Esophageal peristaltic dysfunction in peptic esophagitis

Esophageal exposure to acid is a major determinant in the pathogenesis of reflux esophagitis. In this study, we analyzed the esophageal peristaltic function of 177 patients and asymptomatic volunteers for abnormalities that could lead to prolonged esophageal acid clearance. The subjects were divided into five groups: normal volunteers, patient controls, patients with noninflammatory gastroesophageal reflux disease, patients with mild esophagitis, and ones with severe esophagitis. Manometric data were analyzed for the occurrence of failed primary peristalsis, for the occurrence of feeble peristalsis in the distal esophagus, and for hypotensive lower esophageal sphincter pressure. From an analysis of the data on control patients, peristaltic dysfunction was defined as the occurrence of either failed primary peristalsis or hypotensive peristalsis in the distal esophagus for over half of the test swallows. Peristaltic dysfunction was increasingly prevalent with increasing severity of peptic esophagitis, occurring in 25% of patients with mild esophagitis and 48% of patients with severe esophagitis. A correlation did not exist between the occurrence of peristaltic dysfunction and hypotensive lower esophageal sphincter pressure (less than or equal to 10 mmHg). We conclude that peristaltic dysfunction occurs in a substantial minority of patients with peptic esophagitis and could contribute to increased esophageal exposure to refluxed acid material.     

Improvement in Esophageal Motor Dysfunction with Treatment of Reflux Esophagitis: A Report of Two Cases

We report two patients with reflux esophagitis who had decreased lower esophageal sphincter pressures and marked decreased frequency of peristaltic response to swallowing and peristaltic amplitude on pretreatment esophageal motility tracings. Both patients responded to medical therapy of reflux esophagitis with symptomatic clinical improvement, increased lower esophageal sphincter pressures, and increased frequency of peristaltic propagation and amplitude of peristalsis. Measures to treat reflux esophagitis may he effective in some cases, in part, because they permit healing of esophageal inflammation to improve esophageal motor activity, the latter which results in improvement of esophageal acid clearing.     

轻度反流性食管炎与非糜烂性反流病远端食管酸暴露和食管动力学变化

目的:探讨轻度反流性食管炎(RE)与非糜烂性反流病(NERD)食管远端酸暴露及食管动力变化特点.方法:符合洛杉矶诊断标准的RE30例(LA-A16例,LA-B14例),NERD16例,健康对照组10例被纳入本研究,所有患者及对照组均接受24h食管pH监测及压力测定,比较食管pH监测及测压结果.结果:LA-A组、LA-B组、NERD组DeMeester评分明显高于对照组,差异显著(P<0.05).LA-A组与NERD组比较DeMeester评分无明显差异,但NERD组的立位反流时间百分比与长反流周期数多于LA-A组,差异显著;LA-B组DeMeester评分比LA-A组和NERD组明显增高,LA-B组与LA-A组比较食管pH监测各项指标均存在明显差异.LA-A组、NERD组及对照组比较下食管括约肌静息压(LESP)、食管体部蠕动波幅度(PA)无显著差异,LA-A组和NERD组食管下段PA有增高趋势;LA-B组与LA-A组、NERD组及对照组比较LESP明显降低(P<0.05),LA-B组食管下段PA明显低于LA-A组(P<0.05).RE组无效食管运动(IEM)明显高于对照组,差异显著.结论:轻度RE(LA-B)与NERD远端食管酸暴露存在差异.DeMeester评分、LES功能不全及食管蠕动功能障碍与RE的严重程度呈正相关.LES功能不全及食管蠕动功能障碍可能不是轻度RE(LA-A)及NERD的主要致病因素.IEM与RE关系密切,且与RE有关的食管动力异常主要为IEM.     

