幽门螺杆菌感染与反流性食管炎相关关系分析

[目的]探讨幽门螺杆菌感染与反流性食管炎的相关关系。[方法]将经电子胃镜检查确诊为反流性食管炎患者90例(反流性食管炎组)及慢性胃炎患者100例(慢性胃炎组),同时经13 C尿素呼气试验法进行幽门螺杆菌检测,对比2组幽门螺杆菌感染情况。将反流性食管炎组患者根据内镜分级标准分为4级,比较各级间的幽门螺杆菌感染情况;根据临床症状程度分为轻、中、重度,比较各程度间的幽门螺杆菌感染情况。[结果]反流性食管炎组幽门螺杆菌感染率(36.7%)明显低于慢性胃炎组(65.0%),差异有统计学意义(P0.01)。反流性食管炎组不同内镜分级及不同临床症状程度者间的幽门螺杆菌感染率比较,差异均无统计学意义(P0.05)。[结论]幽门螺杆菌感染可能在反流性食管炎的发生过程中起保护作用,幽门螺杆菌与反流性食管炎及患者症状程度无相关性。     

北京地区反流性食管炎患者幽门螺杆菌感染率调查

目的调查近3年来北京地区反流性食管炎患者幽门螺杆菌(Hp)感染率,分析目前反流性食管炎与Hp感染的相关性。方法选择反流性食管炎患者119例和正常对照组121例,以快速尿素酶试验及13C-尿素呼气试验检测Hp感染。结果反流性食管炎患者Hp感染率(26.89%),显著低于对照组(42.15%),P<0.05。结论Hp可能在反流性食管炎的发病中起到保护作用。     

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相关性研究

[目的]探讨反流性食管炎(RE)与幽门螺杆菌(Hp)的相关性。[方法]慢性浅表性胃炎患者165例,其中合并RE者105例为RE组,另60例不合并RE为对照组,分别在其胃窦大小弯取2块活组织行快速尿素酶试验及病理活检检测Hp。[结果]RE组Hp感染率为35.24%,对照组为63.33%,差异有统计学意义(P0.05)。[结论]Hp感染可能有降低RE发病率的作用。     

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。     

胃食管反流病与幽门螺杆菌相关性研究

目的探讨胃食管反流病(GERD)与幽门螺杆菌(Hp)感染的关系。方法选取2010年8月至2012年10月黑龙江省医院附属消化病医院消化科GERD患者80例,进行胃镜检查及24 h食管pH值监测,按照內镜下有无食管黏膜破损分为非糜烂性反流病(NERD)50例,反流性食管炎(RE)30例,并选取同期就诊的100例慢性浅表性胃炎(CSG)为对照组,分别比较三组Hp感染率。结果NERD组Hp感染率38.0%,RE组Hp感染率为36.7%,CSG组Hp感染率为56%,NERD组及RE组Hp感染率明显低于对照组(P0.05);NERD组及RE组Hp感染率无显著性差异(P0.05)。结论Hp感染可能对GERD发生有一定保护作用;造成GERD不同发生机制不同的主要原因并非Hp感染。     

消化系统疾病

老年人反流性食管炎1119例分析；非糜烂性反流病的临床研究； 胃食管反流病与下消化道功能关系的研究；幽门螺杆菌感染与反流性食管炎：一项病例对照研究；上海地区幽门螺杆菌感染及其危险因素调查。     

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.     

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,…     

反流性食管炎1405例临床和内镜特点分析

目的 分析反流性食管炎患者的临床和内镜检查特点.方法 回顾性分析自2004年9月至2007年1月北京友谊医院诊治的反流性食管炎患者的性别、年龄、是否存在幽门螺旋杆菌感染和食管裂孔疝,并且按照洛杉矶标准进行分级.结果 1405例反流性食管炎患者中,男女比例1.75:l,二者差异有统计学意义(P＜0.01).男、女性患者平均年龄有一定差异(P=0.01).患者发病高峰年龄在40～60岁.根据洛杉矾标准,A、B级分别与C、D级患者间年龄存在差异(P＜0.01).Hp阳性患者277例,感染率明显降低(P＜0.01).合并有食管裂孔疝患者195例,与食管炎严重程度和年龄显著相关(P＜0.01).结论 反流性食管炎男性患者的平均年龄较低,检出量多于女性患者.食管炎患者Hp感染率明显降低.高龄和合并有食管裂孔疝的患者食管炎更严重.患者黏膜破损较易发生在食管右半侧壁.     

