Esophageal motility disorders with thoracic pain of unknown origin

35 patients with angina-like chest pain underwent esophageal manometry after a coronary artery disease had been ruled out by angiography. Furthermore, patients after gastric or esophageal surgery, with pathologic upper gastrointestinal endoscopy or with pathologic gastroesophageal reflux as seen on 24-hour-pH-metry were excluded from this study. 29 out of 35 patients (83%) had a normal manometric study, six patients (17%) had a motility disorder; five of these showed an unspecific dismotility pattern and were asymptomatic while the study was done; only one patient presented with esophageal spasm. Since only this latter patient was symptomatic while the study was done, a correlation between symptoms and this motility disorder seems likely. --If pathologic gastroesophageal reflux has been ruled out, esophageal manometry can establish a diagnosis in only 3% of patients with angina-like chest pain without esophageal symptoms (dysphagia, odynophagia, heartburn or regurgitation). We conclude that this complicated examination should not be done in these patients.     

Esophageal motility disorders

Esophageal motility disorders consist of a complex array of disturbances in normal esophageal function associated with dysphagia, gastroesophageal reflux, and noncardiac chest pain. A thorough knowledge of normal esophageal anatomy and physiology is important to a full understanding of these motility derangements. Through a complicated interaction of neuromuscular and hormonal influences, the voluntary act of swallowing transforms into an automated sequence of peristaltic waves propelling food and liquids into the stomach in concert with coordinated relaxation of the sphincters. Anatomic and physiologic barriers exist within the esophagus protecting against gastroesophageal reflux and aspiration. With improvements in diagnostic tools such as barium contrast radiography, scintigraphy, pH measurements, and esophageal manometrics with provocative testing, motility disorders have become better defined and understood. Primary motility disorders consist of achalasia, diffuse esophageal spasm (DES), "nutcracker esophagus," hypertensive lower esophageal sphincter, and nonspecific esophageal motility dysfunction (NEMD). A host of secondary and miscellaneous motility disorders also affect the esophagus, including scleroderma and other connective tissue diseases, diabetes mellitus, Chagas' disease, chronic idiopathic intestinal pseudo-obstruction, and neuromuscular disorders of striated muscle. Gastroesophageal reflux disease (GERD) may also be promoted by associated motility disturbances. Treatment modalities include surgical myotomy; dilatation; and pharmacologic manipulations, including use of nitrates, calcium-channel blockers, H2-blockers, and psychotropic drugs where appropriate.     

Management of diffuse esophageal spasm with balloon dilatation

Of 1200 patients referred to the esophageal laboratory at Guy's Hospital for investigation of suspected esophageal motility disorders, 61 (5.1%) were diagnosed as diffuse esophageal spasm. Twenty of these patients whose symptoms were severe did not respond to conservative treatment and were treated by balloon dilatation. Results were good in 14 and poor in six patients, which included one esophageal perforation. Diffuse esophageal spasm was diagnosed where more than 30% nonperistaltic activity was demonstrated by manometry. Lower esophageal sphincter pressure and relaxation were normal in all cases except one. Gastroesophageal reflux was present in four of five poor responders who were examined by 24-h ambulatory pH monitoring, and in only one of 10 good responders. Three of the six patients in whom balloon dilatation was successful proceeded to full-length myotomy, with relief of symptoms in two. The indications for, and results of, balloon dilatation in this condition are discussed, and a new radiological sign is described.     

Primary esophageal motility disorders

Esophageal motility disorders often manifest with chest pain and dysphagia. Achalasia is a disorder of the lower esophageal sphincter and the smooth musculature of the esophageal body. In achalasia the lower esophageal sphincter typically fails to relax with swallowing, and the esophageal body fails to undergo peristalsis. In contrast to spastic disorders of the esophagus, achalasia can be progressive and cause pronounced morbidity. Pseudoachalasia mimics achalasia in terms of symptoms but can be caused by infectious disorders or malignancy. Treatment for achalasia is nonstandardized and includes medical, endoscopic, and surgical options. Spastic disorders of the esophagus, such as diffuse esophageal spasm and nutcracker esophagus, and nonspecific esophageal motility disorder are benign and nonprogressive, with similar findings on esophageal manometry. Although the exact cause remains unknown, these disorders may represent a manifestation of gastroesophageal reflux disease. Treatment of spastic disorders includes medical and surgical approaches and is aimed at symptomatic relief.     