Healing of severe reflux esophagitis with PPI does not improve esophageal dysmotility

Esophageal dysmotility is frequently associated with gastroesophageal reflux disease (GERD). The aim of this study was to investigate the relationship between the severity of reflux esophagitis and esophageal dysmotility and evaluate the effect of prolonged treatment with proton pump inhibitor (lansoprazole 30 mg/day) on esophageal motility in patients with severe reflux esophagitis associated with esophageal motility disorder. Twelve healthy subjects (HS) and 100 patients with reflux disease were involved in the study consisting of two parts: (i) comparison of esophageal motility in HS and patients with non-eroseive reflux disease (NERD), mild esophagitis and severe esophagitis; (ii) effect of 3-6 months lansoprazole therapy on esophageal motility in 23 patients with severe esophagitis, pathologic acid reflux and esophageal peristaltic dysfunction. Results included the following. (i) Esophageal dysmotility was noted in both patients with NERD and erosive GERD. (ii) Severe esophagitis was associated with severe esophageal dysmotility. (iii) Healing of severe esophagitis did not improve esophageal dysmotility. The resting lower esophageal sphincter pressure was 3.9 mmHg (range 1.7-20) before treatment and 4.8 mmHg (range 1.2-18.3) after esophagitis healing (P = 0.23, vs. before treatment), the amplitude of distal esophageal contraction was 28.8 mmHg (range 10.9-80.6) before treatment and 33.3 mmHg (range 10.0-72.5) after esophagitis healing (P = 0.59, vs. before treatment) and the frequency of failed peristalsis was 70% (range 0-100%) before treatment and 70% (range 0-100%) after esophagitis healing (P = 0.78, vs. before treatment). Both esophageal motility disorders and acid reflux play important roles in the mechanism of GERD, especially in severe esophagitis. Esophageal dysmotility is not secondary to acid reflux and esophagitis; it should be a primary motility disorder.     

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。     

Esophagitis in progressive systemic scleroderma. Prevalence and risk factors in forty-six patients]

Forty-six patients with progressive systemic sclerosis (37 women and 9 men) were successively evaluated by endoscopy, manometry, and esophageal pH monitoring. Fourteen patients (30.4 percent) had erosive esophagitis. Twenty-four patients were symptomatic; nineteen patients complained of dysplagia. Erosive esophagitis was significantly more frequent in symptomatic patients than in asymptomatic patients (50.0 percent vs 9 percent, P less than 0.01) and especially in patients complaining of dysphagia (57.9 percent vs 11.1 percent, P less than 0.01). Erosive esophagitis was not correlated with symptoms of gastroesophageal reflux. Abnormal esophageal motility was found in 34 patients (73.9 percent). Occurrence of erosive esophagitis was not linked with esophageal dysmotility. In patients with erosive esophagitis lower esophageal sphincter pressures were significantly lower than those in patients without erosive esophagitis. Twenty-four hr-pH monitoring showed pathological gastroesophageal reflux in 20 patients (43.5 percent). Erosive esophagitis was more frequent in patients with pathological gastroesophageal reflux than in patients with normal gastroesophageal reflux (50.0 percent vs 15.4 percent, P less than 0.02) especially in patients with pathological supine nighttime gastroesophageal reflux (61.5 percent vs 18.2 percent, P less than 0.01). Our data suggest that symptoms, dysphagia, diminished lower esophageal sphincter pressures, and pathologic nighttime gastroesophageal reflux are reliable predictors of the presence of erosive esophagitis in patients with progressive systemic sclerosis.     

