以慢性咳嗽为主要表现的胃食管反流病患者的食管功能及反流特点

目的 通过对以慢性咳嗽为主要表现的胃食管反流病(GERD)患者行高分辨食管内压力-阻抗联合测定(MII-HRM)及24h联合多通道腔内阻抗-pH( MII-pH)监测的结果分析,探讨此类患者食管运动功能及胃食管反流的特点.方法 选取2010年3-11月在首都医科大学附属北京朝阳医院就诊的19例GERD伴慢性咳嗽患者为研究对象.应用MII-HRM及24 h MII-pH监测系统测定上食管括约肌(UES)和下食管括约肌压力、食管体部蠕动功能、对液体和黏液性物质的传输功能、立位及卧位酸及非酸反流的次数、近端反流的次数、酸暴露时间、酸清除时间以及食团清除时间.以同期仅表现为典型胃食管反流症状的17例GERD患者作为对照,比较两组间食管运动功能以及胃食管反流参数的差异.结果 与仅表现为典型胃食管反流症状的GERD患者相比,以慢性咳嗽为主要表现的GERD患者的UES静息压力明显更低[(122.55 ±60.48)mm Hg比(86.37±41.35) mm Hg(1 mm Hg =0.133 kPa),P＜0.05],食管体部异常蠕动的比例更高[(9.47±15.63)％比(22.16±17.45)％,P＜0.05],食管体部对液体物质传输能力减低[(88.82±12.23)％比(71.68±23.06)％,P＜0.05],卧位时酸及非酸反流次数及卧位近端非酸反流次数明显增多(P＜0.05),卧位食团清除时间延长(P＜0.05).结论 以慢性咳嗽为主要表现的GERD发病机制可能与单纯典型GERD不同,其与UES静息压力减低、卧位酸及非酸反流、近端反流的增多以及食管清除功能障碍密切相关.     

酸反流与胆汁反流在胃食管反流病中的作用

目的探讨酸反流与胆汁反流在胃食管反流病(GERD)中的作用及相互关系.方法46例GERD患者(反流性食管炎组30例,胃镜阴性组16例)及26例健康对照者在完成食管测压后,应用便携式食管pH监测仪及Bilitec2000胆汁反流监测仪,同时进行24h食管内酸及胆汁反流的动态连续监测.结果GERD患者酸反流及胆汁反流各指标均明显高于健康对照者,且与食管炎严重程度一致.pH＜4总时间百分比与胆红素光吸收值(Abs)＞0.14,总时间百分比存在线性相关关系(r=0.34,P＜0.01).酸反流和胆汁反流共存的双重反流在GERD患者中最为常见,且较单纯反流更易引起严重食管炎.结论GERD患者中较为常见的双重反流对食管粘膜的损伤作用强于单纯酸或胆汁的不完全反流,酸反流与胆汁反流间可能有正性协同作用;联合应用胃镜检查及食管内酸和胆汁反流监测将为GERD的诊治提供可靠的客观依据.     

合并食管外症状的难治性胃食管反流病的临床研究

选取51例难治性GERD患者,分析合并食管外症状和典型反流症状的难治性GERD患者的高分辨率食管测压和24 h pH-阻抗监测数据。结果显示合并食管外症状组弱酸反流事件发生率(41.0%,16/39)高于典型反流症状组(9/12),差异有统计学意义(χ^2=4.238,P=0.040);而两组酸反流、长反流、非酸反流和食管动力之间差异均无统计学意义(P均>0.05)。弱酸反流可能是合并食管外症状难治性GERD的重要发病机制。     