Esophageal dysmotility in patients who have eosinophilic esophagitis

The understanding of esophageal motility alterations in patients who have eosinophilic esophagitis (EE) is in its infancy despite the common presenting complaint of dysphagia. A diversity of motility disorders has been reported in patients who have EE including achalasia, diffuse esophageal spasm, nutcracker esophagus, and nonspecific motility alterations including high-amplitude esophageal body contractions, tertiary contractions, abnormalities in lower esophageal sphincter pressure, and other peristaltic problems. Some evidence suggests that treatment of EE will improve motility. Technological advances such as high-resolution manometry and combined manometry with impedance may provide new insight into more subtle motility abnormalities.     

Esophageal chest pain

Recurrent chest pain frequently results in significant disability and anxiety, even after cardiac disease has been excluded. A stepwise approach is recommended for the diagnosis of pulmonary conditions, musculoskeletal disorders and structural problems of the upper gastrointestinal tract that can produce chest pain. If a search for these disorders proves negative, an esophageal source of chest pain should be strongly suspected. Although gastroesophageal reflux disease is the most common and easily treated cause of esophageal chest pain, esophageal motility disorders should also be considered. Motility disorders include achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal sphincter and nonspecific motility disorders.     

Inflammation and oxidative stress in gastroesophageal reflux disease

The etiology of esophageal mucosal injury is complex, since it may involve the reflux of gastric acid, bile acid, and pancreatic juice, external factors such as drugs and alcohol, or functional factors such as esophagogastric motility. The mechanism of esophageal mucosal injury has gradually been understood at the molecular biological level. It is particularly important that pro-inflammatory factors, such as inflammatory cytokines (interleukin-6 and -8), leukocytes and oxidative stress, have been demonstrated to be involved in the development of gastroesophageal reflux disease (GERD) including nonerosive reflux disease (NERD). In addition, nociceptors such as acid-sensitive vanilloid receptors, protease-activated receptors and substance P have also been implicated in the pathogenesis of neurogenic inflammation in NERD patients with esophageal hypersensitivity. The development of new therapy with anti-inflammatory and anti-oxidant effects is expected to assist in the treatment of intractable NERD/GERD and the prevention of carcinogenesis.     

24h食管pH监测和食管测压及奥美拉唑治疗试验在食管原性胸痛中的应用

目的 :探讨 2 4 h食管 p H监测和食管测压及奥美拉唑治疗试验在食管原性胸痛中的诊断价值。方法 :对食管原性胸痛 6 8例行内镜、食管测压、2 4 h食管 p H监测及 7d的奥美拉唑 (2 0 mg,2次 / d)治疗试验 ,治疗后症状评分比治疗前降低超过 75 %者则为治疗试验阳性。结果 :食管原性胸痛 6 8例中 5 5例 (81% )符合胃食管反流病 (GERD) ,胡桃夹食管 2例 ,早期贲门失驰缓症 3例 ,弥漫性食管痉挛 3例 ,无效食管运动 (IEM) 5例。GERD5 2例测压分析 ,35例(6 7% )符合 IEM诊断标准。奥美拉唑治疗试验对诊断 GERD的敏感性为 93% ,特异性为 85 %。结论 :GERD是食管原性胸痛的主要原因。 2 4 h食管 p H监测和食管测压是诊断食管原性胸痛的主要检查手段 ,奥美拉唑治疗试验是临床诊断GERD简便而实用的方法。     

