Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014848 (achalasia)
 2,804 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 (anti-cholinergic 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.
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PMID:Medical treatment of esophageal motility disorders. 846 20

History taking is the first step in the evaluation of a patient. An analysis of the information obtained provides the basis for the choice and order of diagnostic tests. In addition, it provides the clinician with the necessary information to determine the relevance of "abnormal tests" to the patient's problem. Dysphagia is a reliable symptom that indicates an abnormality in the swallowing mechanism. The history should contain a detailed description of the symptoms associated with dysphagia from the onset. Especially relevant are questions to determine if dysphagia is experienced every day or intermittently, with solid food or liquids or both, as well as presence and timing of associated symptoms such as, choking, coughing and regurgitation, changes in speech, heartburn and chest pain. It is clinically useful to divide swallowing into three phases: oral, pharyngeal and esophageal. Oral dysphagia is usually due to a neurologic disorder, decreased salivary flow or painful oropharyngeal lesions. Pharyngeal dysphagia is most frequently caused by neuromuscular disorders and less frequently by a Zenker's diverticulum, neoplasm or a mucosal web. Esophageal dysphagia is caused by a structural narrowing, such as produced by a peptic stricture, neoplasm or a Schatzki's ring or by a primary motility abnormality, such as achalasia or diffuse esophageal spasm or by motility abnormalities produced by inflammation caused by gastroesophageal reflux, medication-induced esophageal ulceration or infectious esophagitis.
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PMID:Art and science of history taking in the patient with difficulty swallowing. 846 26

In reflux disease the authors emphasize the following diagnostic procedures: a satisfactory case-history, endoscopy, aimed biopsy, radiographic evidence of reflux, radionuclide reflux scintigraphy and pH-metry. As to subsidiary examinations, they recommend Bernstein's perfusion test. In 50% of the patients with non-coronary chest pain the complaints are caused by diseases of the oesophagus. The latter include achalasia, dysphagia, idiopathic diffuse spasm, hyperdynamic oesophagus and irritable oesophagus. In the treatment of reflux disease the stage of the disease is decisive. Treatment is prolonged and the doses of drugs are higher than in duodenal ulcers. The basis are H2 blockers. In severe forms treatment with omeprazole is indicated. Surgery is indicated only in severe mucosal complications. In achalasia of the oesophagus this is disruption of the sphincter by the method of pneumatic dilatation or surgical myotomy. Idiopathic diffuse spasm and other disorders of oesophageal motility respond in different ways to treatment with calcium autagonists and nitrate treatment.
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PMID:[Diagnosis and therapy of esophageal diseases]. 850 59

Extramucosal myotomy involving the external longitudinal and internal circular layers of the musculature of the esophagus represent the surgical therapy in patients with dysphagia and regurgitation or with angina-like chest pain secondary to functional abnormalities of the musculature of the esophagel body and sphincters. Surgery has a palliative function, because cures symptoms and complication such a diverticula, but not the disease. Modern surgical techniques also prevent recurrence of symptoms and complications are minimal with better long-term results than conservative therapy. Myotomy of the lower esophageal sphincter extended to the distal part of the esophageal body (Heller's operation) is performed as first choice or following insucces of dilatation in patients with primary achalasia of the esophagus, using a trans-abdominal or a trans-thoracic approach. Myotomy of the upper esophageal sphincter is indicated in patients with Zenker's diverticulum following diverticulectomy or diverticulopessy. Segmental myotomies are performed after diverticulectomy in patients with epiphrenic pulsion diverticula. Trans-thoracic "long" esophageal myotomy performed from the thoracic portion of the lower esophageal sphincter to the aortic arch is indicated in patients with diffuse esophageal spasm and nutcracker esophagus and sometimes in patients with aspecific abnormalities of the esophageal motor function associated with diverticula. Circular miotomies limited to the external longitudinal layer of the esophageal musculature can be performed at the level of anastomosis in order to gain tissue and reduce tissutal tension. The recent introduction of the endoscopic surgery allowed some of these operations to be performed through minimally invasive approaches. Therefore laparoscopic and thoracoscopic Heller's myotomy is feasible with clinical and functional results similar to those obtained with traditional open approach and with less postoperative discomfort and shorter hospital stay. This paper deals with the indications and surgical techniques of myotomies of the esophageal body both limited and extended to the lower esophageal sphincter.
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PMID:[Myotomy of the esophageal body]. 894 93

