健康人食管测压及影响因素多中心研究

目的 建立不同年龄组食管动力参数正常值及测定方法.方法 应用气液压毛细灌注系统测定3个不同年龄组(Ⅰ组18～39岁,Ⅱ组40～59岁,Ⅲ组≥60岁)健康志愿者食管动力参数.同时观察本测定方法对下食管括约肌(LES)检测的重复性和稳定性.结果 实际入组162名,Ⅰ组62名,Ⅱ组73名,Ⅲ组27名.三组间下食管括约肌长度(LESL)、呼气末下食管括约肌压力(LESP)、LESP平均值、残余压、下食管括约肌松弛率(LESRR)差异无统计学意义(P＞0.05).Ⅰ组吸气末LESP为(28.98±1.11) mmHg,明显低于Ⅲ组[(34.35±1.96)mmHg,P＜0.05].Ⅰ组跨膈压为(9.55±0.62) mmHg,明显低于Ⅱ组[(13.05±0.76) mmHg,P＜0.05].三组食管体部远端和近端收缩波幅和时限差异无统计学意义(P＞0.05).Ⅲ组上食管括约肌压力( UESP)明显低于Ⅰ组、Ⅱ组(P＜0.05).重复性比较,Ⅰ组、Ⅱ组第2次呼气末LESP明显高于第1次(P＜0.05).远端食管蠕动收缩波幅女性明显高于男性(P＜0.05),近端食管蠕动收缩波幅女性与男性无明显差别(P＞0.05).结论 得到不同年龄组食管动力参数的正常值.LES的动力参数不随年龄的增长而变化.而食管体部蠕动收缩能力在40～59岁年龄组最强.老年人UESP明显下降.检测前让受试者有足够的适应时间,有利于得到准确、可靠的LES的动力参数.     

肝硬化患者食管动力与肝功能障碍的关系研究

目的研究肝功能减退对食管动力的影响.方法对无腹水或经治疗腹水消退后的肝硬化患者63例,进行Child-pugh分级,和健康对照组22例分别进行食管测压及24小时pH监测.结果肝硬化组下食管括约肌压力(LESP)、远端食管蠕动波幅(PA)、蠕动时间(PD)和蠕动传导速度(PV)与对照组比较显著异常(P＜0.05).LESP在ChildC级较ChildB级显著下降(P＜0.05),与Child-Pugh分数呈负相关(r＝-0.523,P＜0.01),伴各胃食管酸反流指标显著异常和胃食管反流病(GERD)发生率升高,P均小于0.01.食管静脉曲张程度也显著影响PA、PD和PV(P＜0.05),而LESP无明显下降.结论肝硬化患者食管动力异常和胃食管酸反流的原因除食管静脉曲张外,肝功能减退使其加重和LESP下降.     

食管运动功能在重度反流性食管炎中的地位

目的　通过对重度反流性食管炎(RE)治愈前后食管体部运动功能的研究,了解食管体部运动功能在重度RE中的地位。方法　对70例胃食管反流病患者进行食管压力测定。从中筛选23例重度RE(内镜诊断为洛杉矶C和D级食管炎);且24h食管内pH监测证实为病理性酸反流;食管压力测定证实有食管体部运动障碍患者。给予兰索拉唑30mg/d治疗3~6个月至内镜下食管炎完全愈合后,再行食管压力测定,观察下食管括约肌静息压(LESP)及食管体部运动功能的变化。以湿咽成功率、食管远端收缩波幅和食管蠕动的传导速度作为食管体部运动功能的指标。结果　食管炎治愈前后,LESP[ (6 00±0 86 )mmHg比(5 10±0 87)mmHg, 1kPa=7 5mmHg, P=0 476],食管远端收缩波幅[ (34 1±4 1)mmHg比(37 2±4 0)mmHg,P=0 593]、湿咽成功率[ (33 5±6 5)%比(38 6±7 1 )%,P=0 592 ]比较差异均无统计学意义,其均值仍显著低于正常对照组。结论　治愈食管炎并不能提高LESP及改善食管体部的运动功能。食管体部运动功能障碍和酸反流是RE的重要发病机制,尤其是重度RE。     