Cervical esophageal webs: association with gastroesophageal reflux

Background: We investigated whether there is a significant association between cervical esophageal webs and gastroesophageal reflux on pharyngoesophagography. Methods: We studied 50 patients with cervical esophageal webs on pharyngoesophagrams and 50 control subjects. The control group was matched to the webs group for age, sex, and symptomatology. Patients with cervical esophageal webs and controls were compared to determine the prevalence of gastroesophageal reflux, hiatal hernias, reflux esophagitis, and abnormal esophageal motility. Pearson's chi-square test was used to determine any statistically significant differences in the frequencies of these findings between groups. Results: Thirty-nine (78%) of 50 patients with cervical esophageal webs versus 27 (54%) of 50 patients in the control group had gastroesophageal reflux (p = 0.01). When patients were classified based on degree of gastroesophageal reflux, 22 (44%) of 50 patients with cervical esophageal webs versus 21 (42%) of 50 controls had mild reflux (p = 0.84), whereas 17 (34%) of 50 patients with webs versus six (12%) of 50 controls (p < 0.009) had moderate/marked reflux. Thus, the prevalence of moderate/marked gastroesophageal reflux was significantly greater in patients with webs than in the controls. However, no significant differences were found in the prevalence of mild gastroesophageal reflux, hiatal hernias, reflux esophagitis, or abnormal esophageal motility. Conclusion: We found a significant association between cervical esophageal webs and gastroesophageal reflux independent of age, sex, or symptomatology. Radiologists should be aware of this association, so that patients with cervical esophageal webs on pharyngoesophagography are evaluated for gastroesophageal reflux at the time of the barium study or advised to undergo further testing for gastroesophageal reflux disease. Received: 15 December 2000/Accepted: 24 January 2001     

功能性消化不良者心理因素与食管动力的关系

目的探讨心理因素与功能性消化不良(FD)食管动力的关系。方法使用高分辨率旁道灌注测压系统对20例健康对照组及121例FD进行食管动力测定,同时以焦虑自评量表及抑郁自评量表评定两组的心理状态,并观察食管动力与心理状态的联系。结果9.8%(24/121)的FD患者有食管动力障碍,主要表现为非特异性食管动力障碍70.8%(17/24);胡桃夹食管2例、弥漫性食管痉挛5例;60.7%(73/121)的FD者有心理障碍,其中抑郁障碍38.0%(46/121)、焦虑障碍48.8%(59/121),对照组1例有轻度的抑郁障碍,P<0.01。有心理障碍FD者食管动力障碍发生率(26.0%,19/73)比非心理障碍FD者(10.4%,5/48)显著增高(P<0.05),且前者LES压力、食管体蠕动波幅、持续时间均显著高于后者(P<0.05)。结论食管动力障碍是FD重要功能紊乱之一,长期抑郁或焦虑可能影响FD食管动力。     

Gastroesophageal reflux disease in diabetic patients

Esophageal dysfunctions occur frequently in patients with diabetic autonomic neuropathy, and the complication of gastroesophageal reflux disease (GERD) has also been reported. However, the characteristics of the GERD complicated with diabetes are obscure, because no detail assessment was performed. We recorded esophageal motility and acid reflux simultaneously in diabetic patients, and the correlation between esophageal dysfunction and diabetic neuropathy was examined. Esophageal dysfunctions including GERD were significantly related to diabetic motor neuropathy. Although the GERD is frequently complicated with diabetes, the symptoms are not apparent in diabetic patients. Therefore, physicians treating diabetic patients should have GERD in mind regardless of the symptoms. We also examined the effect of aldose reductase inhibitor (ARI) on the esophageal dysfunction in diabetic patients. Significant improvement of gastroesophageal reflux and esophageal motility were observed in diabetic patients by ARI treatment. ARI may be useful for the treatment of GERD complicated with diabetes.     

Diagnosis and treatment of esophageal motility disorders

Apart from gastroesophageal reflux disease, achalasia, non-cardiac chest pain and functional dysphagia are the most important manifestations of disturbed esophageal motility. Achalasia is characterized by esophageal aperistalsis and impaired deglutitive relaxation of the lower esophageal sphincter. The morphological correlate is a degeneration of nitrergic neurons in the myenteric plexus. Diagnosis is based on barium esophagram or esophageal manometry with the latter setting the gold standard. Endoscopic exclusion of a tumor at the gastroesophageal junction is mandatory. Appropriate therapeutic interventions are pneumatic dilatation or (laparoscopic myotomy) of lower esophageal sphincter. In patients unfit for these procedures endoscopic injection of botulinum toxin into the lower esophageal sphincter is appropriate. Non-cardiac chest pain may be of esophageal origin. Gastroesophageal reflux, spastic motility disorders and visceral hypersensitivity are arguable underlying mechanisms. The most important diagnostic procedure is 24 h esophageal pH metry correlating symptoms and reflux episodes. Proton pump inhibitors and tricyclic antidepressants serving as visceral analgesics are appropriate therapeutic approaches. Functional dysphagia defines the sensation of impaired passage without mechanical obstruction or a neuromuscular disease with known pathology, e.g. scleroderma. Impaired transit is proven by esophageal scintigraphy or radiogram both using solid boluses. Manometry assesses the underlying mechanisms.     