Achalasia is a disease of undertermined etiology characterized by a defect in the innervation of esophageal smooth muscle causing aperistalsis of the esophageal body, increased lower esophageal sphnicter (LES) tone and inappropriate relaxation of the LES during swallowing. Several of the manometric and radiographic features of achalasia are also seen in individuals without the disease but they are reported much more frequently in older populations. We reviewed our cases of new onsst achalasia in patients over age 65 to see if their presentation and response to treatment might differ from that reported in younger patients. We found dysphagia to be the predominant symptom in our elderly patients just as it is in younger patients. Chest pain, on the other hand, was significantly less common. Additionally, our achalasia group had a high response rate to pneumatic dilatation, confirming an earlier study that showed greater efficacy in older patients than in younger patients.
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PMID:Achalasia in patients over 65. 906 35

The aims of this study were to assess the effect of pneumatic dilation on gastroesophageal reflux in achalasia, differentiate esophageal acid due to lactate from acid due to gastroesophageal reflux, and determine if chest pain and heartburn are reliable indicators of gastroesophageal reflux. Eight untreated achalasia patients underwent pre- and postdilation esophageal fluid/food residue lactate and pH analysis, esophageal manometry, 24-hr pH monitoring, and symptom assessment. All patients had a successful clinical outcome and a decrease in lower esophageal sphincter pressure from 29.1 +/- 12.7 to 14.7 +/- 3.8 mm Hg (mean +/- SD; P = 0.04). Abnormal acid exposure was present in two patients before and two patients after dilation. Postdilation acid exposure was mild. Lactate was detected before dilation in all patients. A lactate concentration >2 mmol/liter was associated with acidic residue and one abnormal 24-hr pH profile. There was no correlation between an abnormal 24-hr pH test and age, lower esophageal sphincter pressure, or duration of symptoms prior to treatment. Chest pain and heartburn were unrelated to drops in pH. Gastroesophageal reflux is rare in untreated achalasia and esophageal acidity may result from ingestion of acidic foods or production of lactate. Mild gastroesophageal reflux occurs after dilation but is of no clinical significance. Chest pain and heartburn are not indicators of acid reflux in achalasia.
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PMID:Effect of pneumatic dilation on gastroesophageal reflux in achalasia. 914 54

Esophageal achalasia (EA) has been historically treated by esophageal dilatation or myotomy with or without fundoplication. Botulinum toxin (Botox-Allergan) use in pediatric EA has not been previously described. The authors' objective was to observe the efficacy of botulinum toxin injection into the lower esophageal sphincter (LES) for EA. An 11-year-old boy presented with a 9-month history of frequent pneumonia, productive cough, and a 1-year history of chest discomfort and odynophagia. Chest radiograph showed changes compatible with aspiration. Upper gastrointestinal (UGI) series showed typical narrowing of the LES, and 24-hour pH study showed no reflux. Esophageal manometry showed classic findings of achalasia. An upper gastrointestinal endoscopy was performed showing a huge volume of retained food. A direct four-quadrant injection was performed with a total of 100 U of botulinum toxin into the LES. UGI series showed improvement in esophageal emptying. Esophageal manometry showed impressive improvement in LES pressure (preinjection, 44.1 mm Hg to postinjection mean of 16.6 mm Hg), percent relaxation (preinjection, 30% to postinjection, 58.8%), and duration of relaxation (preinjection, 1.9 seconds to postinjection, 11 seconds). The patient has not had any further respiratory symptoms, chest pain, or odynophagia in 8 months of follow-up. Botulinum toxin injection is simple and effective for EA and merits its study in a prospective manner in the pediatric population.
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PMID:Botulinum toxin use in pediatric esophageal achalasia: a case report. 920 Jan