Aging and esophageal motility in patients with gastroesophageal reflux disease

BACKGROUND: Alterations of esophageal contractions may worsen the esophageal lesions caused by gastroesophageal reflux. The impairment of the contractions may be localized only in the distal esophagus or in the entire esophageal body, and may be worse with the aging process. AIMS: To evaluate the proximal and distal esophageal contractions in patients with gastroesophageal reflux symptoms with or without esophagitis. PATIENTS AND METHODS: We studied esophageal motility in 104 patients with gastroesophageal reflux symptoms, 42 with normal esophageal endoscopic examination, 47 with mild esophagitis and 15 with severe esophagitis. The esophageal contractions were measured by the manometric method at 2, 7, 12 and 17 cm from the upper esophageal sphincter, after five swallows of a 5 mL bolus of water. RESULTS: The amplitude and area under the curve of contractions were lower in patients with severe esophagitis than in patients without esophagitis or with mild esophagitis in the distal part of the esophageal body (17 cm from the upper esophageal sphincter). In the proximal esophageal body there was no difference in amplitude or area under the curve. In the entire esophageal body there was no difference between the three groups of patients in duration, velocity of peristaltic contractions, or proportion of failed, simultaneous, non-propagated or peristaltic contractions. There was no difference between the patients with less than 50 years or with more than 50 years of age. CONCLUSIONS: Patients with severe esophagitis had lower distal esophageal contraction amplitude than patients without esophagitis or with moderate esophagitis. There was no effect of aging on esophageal contractions.     

Esophageal motility and gastric acid secretion in patients with Barrett's esophagus

Patients with Barrett's esophagus (BE) usually have low resting lower esophageal sphincter (LES) pressure, and also have impaired esophageal body motility, with low amplitude and failed peristaltic contractions on swallowing being common. These motor abnormalities contribute to excessive esophageal acid exposure in patients with BE. However, gastric acid secretion is not different between patients with BE and reflux esophagitis.     

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.     

Peristaltic dysfunction associated with nonobstructive dysphagia in reflux disease

An evaluation was done of 325 consecutive patients who underwent esophageal manometry to investigate the relationship between solid food dysphagia and peristaltic dysfunction in gastroesophageal reflux disease. All patients with dysphagia were endoscoped to evaluate for mechanical obstruction. Manometry was done focusing on the incidence of peristaltic dysfunction (failed peristaltic sequences or sequences characterized by foci of hypotensive peristalsis). The major finding was that the severity of manometrically demonstrated peristaltic dysfunction in reflux patients correlated with the prevalence of dysphagia. After excluding patients with esophageal rings or strictures from the analysis, the overall prevalence of dysphagia was 39% among the 157 reflux patients. Within this group, 29% of patients with minimal peristaltic dysfunction experienced dysphagia compared to 78% of patients with severe peristaltic dysfunction. We conclude that peristaltic dysfunction should be considered along with mechanical obstruction as a potential cause of dysphagia in patients with gastroesophageal reflux disease.     

Nonobstructive Dysphagia in Reflux Esophagitis

Dysphagia in the absence of organic esophageal stricture may occur in patients with reflux esophagitis. Although the exact mechanism of this "nonobstructive dysphagia" (NOD) is not known, it is believed to be related to transient segmental esophageal motor disorder. The goals of this study were to determine the frequency of NOD in patients with reflux esophagitis and correlate it with esophageal pH and motility changes. Sixty-three consecutive patients with symptoms of esophageal dysfunction were studied with endoscopy, infusion esophageal manometry, and 24-h ambulatory esophageal pH monitoring. Forty-seven had severe erosive esophagitis unresponsive to medical therapy; 16 with esophageal motility disorders were used as symptomatic controls. Twenty-eight of 63 patients studied experienced NOD during the 24-h pH study; 22 had esophagitis and six had esophageal dysmotility without esophagitis. NOD was noted with similar frequency in the two groups; 22/47 (46.8%) of patients with esophagitis and 6/16 (37.5%) with esophageal dysmotility experienced NOD during the period of study. NOD correlated with pH less than 4.0 in 88.6% of patients with esophagitis but in only 7% of patients with esophageal dysmotility (p less than 0.001). There was no difference in acid reflux patterns in esophagitis patients who experienced NOD (22/47), and in those who did not (25/47). There was no correlation between NOD and baseline esophageal motility abnormalities. In summary, 1) NOD is a common, intermittent symptom that occurred in up to 46.8% of esophagitis patients and 37.5% of symptomatic controls during the 24-h period of this study; 2) NOD correlates with esophageal pH less than 4.0 in patients with esophagitis and not in patients with esophageal dysmotility. These data strongly suggest that acid in the distal esophagus frequently triggers the sensation of dysphagia in esophagitis patients, but not in patients with esophageal motility disorders. Combined ambulatory intraesophageal motility and pH monitoring may further elucidate the mechanism of dysphagia in these patients.     