Barrett食管、反流性食管炎和非糜烂性胃食管反流病的反流物特点

目的应用食管24 h pH-阻抗(MII-pH)等检查方法,分析具有胃食管反流病(GERD)典型症状、并且食管MII-pH检查结果异常的GERD患者,比较分析其各亚型,即Barrett食管(BE)、反流性食管炎(RE)和非糜烂性胃食管反流病(NERD)患者的胃食管反流特点。 方法入选具有典型胃食管反流症状(烧心/反流),并且食管24 h MII-pH检查结果异常的GERD患者,根据内镜检查结果分为BE、RE、NERD三组,收集患者24 h的食管pH-阻抗信息,应用SPSS16.0统计软件进行组间Mann Whitney检验、多因素方差分析,P< 0.05认为具有统计学差异。 结果共入组103例具有典型反流症状且MII-pH监测阳性的GERD患者,其中有15例BE患者、32例RE患者、56例NERD患者。三组患者的平均年龄、性别构成、以及BMI无显著差异性。将三组患者的各项胃食管反流指标数值进行Mann-Whitney检验,显示RE、BE患者的DeMeester评分、pH<4反流时间百分比、长反流周期数显著高于NERD患者,具有显著性差异。BE患者的反流周期数显著多于RE和NERD患者,具有显著性差异。阻抗相关指标在三组患者之间均没有统计学差异。 结论与NERD相比,酸反流对于RE和BE具有更重要的致病意义。     

呼吸系统症状为主的胃食管反流病48例临床分析

目的:观察以呼吸系统症状为主的胃食管反流病(GERD)患者酸反流事件和基础下食管括约肌压力(LESP)的关系。方法:对48例以呼吸系统症状为主的GERD患者的临床特点进行分析,测定食管内PH值和食管压力。结果:有呼吸系统症状的GERD患者,其食管下括约肌功能有所改变;质子泵抑酸剂和促胃肠道动力药物治疗前后24h食管反流变化和食管内pH值变化均有显著性差异;治疗后呼吸系统症状得到改善。结论:胃食管反流可以作为独立原因引起呼吸道病症状,抑酸抗反流治疗对胃食管反流相关的呼吸系统症状有较好的近期疗效。     

胃食管反流病的临床研究

目的 研究胃食管反流病（GERD）的反流症状与诊断关系，以引起临床医生的重视。方法采用典型症状、波利特试验及内镜检查；结果 检出反流性食管炎89例，非糜烂性食管炎291例，Barrett食管41例。结论 反流症状并有效检查为临床提供良好治疗方案。     

19例胃食管反流病患者根除幽门螺杆菌后食管酸反流的变化

目的：在胃食管反流病(GRED)患者根除幽门螺杆菌(Hp)是否会加重胃食管反流目前存在很大争议。本研究将采用食管内24h pH监测及食管测压检查的方法，定量观察GERD患者根除Hp治疗前后食管酸暴露及食管动力的变化。方法：连续选取我院门诊就诊的Hp阳性GERD患者。Hp感染诊断依据RUT和UBT或UBT和血清学检查。所有入选对象均在内镜检查后1～3d内行食管内24h pH监测和食管测压检查，同时评估反流症状。给予1周三联根除Hp治疗(奥美拉唑20mg，克拉霉素0．25g，阿莫仙1．0g，均bid)。疗程结束3个月后^14C—UBT检查，证实Hp根除者复查食管内24h pH监测和食管测压，同时重新评估反流症状。随访期间不用抑酸剂及促动力剂。结果：共23例Hp阳性GERD患者入选了本研究，其中19例患者完成了根除Hp前后的对比研究。在入选时有6例患者内镜下表现符合反流性食管炎，24h食管内pH监测提示病理性反流者10例。在确定根除Hp3个月后反酸、腹痛症状明显改善，食管24h pH监测各项参数与根除前相比均无显著性差异。LESP根除前10mm Hg(7．7—15．9)，根除后15mm Hg(10—20．6)，前后相比有显著性差异。食管体蠕动无明显改变。结论：本研究在GERD患者根除Hp3个月后反流症状有改善，食管酸暴露情况无明显变化，LESP较根除前增高，提示在GERD患者根除Hp有可能改善胃食管反流症状。     

非糜烂性胃食管反流病内脏高敏感机制研究

非糜烂性胃食管反流病(NERD)是指有典型胃食管反流症状而无内镜下食管黏膜损伤的疾病，又称“内镜阴性胃食管反流病”，约占胃食管反流病(GERD)的70％。其临床症状的严重程度与GERD相似，抑酸治疗效果不佳，往往对患者的生活质量产生严重的影响。其发病机制复杂，主要包括酸反流，内脏高敏感，非酸相关性刺激，中枢及外周水平调控失衡等机制。     

