的临床和基础研究来评价。     

Influence of Helicobacter pylori infection on the prevalence of reflux esophagitis in Japanese patients

BACKGROUND AND AIM: Reflux esophagitis is caused by esophageal motor dysfunction in patients with sufficient gastric acid secretion. Helicobacter pylori causes atrophic gastritis and influences gastric acid secretion. Hiatus hernia (HH) of the esophagus causes motor dysfunction in the lower esophagus. Therefore, this study aimed to test whether H. pylori infection, gastric mucosal atrophy and HH are predictive factors for reflux esophagitis. METHODS: Helicobacter pylori infection was examined in 781 patients by the measurement of serum immunoglobulin (Ig)G antibody, bacteriological culture and histological examination of biopsy specimens. The prevalence of HH, endoscopically identified gastric mucosal atrophy (closed- or open-type) and reflux esophagitis were investigated by reviewing endoscopic films. Investigated patients were divided into three age groups, under 49, 50-69, and over 70 years. The prevalence of esophagitis, H. pylori infection, gastric mucosal atrophy, and HH were compared to identify the possible predictive factors for reflux esophagitis by using logistic regression analysis. RESULTS: Sixty-nine patients with reflux esophagitis were found among the 781 investigated cases. The odds ratios of negative H. pylori infection, endoscopically identified closed-type gastric mucosal atrophy, and HH for the prevalence of reflux esophagitis were 1.342, 1.751 and 5.527, respectively. These results indicated that the presence of H. pylori infection was only a weak negative risk factor, and that HH was the most reliable endoscopic predictive factor for reflux esophagitis. CONCLUSION: Helicobacter pylori infection is a weak negative risk factor for the prevalence of reflux esophagitis, while HH is the most reliable predictive factor.     

Reflux esophagitis facilitates low Helicobacter pylori infection rate and gastric inflammation

BACKGROUND: Helicobacter pylori is regarded as an important pathogen in upper gastrointestinal diseases. However, little is known about the relationship between H. pylori infection and reflux esophagitis. Therefore, an investigation was undertaken in Korean subjects regarding the incidence of H. pylori infection, and a histopathological study of reflux esophagitis was also carried out. METHODS: Analysis of gastric biopsy specimens was conducted for 73 patients with reflux esophagitis and 132 control subjects without reflux esophagitis. The H. pylori infection was assessed by using rapid urease test and the immunohistochemical method, and gastric mucosal morphologic change was analyzed according to the updated Sydney system. RESULTS: The prevalence of H. pylori infection was significantly lower in patients with reflux esophagitis than in the non-reflux group. Grade of inflammation and glandular atrophy in the antrum and body were higher in patients in the non-reflux group compared with those in the reflux esophagitis group. CONCLUSIONS: It is suggested that H. pylori infection decreases the risk of reflux esophagitis by inducing atrophic gastritis.     

胃食管反流病与幽门螺杆菌感染的关系探讨

目的探讨胃食管反流病与幽门螺杆菌感染之间的相关性。方法将经过电子胃镜确诊的GERD患者120例及对照组轻度慢性浅表性胃炎患者120例予血清幽门螺杆菌抗体检测和14C呼气试验法进行H.pylori检测,对比两组H.pylori感染情况;将90例反流性食管炎患者分为LA-A、B组及LA-C、D组,对比两组H.pylori感染情况;将120例GERD患者分为轻度症状组、中度症状组、重度症状组及极重度症状组,比较组间H.pylori感染情况。结果 GERD组H.pylori感染的阳性率(39.17%)低于对照组H.pylori感染的阳性率(62.50%),差异有统计学意义(P<0.05)。LA-A、B组H.pylori感染的阳性率(60.87%)高于LA-C、D组H.pylori感染的阳性率(29.55%),差异有统计学意义(P<0.05)。轻度症状组、中度症状组、重度症状组及极重度症状组H.pylori感染的阳性率分别是40.00%、41.67%、40.63%、31.82%。结论幽门螺杆菌感染是反流性食管炎的保护因素,幽门螺杆菌感染与GERD症状的发生无相关性。     

Helicobacter pylori infection correlates with severity of reflux esophagitis: with manometry findings

The role of Helicobacter pylori infection in the development and exacerbation of reflux esophagitis was investigated. The prevalence of Helicobacter pylori infection, the severity of atrophic gastritis, and esophageal motility (determined by esophageal manometry by an infusion catheter method) were assessed in patients with mild (n = 46) and severe (n = 27) reflux esophagitis and subjects without reflux (n = 28). Compared with the prevalence of Helicobacter pylori infection in the non-reflux group, the prevalence in the mild and severe reflux groups (60.7%, 47.8%, and 14.8%, respectively) was significantly (P < 0.05) lower. Atrophic gastritis was milder in both reflux groups than in the non-reflux group. The degree of gastritis was also milder in the severe reflux group than in the mild reflux group. The esophageal sphincter pressure was significantly (P < 0.05) lower in the reflux groups than in the non-reflux group, and the amplitude of primary peristalsis was significantly (P < 0.05) lower in the severe reflux group than in the non-reflux group. There were no significant differences between reflux patients with and without Helicobacter pylori infection in the parameters of esophageal manometry. These data imply that a low prevalence of Helicobacter pylori infection may result in a milder grade of atrophic gastritis, and consequently, exacerbate reflux esophagitis. Received: July 21, 1998 / Accepted: April 28, 1999     

Helicobacter pylori infection and gastroesophageal reflux in children

Some studies suggest that Helicobacter pylori (H. pylori) infection would be a protective factor for the gastroesophageal reflux. The aim of this study was to explore this fact. A group of 72 children, admitted in a pediatric gastroenterology regional center in Northeast Romania, diagnosed with gastroesophageal reflux by 24‐hour continuous esophageal pH monitoring (results were interpreted using the Boix‐Ochoa score), underwent upper endoscopy with gastric biopsy to detect the presence of H. pylori by the rapid urease testing and for bacteriological and histologic examination. 19 children (26.39%) had H. pylori infection, while 53 (73.61%) did not. The grade of esophagitis was classified according to the Los Angeles classification system. Out of 47 children with esophagitis A, 16 (34.04%) had H. pylori infection, while out of the 25 children with esophagitis B, only 3 (12%) had H. pylori infection, with statistic significance (χ² = 54.69, P << 0.05, 95% confidence interval [CI]). Regarding the value of the Boix‐Ochoa score, it appears that the presence of the H. pylori determines lower pH‐metry scores (F = 8.13, P = 0.0015, 95% CI). The presence of the H. pylori was not an important factor in the gastroesophageal reflux. On the other hand its relationship with esophagitis appears to be inverse ratio. The fact that the H. pylori presence is statistically greater in the grade A esophagitis could confirm the hypothesis that the bacteria would slow down the development of the esophagitis.