Lack of effect of metoclopramide and domperidone on esophageal peristalsis and esophageal acid clearance in reflux esophagitis

The acute effects of oral metoclopramide (40 mg/day) and domperidone (80 mg/day) on esophageal motor activity and acid reflux were assessed in a randomized, double-blind, placebo-controlled study in 20 patients with erosive reflux esophagitis. Esophageal motor function was assessed by standard manometry with wet swallows, and reflux events were evaluated by ambulatory 24-hr pH-monitoring. Both drugs caused a significant (P less than 0.05) increase in lower esophageal sphincter pressure lasting at least 120 min. However, neither esophageal body motility, duration of esophageal exposure to acid, nor esophageal clearance were effected by drug administration in comparison to placebo. Side effects were reported in two patients who received metoclopramide, while no adverse effects occurred after domperidone intake. In conclusion, the so-called motility agents metoclopramide and domperidone have few acute effects on esophageal motility in patients with erosive reflux esophagitis.     

The importance of hiatal hernia in reflux esophagitis compared with lower esophageal sphincter pressure or smoking.

The characteristics of gastroesophageal reflux disease have not been adequately defined. To determine the influence on the esophageal mucosa of hiatal hernia, lower esophageal sphincter pressure, acid reflux, and cigarettes and alcohol, we studied the reflux parameters, smoking habits, and alcohol consumption of 184 healthy, ambulatory outpatients who received endoscopy as the initial diagnostic procedure for workup of gastroesophageal reflux. Patients received endoscopic and histologic evaluations of the esophageal mucosa, prolonged ambulatory esophageal pH monitoring, and esophageal manometric determinations. Structural analysis was used to test the plausibility of various clinical theories concerning the most important factors contributing to the development of esophagitis. Statistical analyses revealed the following: (a) the lower esophageal sphincter pressure, acid contact time, and frequency of reflux episodes were highly associated with the presence of a hiatal hernia (p less than 0.003 for all parameters); (b) individuals with esophagitis had 16.5 times as many hiatal hernias as found in normal, healthy people; (c) cigarette smoking was not correlated with esophagitis but was significantly associated with increased lower esophageal sphincter pressure (r = 0.18; p less than 0.03); and (d) smoking was also not associated with increased acid contact time or increased frequency of reflux episodes. We conclude that (a) the presence of a hiatal hernia, not the pressure of the lower esophageal sphincter, is the most important predictor of reflux frequency, acid contact time, and esophagitis; (b) a decreased lower esophageal sphincter pressure, as suggested by structural analysis, is unlikely to be the cause of increased reflux episodes or esophagitis; and (c) if smoking and lower esophageal sphincter pressure are factors in the development of esophagitis, they damage the esophageal mucosa by mechanisms other than increased frequency of reflux episodes or increased acid contact time.     

Gastroesophageal reflux as a pathogenic factor in the development of symptomatic lower esophageal rings

Gastroesophageal reflux (GER) has been suggested as a cause of the lower esophageal (Schatzki) ring. We looked for the presence of GER and reflux injury in a series of 20 patients with lower esophageal ring and dysphagia, using a 24-hour esophageal pH monitoring and upper endoscopy with biopsy. Abnormal GER was documented in 13 of the patients (65%), 10 of whom had erosive reflux changes in the distal esophagus. Seven patients (35%) showed no evidence of pathologic GER or reflux esophagitis. All patients also underwent esophageal manometry. Nonspecific esophageal body motor dysfunction may have contributed to dysphagia in five patients, two of whom had no evidence of abnormal GER. We conclude that GER disease is a frequent cause of the gradually progressive ring stricturing and dysphagia seen in patients with lower esophageal ring. Antireflux therapy, as an adjunct to esophageal dilatation, may be appropriate for many symptomatic lower esophageal ring patients.     