难治性胃食管反流病食管动力异常与反流特点的研究

目的研究难治性胃食管反流病(refractory gastroesophageal reflux disease,rGERD)食管动力学特征和反流特点。方法应用高分辨率食管测压(HRM)监测87例GERD患者和70例rGERD患者食管动力学数据,同时应用便携式24 h食管pH-阻抗监测仪记录两组患者的酸暴露特点、反流类型及反流特点,分析比较两组患者间差异。结果rGERD患者中UES压力、LES压力显著低于GERD患者(P<0.05),rGERD患者LES的长度与GERD患者比较,差异无统计学意义(P>0.05)。rGERD患者中食管动力障碍比例高于GERD患者(70.00%vs 33.33%,χ2=4.891,P<0.05),DCI下降为特征的食管蠕动收缩障碍及间断收缩为特征的食管收缩节律障碍者比例两组比较,差异无统计学意义(57.14%vs 62.07%;42.86%vs 37.93%,χ2=3.275、2.822,P>0.05)。rGERD患者DeMeester评分高于GERD患者(P=0.014),rGERD患者反流性质中弱酸反流及非酸反流明显多于GERD患者(P弱酸=0.001,P非酸=0.017),而酸反流次数差异无统计学意义(P酸=0.385);rGERD患者反流性状中气体反流及气液混合反流次数多于GERD患者(P气=0.022,P气液=0.031),而液体反流次数差异无统计学意义(P液=0.742)。结论rGERD患者与GERD患者相比,存在UES压力偏低、LES压力下降和食管蠕动收缩障碍等食管动力学异常;rGERD患者反流以弱酸反流及碱反流为主,而GERD患者以酸反流为主,同时rGERD患者中气液混合反流所占比例大,而GERD患者以液体反流为主。     

胃食管反流病的外科治疗

胃食管反流病(GERD)包括由病理性胃食管反流引起的反流性食管炎及并发症(食管狭窄、短食管、Barrett食管、哮喘、吸入性肺炎和反流性咽喉炎等)。GERD发病是多因素的，正常情况下，食管胃连接部存在抗反流屏障，可阻止胃内容物进笔食管。抗反流屏障损害、胃排空和食管酸廓清功能障碍是引发GERD的病理机制。     

Duodenogastral reflux burden gastroesophageal reflux disease

The article presents research data of duodenogastral reflux (DGR) role in patients with gastroesophageal reflux disease. It is shown that in the presence DGR, the reflux esophagitis is detected at a higher frequency and outside of esophageal manifestations of the disease. The comorbidities of hepatobiliary zone and pancreas contributes to the DGR development, as well as the syndrome of bacterial overgrowth in the small intestine.     

反流性咽喉炎的研究进展

随着对胃食管反流病认识的深入,其对咽喉部的影响越来越受到临床的关注,研究证明它是导致咽喉部疾病的重要致病因素之一。胃食管反流对消化系统影响的研究很多,但其与咽喉反流性疾病的相关研究甚少,很多基层医生对该病还不甚了解。本文主要对反流性咽喉炎的发病机制、临床表现、诊断方法和治疗作一综述。     

Laryngopharyngeal reflux in patients with reflux esophagitis

AIM： To assess the prevalence of laryngopharyngeal reflux （LPR） in patients with reflux esophagitis and disclose factors contributing to the development of LPR.
METHODS： A total of 167 patients who proved to have reflux esophagitis by endoscopy were enrolled. They received laryngoscopy to grade the reflux findings for the diagnosis of LPR. We used validated questionnaires to identify the presence of laryngopharyngeal symptoms, and stringent criteria of inclusion to increase the specificity of laryngoscopic findings. The data of patients were analyzed statistically to find out factors related to LPR.
RESULTS： The prevalence rate of LPR in studied subjects with reflux esophagitis was 23.9%. Age, hoarseness and hiatus hernia were factors significantly associated with LPR. In 23 patients with a hiatus hernia, the group with LPR was found to have a lower trend of esophagitis grading.
CONCLUSION： Laryngopharyngeal reflux is present in patients with reflux esophagitis, and three predicting factors were identified. However, the development of LPR might be different from that of reflux esophagitis. The importance of hiatus hernia deserves further study.     