经口内镜下肌切开术治疗25例贲门失弛缓症患者的食管动力变化

目的比较贲门失弛缓症(AC)患者接受经口内镜下肌切开术(POEM)前后症状变化和食管动力改变,评价POEM治疗AC的有效性。方法对行POEM治疗的25例AC患者术前及术后1个月使用固态高分辨率食管测压系统(HRM)检测吞咽液体食团时下食管括约肌(LES)动力学参数的变化。结果25例患者POEM术治疗前后Eckardt评分有统计学差异(P0.001);手术前后食管下括约肌长度无明显变化;术前食管下括约肌静息压(LESP)为(27.75±2.44)mmHg,较术后(10.05±1.06)mmHg显著降低,二者差异有统计学意义(P0.001);液体吞咽4 s后的完整松弛压(IRP)在术前术后分别是(21.81±2.57)mmHg和(7.42±0.98)mm Hg,差异有统计学意义(P0.001);食管下括约肌松弛率(LESRR)术后较术前明显升高(P0.05)。结论 POEM能有效改善AC患者的LES松弛障碍,但其远期疗效尚需进一步随访观察。     

高分辨率食管测压下胃食管反流病吞咽延迟时间与食管动力的相关性研究

目的探讨高分辨率食管测压（HRM）下胃食管反流病（GERD）患者吞咽延迟时间（DL）与食管动力的关系。方法51例行HRM且24h食管pH监测诊断为GERD的患者根据HRM结果是否存在食管异常蠕动分成动力异常组（n=28）和阴性组（n=23）,另选择14例非GERD者行HRM作为对照（对照组）,统计分析各组HRM监测结果。结果动力异常组DL（7．27±1．44）S明显高于阴性组的（6．704±41）S和对照组的（5．86±0．96）2,差异均有统计学意义（P〈0．01）,且阴性组也明显高于对照组（P〈0．01）;动力异常组的远端收缩积分（712．49±703．10）mmHg·s·cm明显低于阴性组的（1285．85±850．83）mmHg·s·cm和对照组的（1109．74±611．70）mmHg·s·cm,差异均有统计学意义（P〈0．01）,而阴性组与对照组比较差异无统计学意义（P〉0．05）;各组间食管下括约肌压力、收缩前沿速度及食管下括约肌处食团内部压力差异均无统计学意义（P〉0．05）。结论HRM下DL的延长与GERD患者食管蠕动减弱明显相关,GERD患者表现为更长的DL,证明食管动力的改变是GERD发生发展的重要环节。     

难治性与非难治性胃食管反流病食管动力比较

目的 :比较难治性胃食管反流病(RGERD)与非RGERD食管动力特点的差异。方法 :回顾分析2011年5月至2014年5月我院消化科进行高分辨率食管测压的GERD患者86例,其中RGERD组44例,非RGERD组42例,比较2组患者食管动力特点的差异。结果:RGERD组与非RGERD组食管下括约肌(LES)长度分别为(2.6±0.7)和(3.5±0.9)cm,LES静息压分别为(16.3±8.0)和(20.3±8.6)mmHg(1 mmHg=0.133 kPa),远端波波幅分别为(65.7±30.1)和(80.1±34.9)mmHg,食团内压(IBP)分别为(11.6±4.0)和(13.6±3.7)mmHg,差异有统计学意义(t=5.128、2.235、2.044、2.400,均P0.05)。2组小型蠕动中断百分比差异有统计学意义(P0.05)。结论:LES长度较短、LES静息压偏低、远端波波幅偏低、IBP偏低及小型蠕动中断百分比增加是RGERD的主要食管动力障碍,调控这些因素或许可以为RGERD的治疗提供新的方向。     

不同体位高分辨率食管测压检测下食管括约肌静息压的比较分析

目的 了解不同体位对临床高分辨率食管测压检测下食管括约肌静息压力（LESP）结果的影响.方法 对临床有检查适应证的40例患者行高分辨率测压（HRM）,按照性别、年龄、疾病进行分组比较,分析坐位及平卧位LESP的差异.结果 受检患者下食管括约肌（LES）上缘及下缘距鼻孔平均距离为（42.8±3.3）cm和（45.6±3.7）cm,LES长度为（2.8±0.8）cm.根据受检患者身高分组,组间食管括约肌位置及长度比较差异无统计学意义（P＞0.05）.不同性别患者其平卧位及坐位LESP差异无统计学意义（P＞0.05）.随着年龄的增加,LESP逐渐降低,但体位对其无明显影响.反流性食管炎患者平卧位LESP为（9.38 ±2.95） mmHg,坐位LESP为（11.35±4.09） mmHg,两者比较差异有统计学意义（P＜0.05）;贲门失迟缓症患者平卧位LESP为（46.40±1.13） mmHg,坐位LESP为（43.78±2.38） mmHg,两者比较差异有统计学意义（P＜0.05）.非糜烂性胃食管反流病（NERD）及无明确食管疾病患者不同体位LESP比较差异无统计学意义（P＞0.05）.结论 临床中应根据患者症状采用不同体位进行检查,以增加疾病诊断的敏感性.     

