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)

Early studies confirmed the beneficial effects of calcium channel blockers on the normal oesophagus, which included a decrease in lower oesophageal sphincter tone in achalasia and a decrease in oesophageal contractions and amplitude in diffuse oesophageal spasm. This resulted in the enthusiastic use of the drugs in both disorders. With further experience, and with increased recognition of side effects, the role of these drugs in the 2 disorders has been better clarified. Clinical trials in general have not reflected the improvement observed in the manometric parameters. Only a minority of patients appear to derive sustained symptomatic benefit. Calcium channel blockers may be the initial choice for high or moderate risk patients with achalasia prior to proceeding with pneumatic dilatation or surgical myotomy. In diffuse oesophageal spasm, they are a reasonable first choice for all risk categories.
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PMID:An overview of the role of calcium antagonists in the treatment of achalasia and diffuse oesophageal spasm. 137 16

The charts of 83 children with chest pain who underwent esophageal manometry followed by esophagogastroscopy were reviewed. Forty-seven (57%) had normal esophageal histology and normal motility (group I). Esophagitis and normal motility were demonstrated in 15 children (group II), normal esophageal histology and esophageal dysmotility in 13 (group III), and both esophagitis and abnormal motility in 8 (group IV). Diffuse esophageal spasm and achalasia were the most common motility disorders identified (in seven and four patients, respectively). The presence and duration of symptoms, the age, and the gender were not different among the four patient groups. After six months of H2-receptor blockade, 12 of 15 group II patients were asymptomatic, whereas a significantly smaller percentage (five of 18) of patients with abnormal esophageal motility responded to esophageal dilation or treatment with calcium channel blockade, H2-receptor antagonist, and/or prokinetic agents (P less than 0.01). These data suggest that the evaluation of children with chest pain should include esophageal motility testing and esophagoscopy, even in the absence of other gastrointestinal-associated symptoms, and that while treatment of esophagitis results in resolution of symptoms, motility disorders were relatively refractory to therapy.
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PMID:Spectrum of esophageal disorders in children with chest pain. 156 6

In this paper the pharmacodynamic effects of calcium channel blockers (verapamil, nifedipine, diltiazem, fendiline, nitrendipine, nimodipine, and nisoldipine) on esophageal motility in man and their clinical effects in patients with various forms of primary esophageal motility disorders are critically analysed and summarized. The evaluation of efficacy and safety is mainly focused on nifedipine (Bay a 1040, Adalat; CAS 21829-25-4), since it has been best documented clinical pharmacologically and therapeutically in this field. Nifedipine and--with varying potency--the other calcium antagonists reduce effectively the increased lower esophageal sphincter pressure (LESP) and abnormally high and prolonged peristaltic and nonperistaltic contractions in the esophageal body in patients with achalasia, diffuse esophageal spasm (DES), and other disorders which may cause angina-like chest pain and/or dysphagia. Pharmacodynamic effects on esophageal motility are closely correlated with the plasma concentration of nifedipine in healthy volunteers and in patients. However, a final judgement on the therapeutic value of these compounds in esophageal motor abnormalities cannot be given due to conflicting results from clinical studies with fairly small numbers of patients and varying study designs. Among the different calcium antagonists investigated nifedipine represents the best investigated and the most suitable compound for the treatment of primary hypertensive esophageal motor disorders.
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PMID:Clinical efficacy of nifedipine and other calcium antagonists in patients with primary esophageal motor dysfunctions. 193 Mar 46

The authors review the recent literature about the classification of primary motor disorders of the oesophagus: achalasia, diffuse oesophageal spasm, nutcracker oesophagus, hypertensive lower oesophageal sphincter and non-specific intermediary disorders. In fact these motility disorders belong to a spectrum of diseases closely related, with chronological transformation of a specific disorder to another one or to intermediary disorders. Most of the recent pathophysiological research concerned primary achalasia, secondary achalasia syndromes being a kind of experimental model. These studies point to a morphological or functional deficiency of postganglionic nerves inhibiting the lower oesophageal sphincter (LOS) through noncholinergic nonadrenergic neurotransmitters. Recent advances in the treatment of achalasia and other motility disorders are not yet based on these findings. Although calcium channel blockers, like nifedipine, lower LOS basal pressure, they are not very useful on long term relief of symptoms of achalasia. Pneumatic dilatations or cardiomyotomy still remain the best methods of treatment of this disease.
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PMID:[Current advances in the physiopathology of primary motility disorders of the esophagus]. 198 73

The effect of nifedipine (10-20 mg) on esophageal motility was tested in 18 patients with clinical esophageal syndrome and radiologic aspect suggesting esophageal spasm. The drug was administered 20-30 min prior to the second radiologic examination. In 3 cases of achalasia the drug was administered in doses of 10 mg/day for 10 days before the second X-ray examination. Fiber esophagoscopy was performed in all the cases. The initial radiologic aspect was favourably influenced by nifedipine administration in 12 cases confirmed as esophageal spasm. The other 6 patients who did not benefit by the test were cases of organic diseases: 2 post caustic stenoses and 4 cases of eso-cardio-tuberal neoplasm. In the 3 cases of achalasia, treatment with nifedipine led to clinical improvement with relaxation of inferior esophageal contraction on radiologic examination. The study demonstrated the favourable contribution of calcium channel inhibitors to the diagnosis and treatment of esophageal motility disturbances.
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PMID:The diagnostic and therapeutic contribution of calcium channel inhibitors (nifedipine) in esophageal spasm. 228 70