序贯疗法与三联疗法根除幽门螺杆菌的疗效及对反流性食管炎愈合率的影响

目的比较10天序贯疗法与10天标准三联疗法根除幽门螺杆菌（HP）的疗效,并观察根除HP对反流性食管炎愈合率的影响。方法将76例反流性食管炎合并HP感染的患者随机分为3组：序贯疗法治疗组32例,埃索美拉唑＋阿莫西林,每日2次,共用5天,随后5天用埃索美拉唑＋克拉霉素＋替硝唑,每日2次;三联疗法治疗组24例,埃索美拉唑＋克拉霉素＋阿莫西林,每日2次,疗程10天,两组抗HP疗程结束后继续给予埃索美拉唑,每日2次,总疗程8周;对照组20例：单用埃索美拉唑,每Et2次,疗程8周。疗程结束后复查胃镜,并行HP检测。结果序贯疗法与三联疗法对幽门螺杆菌的根除率分别为87．50％和58．33％,两组比较差异有统计学意义（P〈0．05）。HP根除患者和未根除患者食管炎治愈率分别为83．33％和91．18％,两者比较差异无统计学意义;3组食管炎的治愈率分别为87．50％、83．33％和90％,三者之间比较差异无统计学意义。结论在食管炎患者中,序贯疗法HP根除率明显优于三联疗法;根除幽门螺杆菌对反流性食管炎8周愈合率无明显影响。     

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.     

Corpus gastritis and erosive esophagitis: a report from the Middle East.

OBJECTIVE: To assess whether corpus gastritis due to Helicobacter pylori protects against erosive esophagitis in an area with high prevalence of H. pylori infection. METHODS: Biopsies obtained from gastric corpus and antrum in 151 patients with symptoms of gastroesophageal reflux disease were studied for presence of H. pylori and endoscopic evidence of gastritis. Presence and grade of esophagitis at endoscopy was recorded. RESULTS: Fifty-four (36%) patients had endoscopic esophagitis. Patients with severe esophagitis (>or= grade II) less often had active gastritis (15/45 vs. 55/98; p=0.02) and had a lower density of H. pylori (p=0.0003) than those without esophagitis. CONCLUSION: Active corpus gastritis due to H. pylori infection may protect against erosive esophagitis in patients with gastroesophageal reflux disease in the Middle East.     

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.     

Characteristics of gastritis in patients with Helicobacter pylori-positive reflux esophagitis

BACKGROUND AND AIM: The influence of Helicobacter pylori on gastric acid secretion differs with the status of gastritis. The histological characteristics of gastritis in H. pylori-positive patients with reflux esophagitis have not been fully investigated. We therefore studied the pattern of endoscopic gastric mucosal atrophy and degree of histological gastritis in such patients. METHODS: Subjects comprised 41 H. pylori-positive patients with reflux esophagitis, 41 age- and sex-matched patients with duodenal ulcer, and 41 patients with early gastric cancer. The endoscopic pattern of gastric mucosal atrophy was reviewed, and the degree of histological gastritis in biopsy specimens from the antrum and corpus was assessed in accordance with the updated Sydney system. RESULTS: The grade of endoscopic and histological gastric mucosal atrophy in patients with reflux esophagitis was significantly lower than that in patients with gastric cancer, and the histological scores for antral atrophy and metaplasia in patients with reflux esophagitis tended to be lower than those in patients with duodenal ulcer. In patients with reflux esophagitis and duodenal ulcer, the scores for antral inflammation and activity tended to be higher than those for the corpus. Conversely, the inflammation and activity score in patients with early gastric cancer showed a corpus-predominant gastritis pattern. CONCLUSION: In H. pylori-positive patients with reflux esophagitis, the degree of endoscopic gastric mucosal atrophy is low and histologically there is an antral-predominant gastritis pattern. Therefore, gastric acid secretion in H. pylori-positive patients with reflux esophagitis may be augmented by H. pylori infection.     

The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with Barrett's esophagus in Japan

OBJECTIVES: The acidity of the refluxate into the esophagus is a key factor for the pathogenesis of gastroesophageal reflux disease. Helicobacter pylori (H. pylori) infection can influence gastric acid secretion. We have reported that H. pylori infection prevents reflux esophagitis by decreasing gastric acid secretion in Japanese patients, but the role of this organism in Barrett's esophagus is unclear. The aim of this study was to investigate the prevalence of H. pylori infection and gastric acid secretion in Japanese patients with reflux esophagitis with or without Barrett's esophagus. METHODS: We enrolled 112 reflux esophagitis patients who were examined for the status of H. pylori and acid secretion in this study. They were divided into three groups, according to the presence or absence of Barrett's esophagus as follows: reflux esophagitis group without Barrett's esophagus (reflux esophagitis alone) (80 patients); short-segment Barrett's esophagus group (16 patients); and long-segment Barrett's esophagus group (LSBE) (16 patients). Age- and sex-matched control subjects were also assigned to the 80 patients with reflux esophagitis alone. The prevalence of H. pylori infection was determined by histology, rapid urease tests, and serum IgG antibodies. Gastric acid secretion was evaluated by the endoscopic gastrin test (EGT). RESULTS: The overall prevalence of H. pylori infection in the reflux esophagitis patient group (24.1%) was significantly lower than the control group (71.2%) (odds ratio 0.13, 95% confidence interval 0.07-0.24; p < 0.0001). The prevalence of H. pylori infection in the patients with Barrett's esophagus tended to be lower than that in the patients with reflux esophagitis alone (reflux esophagitis alone; 30.0%, SSBE; 18.7%, LSBE; 0%), especially in the patients with LSBE compared with the reflux esophagitis alone group (p < 0.01). The EGT value of the respective reflux esophagitis patient group was significantly higher than the control group. The EGT value in the patients with Barrett's esophagus tended to be higher than that in the patients with reflux esophagitis alone, but the difference was not statistically significant. When examined in H. pylori-negative subjects, no difference was found in the EGT value between the control subjects and the patients with reflux esophagitis alone, but it was significantly higher in patients with Barrett's esophagus than the control subjects (p < 0.05). On the other hand, when examined in the H. pylori-positive subjects, the EGT value was significantly higher in the patients with reflux esophagitis alone than in the control subjects (p < 0.01). CONCLUSIONS: H. pylori infection may play a protective role in the development of Barrett's esophagus, especially in the development of LSBE in Japan. Gastric acid hypersecretion may be concerned with the development of Barrett's esophagus in addition to the absence of H. pylori infection.     