无效食管动力在胃食管反流病中作用的探讨

目的探讨无效食管动力(IEM)在胃食管反流病(GERD)发病中的作用。方法选取2014年7月至2016年2月在上海同济大学附属东方医院就诊的GERD患者,所有患者均接受高分辨率(HRM)食管测压和24h动态pH监测,排除食管-胃连接处(EGJ)压力和(或)形态异常的情况,共纳入49例GERD患者。根据HRM测压下食管远端收缩积分(DCI)将GERD患者分为IEM组、异常动力组和正常动力组。比较各组间食管动力及反流情况。结果 49例GERD患者中,IEM组19例,异常动力组15例,正常动力组15例。IEM组中反流性食管炎所占比例显著高于异常动力组和正常动力组(P0.05),正常动力组与异常动力组相比较差异无统计学意义。IEM组平均吞咽DCI显著低于异常动力组及正常动力组(P0.01),异常动力组显著低于正常动力组(P0.01)。IEM组食管体部蠕动中断长度相较于异常动力组及正常动力组显著延长(P0.01),异常动力组较正常动力组显著延长(P0.01)。各组间酸反流次数、弱酸反流次数、非酸反流次数和总反流次数比较差异无统计学意义。IEM组DeMeester得分及合计酸反流时间较异常动力组及正常动力组显著增加,差异有统计学意义(P0.05),异常动力组及正常动力组DeMeester得分及合计酸反流时间比较差异无统计学意义。49例GERD患者中,平均吞咽DCI与食管蠕动中断长度呈负相关(P0.01),平均吞咽DCI与合计酸反流时间呈负相关(P0.01)。结论 GERD患者中食管动力障碍与酸反流相关,食管体部收缩力度减弱,蠕动中断延长,与酸反流严重程度相关。IEM患者食管收缩力度较弱,酸反流时间较长,更易导致食管炎发生。     

远端收缩积分和无效食管动力与胃食管反流的关系

目的探讨食管高分辨率测压（HRM）下远端收缩积分（DCI）和无效食管动力（IEM）与GERD 患者反流情况的关系。方法共纳入69例 GERD 患者，均完成食管 HRM、24 h pH 联合阻抗监测检查。应用 Pearson 相关分析研究 DCI、无效吞咽次数和 DeMeester 评分的相关性。根据10次5 mL液体吞咽试验发生无效吞咽的次数分成3组，5～10次无效吞咽为 IEM 组（21例），1～4次无效吞咽为动力异常组（19例），0次无效吞咽为动力正常组（29例），采用 t 检验比较3组平均 DCI、残余的有效吞咽 DCI 平均值、DeMeester 评分、酸反流时间、食团暴露时间、近端反流次数的差异。结果69例 GERD患者中，其10次5 mL 液体吞咽平均 DCI 和 DeMeester 评分呈负相关（r＝－0．363，P ＝0．003），无效吞咽次数和 DeMeester 评分呈正相关（r＝0．374，P ＝0．002）。动力正常组、动力异常组和 IEM 组10次5 mL液体吞咽平均 DCI 分别为（1458．96±545．10）、（986．48±577．50）和（288．50±167．25）mmHg·s·cm， IEM 组低于动力正常组和动力异常组（t＝－11．42、－2．12，P 均＜0．05）。动力正常组、动力异常组和IEM 组残余的有效吞咽 DCI 平均值分别为（1458．96±545．10）、（1187．90±669．40）和（450．78±350．73）mmHg·s·cm，IEM 组低于动力正常组和动力异常组（t＝－8．05、－5．27，P 均＜0．01）。IEM组的 DeMeester 评分为（15．42±8．79）分，高于动力正常组的（6．34±3．45）分，差异有统计学意义（t ＝2．43，P ＜0．05）。IEM 组的酸反流时间、食团暴露时间分别为（54．93±37．07）min、（0．64±0．49）％，分别长于动力异常组的（37．37±22．66）min、（0．52±0．24）％，动力正常组的（21．22±13．98）min、（0．39±0．14）％，差异均有统计学意义（t＝2．36、2．17，2．60、2．54，P 均＜0．05）。IEM 组和动力异常组的总反流次数分别为（67．10±32．94）、（57．26±38．90）次，均多于动力正常组的（44．61±23．84）次，差异均有统计学意义（t＝2．48、2．17，P 均＜0．05）。结论DCI 和无效吞咽次数在一定程度上可预测GERD 患者发生反流的情况，IEM 组食管体部收缩力度最弱，食管对反流物的廓清能力最差。     