Utilizing the rationale that the calcium channel blocker nifedipine decreases lower esophageal sphincter pressure, we performed a double-blind, placebo-controlled, crossover trial of sublingual nifedipine in achalasia, a disorder whose treatment depends on reduction in lower esophageal sphincter pressure. Ten patients participated in this trial, completed diaries, underwent manometric determinations of lower esophageal sphincter pressure, and had testing of esophageal emptying rates by a solid-meal radionuclide method. Nifedipine, titrated to a dose of 10-30 mg before meals, was well tolerated. Compared with placebo, nifedipine significantly reduced the frequency of dysphagia, but some symptoms of dysphagia, regurgitation, or nocturnal cough were still present most days. Nifedipine significantly reduced lower esophageal sphincter pressure by 28%, a value approximately one-half that achieved by successful pneumatic dilatation or myotomy. Esophageal emptying rates, as determined by the radionuclide method, were unchanged by nifedipine. We concluded that 1) nifedipine reduces symptoms of achalasia, but substantial symptoms do remain during such therapy; 2) the suboptimal effect results from the limited, although statistically significant, effect of nifedipine on reduction of lower esophageal sphincter pressure; and 3) although we believe that nifedipine may be recommended as treatment for achalasia in the subset of patients whose overall medical condition places them at high risk for forceful dilatation or surgery, it cannot be recommended as a standard alternative to these other modalities.
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PMID:The role of nifedipine therapy in achalasia: results of a randomized, double-blind, placebo-controlled study. 267 48

Clinical uses of calcium channel blockers are expanding. In addition to the established uses in patients with arrhythmias, angina pectoris or hypertension, newer and to some extent investigational uses indicate widespread application. For instance, their use has been reported in hypertrophic cardiomyopathy and cold cardioplegia, as well as in pulmonary hypertension, antiplatelet therapy, asthma, achalasia and oesophageal spasm, increased intraocular pressure and in cerebral vasospasm. Their use in obstetrical practice has been proposed. Thus, the presentation of a patient who is treated with calcium channel blockers and who requires anaesthesia will become more common. Calcium channel blockers may, under certain circumstances, potentiate haemodynamic and MAC depressive effects of inhalation agents. There is also evidence that the effects of neuromuscular blocking agents may be potentiated. The anaesthetist should be aware that the potential for interactions exists with digoxin, propranolol, quinidine, theophylline or dantrolene. Of interest and some significance are the anaesthetic implications of pathophysiological alterations that can be induced by calcium channel blockers, by affecting lower oesophageal tone, intracranial hypertension, bronchomotor tone (asthma), muscular dystrophy, neuromuscular function, hypoxic pulmonary vasoconstriction, malignant hyperthermia, inhibition of platelet aggregation and hyperkalemia. Despite these significant potential anaesthetic implications and because, at this time, in some instances withdrawal has clearly demonstrated increase in the signs of myocardial ischaemia, it would not seem necessary to recommend preoperative discontinuation of calcium channel blocker medication in patients presenting for anaesthesia. It is, however, appropriate that there is a high index of awareness of potential problems, unless there is some modification in inhalation anaesthetic concentrations and neuromuscular blocker dosage. Monitoring of cardiovascular and neuromuscular functions is essential. Calcium channel blockers would appear to be currently the drugs of choice for angina pectoris, arrhythmias or hypertension in patients with associated chronic obstructive pulmonary disease.
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PMID:Anaesthetic implications of calcium channel blockers. 286 80

We described an 84-year-old woman with symptomatic achalasia who refused both dilation and surgical treatment. She was treated with the calcium channel blocking drug nifedipine, with significant relief of symptoms. Objective evidence of response to the drug was confirmed by using an egg salad sandwich meal labeled with 99mTc-DTPA.
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PMID:Nifedipine for the poor-risk elderly patient with achalasia: objective response demonstrated by solid meal study. 636 79

Esophageal motor disorders may be clearly primary, as in achalasia or diffuse esophageal spasm (DES), or clearly secondary, as in scleroderma or intrathoracic malignancy. In patients with gastroesophageal reflux, abnormal motility of the esophageal body and stomach, and lower esophageal spasm (LES) appear to predispose patients to reflux. It is possible that esophagitis caused by refluxed gastric material then further impairs motility, propagating the injury. Therapeutically, appropriate use of recently available medications, such as calcium channel blockers and metoclopramide, and new applications of previously available agents, such as hydralazine and bethanechol, have improved our ability to relieve symptoms and at times restore more normal motility.
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PMID:Motor disorders of the esophagus: diagnosis and treatment. 646 93

Achalasia is a primary esophageal motor disorder characterized by lack of esophageal peristalsis and poor lower esophageal sphincter (LES) relaxation. Clinically, achalasia manifests as progressive dysphagia to solids and liquids and mild weight loss. Predisposition to esophageal cancer is not prevalent, but certain tumors may mimic achalasia. The diagnosis of achalasia is relatively easy to make with a good history, radiography, and esophageal motility testing. The esophagogram reveals a typical bird-beak narrowing of the esophagogastric junction and esophageal dilation, the degree of which depends on the stage of the disease. Esophageal manometry reveals poor LES relaxation, aperistalsis, and often elevated intraesophageal pressure. Endoscopic examination is important to rule out malignancy as the cause of achalasia. The traditional treatment of achalasia is forceful dilation of the LES. Bougienage may be helpful in some cases. Pharmacological agents, such as nitroglycerin and calcium channel blockers, provide some relief by decreasing LES pressure. However, they are not a viable, long-term choice. Surgical myotomy offers slightly better results than pneumatic dilation, but it is accompanied by some increased gastroesophageal reflux. Laparoscopic and thoroscopic myotomy are in their infancy, and, if successful, they will make surgical treatment much more attractive. Intrasphincteric botulinum toxin injection is the newest form of therapy. Its safety and ease of administration are very encouraging, but long-term results are not available.
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PMID:Achalasia. 877 90


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