Ambulatory esophageal pressure and pH monitoring in patients with high-grade reflux esophagitis

Using conventional manometry and 24-hr ambulatory pressure and pH monitoring, we investigated esophageal motility and the esophageal motor response to reflux in 11 patients with reflux esophagitis Savary-Miller grade III and IV, and an age- and sex-matched group of 11 healthy controls. The patients had a significantly increased esophageal acid exposure. Conventional manometry showed a significantly decreased LES pressure and distal peristaltic amplitude in patients. The 24-hr monitoring yielded a significant decrease in peristaltic contraction duration and peristaltic propagation velocity in the patient group. Distal peristaltic amplitude was not decreased. Analysis of the contractions occurring in the 2-min period after each reflux episode showed a reduced number of contractions during the upright period, caused by a significantly decreased number of peristaltic contractions. During the supine period, there was a trend towards an increased number of contractions. It is concluded that esophageal motor activity and the response to reflux are impaired in patients with high-grade reflux esophagitis. However, the abnormalities found are only minor and are unlikely to play an important role in the pathogenesis of reflux esophagitis.     

Physiological studies on nitric oxide in the lower esophageal sphincter of patients with reflux esophagitis

BACKGROUND/AIMS: Nitric oxide has recently been shown to be a neurotransmitter in the non-adrenergic non-cholinergic inhibitory nerves in the digestive tract. To clarify the significance of nitric oxide in the lower esophageal sphincter of patients with reflux esophagitis, we have investigated enteric nerve responses in lower esophageal sphincter specimens obtained from the patients with gastric cancer who had reflux esophagitis, using the normal lower esophageal sphincter as a control. METHODOLOGY: Lower esophageal sphincter specimens were obtained from 6 patients who had gastric cancer with reflux esophagitis, and normal lower esophageal sphincter specimens were obtained from 12 patients who had gastric cancer without gastroesophageal reflux disease. A mechanograph was used to evaluate in vitro lower esophageal sphincter muscle responses to electrical field stimulation of the adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers, and NG-nitro-L-arginine and L-arginine. RESULTS: 1) Cholinergic nerves were more dominant in the normal lower esophageal sphincter than in the lower esophageal sphincter with reflux esophagitis (p < 0.01); 2) non-adrenergic non-cholinergic inhibitory nerves were significantly found to act more on the lower esophageal sphincter with reflux esophagitis than those in the normal lower esophageal sphincter (p < 0.01); 3) nitric oxide mediates the relaxation reaction via non-adrenergic non-cholinergic inhibitory nerves in the normal lower esophageal sphincter and the lower esophageal sphincter with reflux esophagitis; 4) The relaxation reaction of nitric oxide was observed in the normal lower esophageal sphincter and increased in the lower esophageal sphincter with reflux esophagitis. CONCLUSIONS: These findings suggest that the cholinergic and non-adrenergic non-cholinergic inhibitory nerves play important roles in regulating contraction and relaxation of the human lower esophageal sphincter, and nitric oxide plays an important role in non-adrenergic non-cholinergic inhibitory nerves of the human lower esophageal sphincter. In addition, a decrease of the action of cholinergic nerves and an increase of the action of non-adrenergic non-cholinergic inhibitory nerves by nitric oxide may be largely related to the low lower esophageal sphincter pressure observed in the patients with reflux esophagitis.     