食管动力学障碍不同亚型对胃食管反流病的影响

目的探讨食管动力学障碍不同亚型在胃食管反流病(gastroesophageal reflux disease,GERD)中的作用。方法收集40例GERD典型症状患者,全部行食管高分辨率测压(high-resolution manometry,HRM)和24 h食管动态p H阻抗监测,根据HRM结果,分为动力正常组、失蠕动收缩组、弱蠕动收缩组、间断收缩组。分析食管动力学障碍不同亚型及正常食管动力患者胃食管病理性反流情况。结果 40例典型GERD症状患者中动力正常组10例(25.0%),失蠕动收缩组11例(27.5%),弱蠕动收缩组19例(47.5%),间断收缩组30例(75.0%)。失蠕动收缩组及弱蠕动收缩组反流次数明显多于食管动力正常组(96.7±65.5、92.7±49.1 vs 69.5±31.3,P0.05),以弱酸反流(53.3±52.2、47.7±34.6 vs 20.3±15.3,P0.05)为主;而病理性酸暴露程度无明显差别。与食管动力正常组相比,间断收缩组患者总p H4时间(%)明显升高(8.4±3.9 vs 14.3±7.6,P0.05);De Meester评分有升高趋势,但差异无统计学意义(27.9±43.9 vs 50.6±60.6,P0.05)。结论食管收缩力差的患者更易出现反流次数增加且以弱酸反流为主;而食管收缩模式障碍的患者则与食管远端酸暴露更为相关。     

Upper esophageal motility disorders

This article begins with a summary of the anatomy and physiology of the upper esophageal region. The appropriate diagnostic tools used in the evaluation of upper esophageal motility disorders are then detailed including cineradiography, manometry, and other modalities. Specific clinical disorders associated with pharyngeal, UES, or upper esophageal dysfunction are described followed by a section on treatment.     

Physiology of normal esophageal motility

The esophagus consists of 2 different parts. In humans, the cervical esophagus is composed of striated muscles and the thoracic esophagus is composed of phasic smooth muscles. The striated muscle esophagus is innervated by the lower motor neurons and peristalsis in this segment is due to sequential activation of the motor neurons in the nucleus ambiguus. Both primary and secondary peristaltic contractions are centrally mediated. The smooth muscle of esophagus is phasic in nature and is innervated by intramural inhibitory (nitric oxide releasing) and excitatory (acetylcholine releasing) neurons that receive inputs from separate sets of preganglionic neurons located in the dorsal motor nucleus of vagus. The primary peristalsis in this segment involves both central and peripheral mechanisms. The primary peristalsis consists of inhibition (called deglutitive inhibition) followed by excitation. The secondary peristalsis is entirely due to peripheral mechanisms and also involves inhibition followed by excitation. The lower esophageal sphincter (LES) is characterized by tonic muscle that is different from the muscle of the esophageal body. The LES, like the esophageal body smooth muscle, is also innervated by the inhibitory and excitatory neurons. The LES maintains tonic closure because of its myogenic property. The LES tone is modulated by the inhibitory and the excitatory nerves. Inhibitory nerves mediate LES relaxation and the excitatory nerves mediate reflex contraction or rebound contraction of the LES. Clinical disorders of esophageal motility can be classified on the basis of disorders of the inhibitory and excitatory innervations and the smooth muscles.     

Intraluminal pH esophageal motility.

The aim of the present study was to investigate the effect of intraluminal pH on motor activity of the lower esophageal body. Liquid boluses of different pH values (7 to 2) were infused in the esophagus of 14 normal subjects during manometric recording of motor activity. Each test infusion elicited an esophageal motor response, either secondary peristalsis or simultaneous contractions. Secondary peristalsis was elicited by similar volumes of perfusates at pH 7, 6, 5, but significantly less volumes were needed with perfusates pH 4, 3, and 2. Simultaneous motor activity was not affected by intraesophageal pH value in the range investigated.     