Pathophysiology of GERD: mechanisms of gastroesophageal reflux and prolonged esophageal acid exposure time

GERD is characterized by excessive esophageal acid exposure time. This suggests that either the rate of gastroesophageal reflux (GER) is higher and/or that the esophageal acid clearance time is longer. Transient LES relaxation (TLESR) is the single most common mechanism underlying GER in both normal subjects and patients with GERD. Whether or not the rate of TLESRs is higher in patients with GERD remains unclear. It is in the sitting or upright position that acid reflux mainly occurs, however, there seems to be no difference in the rate of TLESRs between both groups. The rate of TLESRs accompanied by acid reflux has been consistently shown to be significantly greater in patients with GERD than in normal subjects. Other mechanisms of reflux in patients with severe GERD are a hypotensive LES and ineffective esophageal motility which is found in severe GERD and which impairs bolus clearance of acid and thus increases acid contact time with the esophageal mucosa.     

Pathophysiology of gastroesophageal reflux disease: motility factors

Reflux esophagitis (RE) is characterized by excessive esophageal acid exposure. The number of acid reflux episodes, the way acid comes up after reflux and the delay of acid bolus clearance cause excessive esophageal acid exposure. Transient lower esophageal sphincter relaxation(TLESR) is the major mechanism of acid reflux in both healthy subjects (HS) and in patients with acid reflux disease, but there is no difference in the rate of TLESRs or in the rate of acid reflux during TLESRs above the LES between HS and patients with severe RE. In patients with severe RE, refluxed acid above the LES rises more easily to the proximal esophagus but it does not clear easily from the esophagus when compared with HS. The pathophysiology of non-erosive reflux disease (NERD) is poorly understood, however with regard to esophageal motility in patients with NERD, the LES pressure, the pressure wave amplitude and the rates of successful primary peristalsis were similar to that of HS but the triggering of secondary peristalsis was defective. This may lead to prolonged contact time between refluxed gastric acid and esophageal mucosa thereby leading to symptoms.     

Lansoprazole-induced improvement of esophageal submucosal injury

The proton pumpvinhibitor, lansoprazole, is reported to have acid secretion inhibiting effect as well as anti-inflammatory effects such as inhibition of cytokine secretion from inflammatory cells. Clinically, excellent efficacy of lansoprazole is reported for not only gastric ulcer but also gastroesophageal reflux disease (GERD). Since GERD is categorized endoscopically into erosive esophagitis and non-erosive reflux disease, it is important to make accurate assessment of any improvement in the inflammatory process when using endoscopic ultrasonography (EUS) capable of visualizing the submucosal structure. We report here our experience in assessing the effect of treatment with lansoprazole on esophageal wall structure using EUS in patients with GERD. At baseline (before treatment), EUS showed abnormalities in the mucosa, submucosa and muscularis propria caused by inflammation, thickening of the entire esophageal wall and changes in the contractile properties of esophageal smooth muscles reflecting the effects of inflammation on the entire wall of the lower esophagus in reflux esophagitis regardless of whether it is erosive or endoscopically-negative. Treatment with lansoprazole resulted in normalization of esophageal wall structure and improvement of motility, suggesting that lansoprazole improves not only mucosal inflammation but also submucosal inflammation in GERD.     

