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)

A 52-year-old man developed achalasia and a lung abscess due to aspiration pneumonia. We conducted a right upper lobectomy by thoracotomy for the abscess and, 2 weeks later, video-assisted thoracoscopic myotomy and fundoplication (modified Belsey Mark IV procedure) though the left thorax for achalasia. Three months after surgery, the patient was free of dysphasia and chest pain and had regained his original weight. Esophageal myotomy and fundoplication using video-assisted thoracoscopy appear to be feasible in treating achalasia involving impaired pulmonary function.
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PMID:Video-assisted thoracoscopic esophagomyotomy for achalasia after pulmonary lobectomy. 1061 1

Dysphagia and chest pain are the two commonest symptoms of abnormalities of oesophageal motility. Dysphagia is to be distinguished into high or oropharyngeal and low or oesophageal dysphagia. Oropharyngeal dysphagia pertains to dysfunction of the pars cricopharyngea of the M. constrictor pharyngis inferior (M. cricopharyngeus), which is frequently associated with a Zenker diverticulum. Treatment consists of endoscopical or surgical myotomy and diverticulectomy. In achalasia there is incomplete relaxation of the lower esophageal sphincter with aperistalsis. The main treatment modalities are endoscopic pneumodilation and surgical myotomy of this sphincter. In dysphagia or non-cardiac chest pain spastic or hypocontractile abnormalities of the oesophageal motility can be involved, these are often difficult to treat. Disorders of gastric motility are mainly gastroparesis and functional dyspepsia. In diabetic gastroparesis, adequate monitoring of the blood sugar level is also necessary. New insights into the pathophysiology of functional dyspepsia concern abnormal visceral sensitivity and reduced adaptive relaxation of the stomach during intake of food.
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PMID:[Gastrointestinal surgery and gastroenterology. VII. Proximal motility disorders in the digestive tract]. 1074 45

In this article we report our experience in 100 consecutive achalasia patients who were treated with laparoscopic Heller myotomy and Dor antireflux fundoplication, with particular regard to the technical problems encountered, the learning curve, and the long-term follow-up. The operation was completed laparoscopically in 94 patients, with a median operative duration of 150 minutes, and a continuous steady reduction in the operating time from the first patients to the last. In six patients the operation was completed through "open" access. Postoperative complications were recorded in six cases. Follow-up was completed in all 100 patients, with a median follow-up of 24 months. Overall, actuarial life-table analysis showed a probability of 90% that patients would be symptom free over a 5-year period. Radiologic assessment showed a significant reduction in the esophageal diameter, and manometry showed a significant reduction in the lower esophageal sphincter resting pressure and residual pressure. Twenty-four-hour pH monitoring showed postoperative reflux in 6.9% of the patients. Persistent dysphagia or chest pain was reported by eight patients, which constituted treatment failures. Seven of these eight patients were eventually treated with multiple pneumatic dilatations, which were successful in six cases. It was concluded that laparoscopic Heller myotomy with Dor fundoplication is a feasible and effective treatment for achalasia, with an actuarial success rate of 90% at 5 years.
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PMID:Treatment of esophageal achalasia with laparoscopic Heller myotomy and Dor partial anterior fundoplication: prospective evaluation of 100 consecutive patients. 1076 91

Swallowing is a complex mechanism based on the coordinated collaboration 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 primary esophageal motility disorders--achalasia, diffuse esophageal spasm, hypercontractile esophagus ('nutcracker esophagus') and non-specific motility disorder--are of unknown etiology. Other esophageal diseases, such as cervical diverticula or gastroesophageal reflux disease, might also be caused by a primary esophageal motility disorder. Medical treatment of esophageal disorders with esophageal hyper- or dysmotility requires agents that reduce esophageal contractile force (anticholinergic agents, nitrates, calcium antagonists). Despite the beneficial effect of the various drugs on esophageal motility parameters, the clinical benefit of medical treatment of esophageal motility disorders is rather disappointing. Calcium channel antagonist, alone or in combination with anticholinergics or nitrates, can be used as a medical trial, especially in mild achalasia. However, medical therapy is clearly inferior to pneumatic balloon dilation therapy. Recently, botulinum toxin injection was suggested as a therapeutic option in achalasia patients with good results on lower esophageal sphincter pressure (LESP) and symptom scores that were similar to the results achieved by pneumatic balloon dilation. Hypercontractile esophagus shows a good manometric response to calcium channel antagonists, but only little clinical effect in terms of improvement of symptoms. Diffuse esophageal spasm is a relatively rare disease and few clinical studies are available. The use of calcium channel antagonists can be beneficial, at least in some patients with diffuse esophageal spasm. From clinical and epidemiological studies, there is some evidence of a 'psychological' component in the pathogenesis or perception of esophageal symptoms. There is some clinical benefit from centrally acting drugs such as benzodiazepines or antidepressants. With the exception of botulinum toxin for achalasia, medical therapy of primary esophageal motility disorders is rather limited and the clinical results are poor. Further understanding of esophageal pathophysiology as well as development of new receptor-selective drugs might increase our chances of a successful treatment of primary esophageal motility disorders.
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PMID:Esophageal pharmacology and treatment of primary motility disorders. 1077 Mar 58