Medical treatment of esophageal motility disorders

Swallowing is a complex mechanism that is based on the coordinated interplay of tongue, pharynx, and esophagus. Disturbances of this interplay or disorders of one or several of these components lead to dysphagia, non-cardiac chest pain, or regurgitation. The major esophageal motility disorders include achalasia, diffuse esophageal spasm, hypercontractile esophagus (nutcracker esophagus), and hypocontractile esophagus (scleroderma esophagus). Other esophageal diseases such as hypopharyngeal (Zenker's) diverticula or gastroesophageal reflux disease also may be sequelae of primary esophageal motility disorder. Finally, a substantial group of patients referred for evaluation of possible esophageal motor disorders have milder degrees of dysmotility—referred to as nonspecific esophageal motor disorder—that are of unclear clinical significance. Medical treatment of esophageal motility disorders involves the uses of agents that either reduce (anticholinergic agents, nitrates, calcium antagonists) or enhance (prokinetic agents) esophageal contractility. Despite the beneficial effect of the various drugs on esophageal motility parameters, the clinical benefit of medical treatment is often disappointing. From clinical and epidemiological studies there is some evidence for a psychological component in the pathogenesis or perception of esophageal symptoms. Further understanding of esophageal pathophysiology, as well as development of new receptor selective drugs, might increase our chances of successful treatment of esophageal motility disorders.     

Indices of esophageal motility in diabetics

A clinical-esophagomanometric study of 38 patients with diabetes mellitus has shown that a lowered tone of the inferior esophageal sphincter, a decrease in the amplitise and rate of esophageal peristalsis and the appearance of abnormal contractions (2- and 3-peak, spontaneous) in the esophageal body are typical of patients with diabetes mellitus complicated by neuropathy. Disorders of the esophageal motility should be taken into account while interpreting mechanisms of development of esophagitis, inflammatory processes in the bronchopulmonary system and retrosternal pains in diabetes patients.     

Effect of clarithromycin on esophageal motility

As clarithromycin (CLA), an antibiotic commonly used for Helicobacter pylori eradication, stimulates gastroduodenal motility, we investigated whether it also stimulates esophageal motility. In 15 normal subjects, esophageal motility was recorded using a low-compliance manometric system with two ports in the esophageal body, one port in the lower esophageal sphincter (LES), and five ports in the antroduodenal tract to monitor the occurrence of phases I-III of the migrating motor complex. Thirty minutes after the occurrence of a duodenal phase III, we infused intravenously, randomly, and in a double-blind manner, CLA 100 mg in five subjects (group A), CLA 250 mg in five subjects (group B), and normal saline in the remaining five subjects (group C). LES tone and post-deglutitive residual pressure, as well as the amplitude and duration of the esophageal contractions, were measured each minute and averaged over a post-infusion period of 30 min. Both group A and B showed a LES tone significantly higher than that of group C after CLA infusion, whereas the post-deglutitive residual pressure was not significantly different from that of group C. The LES tone of group B was significantly higher than that of group A. Group B, but not group A, showed a wave amplitude and duration significantly higher than that of group C. In conclusion, CLA is able to stimulate LES tone and esophageal contractions with a dose-related effect.     

Treatment of spastic esophageal motility disorders

Treatment of spastic motility disorders continues to be challenging.Therapeutic options remain limited due in part to our lack of understanding of the pathophysiology and significance of these disorders. Furthermore, most of therapeutic trials to date are hampered by the poorly designed nature of the study, including the small size of the trials and the lack of placebo arm. Most of the available information suggests that there seems to be an important dissociation between symptoms (chest pain/dysphagia) and esophageal dysmotility. Drug treatment aimed at visceral sensitivity seems more effective in relieving symptoms than spasmolytic medications. Recent trials with Botox, nitric oxide derivatives, and SSRIs offer promising results. Rigorous study design that includes large placebo-controlled trials is needed in this area.     

Analysis of clinical features and motility characteristics of ineffective esophageal motility

正Objective To clarify the correlation between the clinical characteristics,esophageal motility features and esophageal acid exposure in patients with ineffective esophageal motility (IEM).Methods From January 2016to March 2018,at Peking University First Hospital,22 IEM patients diagnosed by esophagus high-resolution