Diagnosis of esophageal motility disorders

Esophageal motility disorders are now known to be a heterogeneous group of conditions that commonly cause dysphagia and chest pain. Motor dysphagia is usually provoked by solids and liquids (in contrast to mechanical dysphagia, which is usually provoked by solids only). Chest pain with these disorders is nonspecific and can mimic angina pectoris. In many patients with diffuse esophageal spasm or nutcracker esophagus, pain appears to be caused by abnormal sensory function rather than contraction abnormalities. Barium esophagography and esophageal manometry are complementary studies in the evaluation of motility disorders.     

幽门螺杆菌感染对胃食管反流病患者食管酸暴露及食管动力的影响

目的分析幽门螺杆菌（helicobacterpylor,Hp）感染胃食管反流病（gastroesophagealrefluxdisease,GERD）患者食管远端酸暴露及食管动力变化特点,探讨Hp感染与GERD的关系。方法GERD患者80例,分为Hp阳性组30例,Hp阴性组50例,同期20例慢性浅表性胃炎患者为对照组,对3组进行食管动力学检测和食管24hpH监测。结果Hp阳性组与Hp阴性组DeMeester评分、食管下括约肌压力、24hpH监测各项指标及食管动力学各项指标比较差异均无统计学意义（P〉O．05）;2组DeMeester评分均高于对照组（P〈0．05）,食管下括约肌压力低于对照组（P〈0．05）。结论GERD患者食管下括约肌压力较正常人群低,且存在过量酸反流;Hp感染与GERD发生可能无明显关系。     

Esophageal manifestation in patients with scleroderma

The esophagus is the most commonly affected part of the gastrointestinal system in patients with systemic sclerosis (SSc). Esophageal involvement may lead to a significant reduction in patient quality of life. The exact pathophysiology is complex and not yet fully elucidated. Ultimately, esophageal smooth muscle becomes atrophied and replaced by fibrous tissue leading to severe motility disturbance of the distal esophagus. Symptoms are mainly attributed to gastroesophageal reflux disease and to esophageal dysmotility. Compelling evidence has correlated esophageal involvement to the severity of pulmonary disease. No formed guidelines exist about the diagnostic modalities used to assess esophageal disease in patients with SSc, though upper gastrointestinal endoscopy is the first and most important modality used as it can reveal alterations commonly observed in patients with SSc. Further exploration can be made by high resolution manometry and pH-impedance study. Proton pump inhibitors remain the mainstay of treatment, while prokinetic agents are commonly used as add-on therapy in patients with symptoms attributed to gastroesophageal reflux disease not responding to standard therapy as well as to motility disturbances. Gastroesophageal reflux disease symptoms in patients with SSc are frequently difficult to manage, and new therapeutic modalities are emerging. The role of surgical treatment is restricted and should only be preserved for resistant cases.     

Lower-esophageal sphincter function does not determine resting upper-esophageal sphincter pressure.

Records of 269 esophageal motility studies were reviewed to determine the relationship between lower-esophageal sphincter (LES) function and upper-esophageal sphincter (UES) pressure. Average and greatest UES pressures were similar in patients with LES pressures less than 10 mm Hg or greater than 20 mm Hg, and in patients with and without gastroesophageal reflux as determined by an intraesophageal pH electrode test. Although teliologically appealing, the belief that patients with weak lower-esophageal sphincters and gastroesophageal reflux have stronger upper-esophageal sphincters to guard against pharyngeal reflux and aspiration cannot be confirmed by current manometric techniques.     

肝硬化患者血清一氧化氮和食管动力关系的研究

目的: 探讨肝硬化患者血清一氧化氮(NO)与食管动力的关系。方法: 35 例肝硬化患者(HC)和30 例健康人(HS)采用硝酸还原酶法测定血清NO含量;核素法测定食管液体通过时间和胃食管反流。结果: HC组血浆NO含量显著高于HS组(P<0.01);HC组胃食管反流发生率显著高于HS组;HC组中胃食管反流患者的NO含量显著高于无胃食管反流的患者(P<0.01),HC组的食管液体通过时间较HS组显著延长(P<0.01),但NO含量与食管通过时间无相关性(P>0.05)。结论: 肝硬化患者血浆NO含量的升高可能使食管下括约肌(LES)松弛而产生胃食管反流,但不影响食管蠕动功能。