Transient Lower Esophageal Sphincter Relaxations and Esophageal Body Muscular Contractile Response in Reflux Esophagitis

In patients with gastroesophageal reflux disease (GERD), transient lower esophageal sphincter relaxations (TLESRs) are more frequently accompanied by acid reflux than in normals. The role of esophageal tone during gastroesophageal reflux events is unknown. We studied the tonic motor activity in the body of the esophagus during TLESRs with and without acid reflux in 11 patients with erosive esophagitis and compared the results with those previously obtained in healthy subjects. Esophageal peristaltic contractions were recorded 13, 8, and 3 cm above a sleeve that measured LES pressure. An intraluminal balloon was inflated 8 cm above the sleeve to induce an esophageal tonic contraction [artificial high pressure zone (HPZ)]. The percentage of TLESRs with acid reflux was significantly higher in patients with esophagitis than in healthy controls (58.3% vs 37.3%, P < 0.05). TLESRs per se were not associated with an inhibition or increase in esophageal body contractility, which, however, changed substantially immediately after reflux. In patients with esophagitis the esophageal body tonic contractility was inhibited in 59.5% of TLESRs vs 36% in controls (P < 0.05). Esophageal contractions during TLESRs traveled down the esophagus in 77% of the instances in patients vs 96.5% in controls (P < 0.05). In conclusion, gastroesophageal reflux during TLESRs was more frequently associated with inhibition of esophageal body tonic contractility in patients with esophagitis than in normals. The different response of the esophageal body to reflux observed in GERD patients may partially contribute to the higher prevalence of reflux during TLESRs in these patients.     

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。     

胆碱能神经对反流性食管炎食管动力的影响

目的研究内源性胆碱能神经在反流性食管炎食管动力机制异常中的作用.方法经下食管括约肌切开制备反流性食管炎的猫模型,用连续水灌注测压系统检测正常猫及反流性食管炎的猫食管体部动力;用分光光度法分别测定正常猫及反流性食管炎的猫食管中段、远段肌组织中的乙酰胆碱转移酶和乙酰胆碱酯酶活力.结果反流性食管炎组食管远段平均收缩波幅度明显低于正常对照组(P＜0.0001),食管远段传导速度低于正常对照组(P＜0.05);反流性食管炎时食管中段及远段肌组织中乙酰胆碱转移酶活力均低于正常对照组的中段及远段(P＜0.05及P＜0.0001),以远段更明显(P＜0.0001).反流性食管炎组食管中段及远段肌组织中的乙酰胆碱酯酶活力与对照组比较差异均无显著性(P＞0.05).结论反流性食管炎可导致食管远段动力低下,内源性胆碱能神经功能异常是其重要机制之一.     

Esophageal striated muscle contractions in patients with gastroesophageal reflux symptoms

Although there are studies showing that the amplitude of contraction in the distal esophageal body may be lower in gastroesophageal reflux (GER) disease than in asymptomatic subjects, there are no data about proximal striated muscle contraction in this disease. We studied the esophageal contraction 2 or 3 cm below the upper esophageal sphincter in response to swallowing a 5-ml bolus of water in 122 consecutive patients submitted to esophageal manometry who complained of heartburn and acid regurgitation. Sixty-nine had esophagitis seen at endoscopy. Thirty-three also complained of dysphagia. No patients had esophageal stenosis, esophageal motility abnormalities in distal esophagus, chest pain, or extraesophageal manifestations of GER. We also studied 20 patients with systemic sclerosis (SSc), a disease with no involvement of striated muscle. When we measured the amplitude, duration, and area under the curve (AUC) of the proximal esophageal contraction, we did not find any differences (P > 0.05) between patients with esophagitis (N = 69) or without esophagitis (N = 53), with dysphagia (N = 33) or without dysphagia (N = 89), with mild (N = 55) or severe (N = 14) esophagitis, or younger than 40 years (N = 45) or older than 60 years (N = 19). There was also no difference between patients with GER symptoms and patients with SSc (P > 0.05). We conclude that patients with GER symptoms with or without esophagitis and with or without dysphagia have similar esophageal striated muscle contractions.