Achalasia is a primary esophageal motor disorder of unknown etiology producing complaints of dysphagia, regurgitation, and chest pain. The current treatments for achalasia involve the reduction of lower esophageal sphincter (LES) pressure resulting in improved esophageal emptying. Calcium channel blockers and nitrates, once used as initial treatment strategy for early achalasia, are now only used in patients who are not candidates for pneumatic dilation or surgery and those not responding to botulinum toxin injections. By virtue of the more rigid balloons, the current pneumatic dilators are more effective and have better efficacy than the older more compliant balloons. The graded approach to pneumatic dilation using the Rigiflex balloons (3.0, 3.5, and 4.0 cm) are now the most commonly used nonsurgical means of treating patients with achalasia, resulting in symptom improvement in up to 90% of patients. Surgical myotomy, once with high morbidity and long hospital stay, can now be performed laparoscopically with similar efficacy to the open surgical approach (94% vs. 84%, respectively), reduced morbidity, and hospitalization time. Given the advances in both balloon dilation and laparoscopic myotomy, most patients with achalasia can now choose between these two equally efficacious treatment options. Botulinum toxin injection of the LES should be reserved for patients who cannot undergo balloon dilation and are not surgical candidates.
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PMID:Current therapies for achalasia: comparison and efficacy. 1047 92

Achalasia is a primary esophageal motor disorder of unknown cause that produces complaints of dysphagia, regurgitation, and chest pain. The current treatments for achalasia involve the reduction of lower esophageal sphincter (LES) pressure, resulting in improved esophageal emptying. Calcium channel blockers and nitrates, once used as an initial treatment strategy for early achalasia, are now used only in patients who are not candidates for pneumatic dilation or surgery, and in patients who do not respond to botulinum toxin injections. Because of the more rigid balloons, the current pneumatic dilators are more effective than the older, more compliant balloons. The graded approach to pneumatic dilation, using the Rigiflex (Boston Scientific Corp, Boston, MA) balloons (3.0, 3.5, and 4.0 cm) is now the most commonly used nonsurgical means of treating patients with achalasia, resulting in symptom improvement in up to 90% of patients. Surgical myotomy, once plagued by high morbidity and long hospital stay, can now be performed laparoscopically, with similar efficacy to the open surgical approach (94% versus 84%, respectively), reduced morbidity, and reduced hospitalization time. Because of the advances in both balloon dilation and laparoscopic myotomy, most patients with achalasia can now choose between these two equally efficacious treatment options. Botulinum toxin injection of the LES should be reserved for patients who can not undergo balloon dilation and are not surgical candidates.
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PMID:Achalasia: diagnosis and management. 1043 97

The esophageal primary motor disorders like achalasia, diffuse esophageal spasm or the nutcracker can involve the upper esophageal sphincter, the esophageal body, the lower esophageal sphincter or a combination of them. This article will focus on the esophageal body and abnormal peristalsis. A normal esophageal peristaltic contraction occurs after a latency period following a swallow and requires a minimum amplitude to be propulsive. Abnormal latencies may generate simultaneous contractions whereas low amplitude contractions may be inefficient i.e. GERD and high amplitude contractions my provoke chest pain or dysfagia i.e. diffuse spasm. The latency period between deglutition and contraction is due to a muscle inhibition immediately after the swallow. This inhibition is due to release of NO by an inhibitory neurone located in the myenteric plexus. At the end of the inhibition, the contraction occurs due to release of acetyl choline by an excitatory cholinergic neurone. The exact interplay between these two neurones will determine the <<timing>> or propagation velocity and the amplitude of esophageal contractions. Patients with achalasia have a predominant loss of inhibitory neurones (VIP and NOS) with a relative preservation of excitatory cholinergic neurones. The histophatologic and immunohistochemical status in patients with esophageal primary motor disorders other than achalasia is poorly characterised Examples of deglutitive inhibition in the esophagus can be observed during the relaxation of the lower esophageal sphincter or when a subject swallows very frequently. In order to quantify deglutitive inhibition we developed a method that induces an artificial high pressure zone in the mid esophageal body. During the latency period after a swallow, the high pressure zone relaxes (is inhibited). With this method, we could measure the magnitude and duration of the inhibitory phenomenon. There is a very good correlation between the degree of deglutitive inhibition and propagation velocity of esophageal contractions. The less inhibition, the faster the propagation velocity of contractions. Simultaneous contractions are the consequence of absent inhibition. Patients with esophageal primary motor disorders may have very fast propagating contractions and a small percentage of simultaneous contractions or up to 100% of simultaneous contractions. The correlation between the degree of inhibition and propagation velocity of contractions suggests that the different primary motor disorders are the expression of a progressive failure in esophageal inhibition.
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PMID:[Role of deglutitive inhibition in the pathophysiology of esophageal primary motor disorders]. 1060 60


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