Upright versus supine reflux in gastroesophageal reflux disease

BACKGROUND: Postural measures are early recommendations in the management of heartburn, and are aimed at preventing acid reflux through an incompetent lower esophageal sphincter (LES). However, LES incompetence is found in only a minority of patients, and transient LES relaxations, primarily in the upright position, are currently recognized as the main pathophysiological abnormality in gastroesophageal reflux disease (GERD). We investigated the importance of supine acid reflux in patients with GERD. METHODS: Upon review of their clinical, manometric, pH monitoring and endoscopic characteristics, 85 patients with reflux symptoms were classified into three groups: Group A (n=22), consisting of symptomatic patients without esophagitis or pathological reflux; group B (n=38), symptomatic patients with reflux but no endoscopic esophagitis; and group C (n=25), symptomatic patients with both ulcerative or complicated esophagitis and pathological reflux. RESULTS: All groups were similar in age distribution. Groups B and C had a higher prevalence of hiatal hernia and reflux symptoms. Manometry revealed similar LES pressures in groups A and B, but lower LES pressure in group C (P < 0.005). In groups A and B, supine reflux, in terms of percentage of time with pH < 4, was less pronounced than upright reflux (P < 0.0001). In contrast, group C supine reflux was as pronounced as the upright reflux. CONCLUSIONS: The majority of patients reflux in the upright position. Only patients with complicated esophagitis have significant bipositional acid reflux. These findings suggest that unless the patient has severe reflux disease, postural measures may not be indicated.     

Gastroesophageal reflux disease--from reflux episodes to mucosal inflammation

Gastroesophageal reflux disease (GERD) affects 20-30% of the population in Western countries, and is one of the most common clinical problems in daily practice. GERD-associated functional and structural abnormalities are caused by recurrent exposure of the esophagus to acidic and nonacidic refluxate of gastric contents (containing duodenal and intestinal proteases as well as acid and gastric pepsin) from the stomach. Major progress has been made in the understanding of the molecular pathogenesis of GERD-associated mucosal inflammation, suggesting a complex and multifactorial pathogenesis and immune-mediated effects. This Review summarizes the complexity of mucosal pathogenesis, including microscopic changes, mucosal inflammation and GERD-specific molecular mediators, in the context of the clinical features and pathophysiological characteristics of GERD. The abnormal exposure of the esophagus to luminal contents leads to chronic mucosal inflammation that is characterized by the release of IL-8 specifically, as well as other proinflammatory mediators, from the esophageal mucosa. Evidence from animal studies indicates a stepwise inflammatory response by the epithelium, which attracts immune effector cells to infiltrate the mucosa. From bench to bedside, these novel molecular findings might provide new treatment options beyond current acid-suppressive therapy and the principle of inhibition of transient lower esophageal sphincter relaxation.     

Gastroesophageal reflux

Gastroesophageal reflux disease (GERD) is the most common disease of the gastrointestinal system. Heartburn, regurgitation, and dysphagia are the most common symptoms of GERD. However, chest pain, chronic cough, laryngitis, hoarseness, and other otolaryngologic manifestation can be the primary manifestations of the disease. Endoscopy, barium studies, and especially pH monitoring and therapeutic trials may help in establishing the diagnosis of GERD. The introduction of H2 antagonists and especially of proton pump inhibitors (PPI) has brought symptomatic relief in most patients. However, surgical procedures, especially laparoscopic fundoplication, are still required in some patients. Barrett's esophagitis is the most common complication of GERD and is associated with a high prevalence of esophageal adenocarcinoma. Whether or not treatment with either PPIs or H2 antagonists can prevent this complication is still under investigation.