Reflux esophagitis patients in Singapore have motor and acid exposure abnormalities similar to patients in the Western hemisphere

OBJECTIVE: Endoscopic esophagitis is less common in the East than in the West. The reason for this is unknown. This study examines prospectively the relationship between endoscopic esophagitis and lower esophageal sphincter pressure, distal esophageal contractility, esophageal peristaltic performance, esophageal acid exposure, gastric acid output, and Helicobacter pylori (H. pylori) status in a consecutive series of Asian patients. METHODS: Esophageal manometry and ambulatory pH monitoring were carried out in 48 patients with endoscopic esophagitis and 208 patients with symptoms suspicious of gastroesophageal reflux disease but without esophagitis. Gastric acid output and H. pylori serology were determined in 22 of the esophagitis group and 36 of the nonesophagitis group. RESULTS: Compared to the nonesophagitis patients, esophagitis patients had a higher prevalence of hypotensive lower esophageal sphincter (49% vs 24%, p < 0.001), impaired esophageal contractility (45% vs 22%, p < 0.005), poor peristaltic performance (23% vs 12%, p < 0.05), and pathological acid reflux (48% vs 27%, p < 0.005). However, there was no difference in the two groups with respect to gastric acid output and H. pylori positivity. CONCLUSIONS: Lower esophageal sphincter competence, esophageal peristaltic contractility, and esophageal acid exposure were important factors in the pathogenesis of reflux esophagitis--results identical to Western studies. Gastric acid output per se and H. pylori infection might not be responsible for susceptibility to esophagitis.     

Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis

OBJECTIVE: Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan. METHODS: A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio. RESULTS: H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it. CONCLUSIONS: These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.     

Helicobacter pylori Infection Has No Role in the Pathogenesis of Reflux Esophagitis

In a prospective study of consecutive patientswith reflux esophagitis and/or hiatal hernia andBarrett's esophagus, the prevalence of Helicobacterpylori was assessed. Antral biopsy specimens werestudied and a serum sample for detection of IgGantibodies against Helicobacter pylori was taken. As areference group patients presenting with a normalesophagus, stomach, and duodenum were taken. Refluxesophagitis was diagnosed in 118 patients, hiatal herniawithout esophageal inflammation in 109, and Barrett'sesophagus in 13. Helicobacter pylori was present in 74(30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacterpylori was significantly lower in all groups comparedwith the reference group (P < 0.001). There was nodifference when patients with esophagitis, Barrett'sesophagus, or hiatal hernia were compared. Patients withesophagitis and Helicobacter pylori in their antrum aresignificantly older than esophagitis patients withoutconcomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). Itis concluded that the prevalence of Helicobacter pyloriinfection in patients with gastroesophageal refluxdisease is significantly lower than in the reference group, irrespective of the severity ofesophagitis. Helicobacter pylori infection has no rolein the pathogenesis of reflux esophagitis.     

Clinical characteristics of Japanese reflux esophagitis patients as determined by Los Angeles classification

BACKGROUND: Recent studies have shown that the number of patients with reflux esophagitis is increasing in Japan, but the prevalence and risk factors associated with reflux esophagitis in Japanese patients are not well defined. METHODS: By using all endoscopic records in the Katta General Hospital from April through to September 1999, we identified 392 patients. We examined the Los Angeles classification, peptic ulcer, gastric mucosal atrophy, hiatal hernia and other medical variable factors for their contribution to esophagitis in the patients. RESULTS: Patients (13.8%) were diagnosed as having reflux esophagitis with a mucosal break. In a multivariate analysis, reflux esophagitis was associated with hiatal hernia (odds ratio (OR) 2.276, 95% confidence interval (CI) 1.164-4.450), with patients over 65 years of age (OR 2.521, 95% CI 1.238-5.134) and the open type of gastric mucosal atrophy (OR 0.420, 95% CI 0.225-0.785). There was no significant difference between esophagitis and Helicobacter pylori infection and peptic ulcer. CONCLUSIONS: We observed that age, hiatal hernia and a lower rate of gastric mucosal atrophy were associated with the proportion of mucosal breaks accompanying esophagitis.