Botulinum toxin (BTX) is one of the most potent inhibitors of acetylcholine from nerve endings, and this accounts for its toxic properties as well as its therapeutic application in a variety of neuromuscular syndromes. This review focuses on the growing use of BTX in the so-called 'spastic' disorders of the gastrointestinal tract. These include achalasia, for which the short-term efficacy of the intrasphincteric injection of BTX has been well established. However, because of the chronicity of this condition, repeated injections of the toxin may be required at regular intervals. In contrast, the relatively short duration of action may be an advantage in disorders such as chronic anal fissure, where the benefit of this therapy has now been demonstrated in hundreds of patients. There are many other sphincteric and non-sphincteric syndromes in the gut for which the efficacy of this agent is being actively tested. These include non-cardiac chest pain, post-operative pylorospasm and sphincter of Oddi dysfunction. Skeletal muscle sphincters, such as the upper oesophageal sphincter or the external anal sphincter/puborectalis muscle, may also be targeted, with good effect. In some of these conditions, the local injection of BTX may serve as a useful therapeutic trial, facilitating the decision to institute more invasive forms of therapy. The cumulative short-term experience with BTX in the gut to date suggests that it is a relatively simple and safe therapy. The use of BTX represents a novel approach for gastrointestinal motility disorders, and the rapidly expanding list of successful applications holds promise for a more widespread use of similar agents in the future. Additional studies on long-term outcome are eagerly awaited.
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PMID:Botulinum toxin for spastic gastrointestinal disorders. 1103 Jun 39

Noncardiac (unexplained) chest pain may be caused by esophageal disorders, psychiatric problems, or visceral hypersensitivity of unknown etiology. The most treatable etiologies, in order of their frequency, include gastroesophageal reflux disease (GERD), panic disorders, visceral hypersensitivity (ie, the irritable esophagus), and achalasia. Ensure the diagnosis is correct, and exclude important cardiac disease. In the younger patient, this may require an EKG, stress test, and echocardiogram, while older patients will need coronary angiography. Reassure the patient that there is no evidence of serious disease, and discuss the prognosis.
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PMID:Noncardiac (Unexplained) Chest Pain. 1109 93

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.
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PMID:Primary esophageal motility disorders. 1149 31

Patients with recurrent angina-like chest pain with normal coronary vessels are deemed to have the syndrome of noncardiac chest pain (NCCP). These patients, despite having significant cardiac disease ruled out, often spend a restricted lifestyle believing they have cardiac disease. These recurrent episodes of chest pain may be related to gastroesophageal reflux disease (GERD), spastic motility disorders of the esophagus and esophageal (visceral) hyperalgesia. These disease entities are often difficult to diagnose and treat except for GERD and achalasia. Recent prospective double-blind studies have shown that about 44% of these patients may have underlying GERD. There is now more evidence to support the practice of empiric use of proton pump inhibitors (PPIs) as the first step in therapy. Newer modalities for diagnosis like endoscopic ultrasonography (EUS) showed that this group of patients had sustained muscular contractions of longer that 68 s during chest pain. These sustained contractions noted on EUS were secondary to isometric contraction of the circular muscle which did not cause luminal constriction nor was related to contraction of the longitudinal muscles which cannot be recorded by pressure manometry. Treatment is difficult if patients do not respond to high-dose PPIs. Other medications which are known to alter visceral hyperalgesia in low doses, such as tricyclic antidepressants like imipramine and desyrel, can be tried. Psychological intervention may be useful in the management of some of these patie
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PMID:Update on noncardiac chest pain. 1127 32

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.
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PMID:[Diagnosis and treatment of esophageal motility disorders]. 1130 49

Oesophageal motility disorders comprise various abnormal manometric patterns which usually present with dysphagia or chest pain. Some, such as achalasia, are diseases with a well defined pathology, characteristic manometric features, and good response to treatments directed at the pathophysiological abnormalities. Other disorders, such as diffuse oesophageal spasm and hypercontracting oesophagus, have no well defined pathology and could represent a range of motility changes associated with subtle neuropathic changes, gastro-oesophageal reflux, and anxiety states. Although manometric patterns have been defined for these disorders, the relation with symptoms is poorly defined and the response to medical or surgical therapy unpredictable. Hypocontracting oesophagus is generally caused by weak musculature commonly associated with gastro-oesophageal reflux disease. Secondary oesophageal motility disorders can be caused by collagen vascular diseases, diabetes, Chagas' disease, amyloidosis, alcoholism, myxo-oedema, multiple sclerosis, idiopathic pseudo-obstruction, or the ageing process.
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PMID:Oesophageal motility disorders. 1180 95


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