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

Nervous control of gastrointestinal motility is extremely complex, is regulated by the enteric system, the "brain of the gut", and modulated by extrinsic nerves. This system with its multiplicity of transmitters and receptors does not always allow a clear interpretation of experimental data, especially with compounds lacking specificity. In this review the complex situation is described particularly in relation to receptor populations (cholinergic, adrenergic, dopamine, histamine, 5-hydroxytryptamine, opioid, gamma-aminobutyric acid (GABA), prostanoid and dihydropyridine receptors), therapeutic aspects of drugs and their usefulness in children. Newer principles with known drugs and promising new compounds with a more appropriate kinetic or fewer side-effects, deriving from distinct pharmacological groups, as candidates for the treatment of gastrointestinal disorders are considered e.g. anticholinergics (prifinium or actilonium bromide), adrenergic alpha 2-agonists (clonidine, lidamidine) for diarrhoea in diabetic neuropathy, adrenergic beta-blockers for shortening postoperative ileus (propranolol), dopamine receptor antagonists (metoclopramide, domperidone, alizapride) and another prokinetic substance (cisapride) which may be useful for a number of applications as gastro-oesophageal reflux, gastro-paresis, intestinal pseudo-obstruction, cystic fibrosis and constipation, morphine derivatives (e.g. loperamide) for intractable diarrhoea and calcium antagonists (e.g. nifedipine) for achalasia. Increasing experience in digestive tract pharmacology and reliable clinical studies will furthermore be the basis for a more specific and better tolerated therapy of gastrointestinal motility disorders in adults and children.
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PMID:Rational pharmacotherapy of gastrointestinal motility disorders. 266 4

The effect of cimetropium bromide, a new anticholinergic agent, in patients with primary achalasia was studied. Twenty such patients (12 females and 8 males, mean age 38 years, range 15-56) were studied. Diagnosis was performed by radiology, endoscopy, and manometry. Lower esophageal sphincter pressure and body wave amplitude were measured by means of a five-channel catheter constantly perfused by a low-compliance pneumohydraulic pump. Patient received cimetropium bromide 10 mg intravenously over 3 min or placebo in a double-blind manner. In five patients esophageal transit evaluated by scintiscanning was studied on separate occasions after cimetropium bromide or placebo. Baseline mean lower esophageal sphincter pressure was 46 +/- 5 mm Hg and mean amplitude of body waves was 30 +/- 8 mm Hg. Cimetropium bromide induced a significant decrease in sphincter pressure and body wave amplitude that measured 13 +/- 3 mm Hg and 8 +/- 4 mm Hg, respectively, 15 min after the end of infusion. The decrease was maintained for 45 +/- 5 min. A marked reduction in repetitive body waves was also noted. Esophageal transit was also accelerated with cimetropium bromide. Maximal stomach radioactivity was observed after 8 +/- 1.8 sec while with placebo this was reached after 65 +/- 1.5 sec (P < 0.01). It is concluded with cimetropium bromide reduces LES pressure and shortens transit in primary esophageal achalasia. It may be useful in the treatment of this esophageal motility disorder.
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PMID:Effect of cimetropium bromide on esophageal motility and transit in patients affected by primary achalasia. 802 47

Achalasia is an esophageal motility disorder of unknown etiology. Several studies suggest possible herpes or measles virus etiology, but results are inconclusive. The aim of this study was to test whether herpesvirus (HV), measles (MV), or human papilloma virus (HPV) sequences could be detected in myotomy specimens from a wide spectrum of achalasia patients, using the polymerase chain reaction (PCR) technique. Myotomy specimens from 13 achalasia patients, esophagectomy specimens from nine esophageal cancer patients, and autopsy specimens from six fetuses were studied with the PCR technique. Paired oligonucleotide primers of HV (HSV-1 and 2, CMV, EBV, VZV, and HHV-6), MV and HPV sequences and exon 3 of the HPRT gene were used for the PCR DNA amplification. Amplified products were resolved on agarose gels and stained with ethidium bromide. All specimens yielded the appropriate-sized products for exon 3 of the HPRT and viral controls. No amplified products were seen in the achalasia specimens or controls corresponding to any of the virus sequences tested. The absence of HV, MV, and HPV sequences suggests that these viruses are not associated with achalasia but does not exclude the possibility of a previously unidentified virus as a causal agent. Further studies aimed at identifying an unknown viral agent as a cause for achalasia are warranted.
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PMID:Achalasia is not associated with measles or known herpes and human papilloma viruses. 905 10

The present study involved a total of 25 patients presenting with oesophageal achalasia who had undergone balloon cardiodilation. The complex of rehabilitative measures concluded the application of an ultrahigh-frequency electromagnetic fields (decimeter wave (DMW) therapy) to the collar region and general iodine bromide baths. The treatment resulted in the elimination of dysphagia syndrome during consumption of solid food in 80% of the patients. Simultaneously, the oesophagogastroscopic study revealed the improvement of the state of oesophageal mucosa. Moreover, the thyrotropin level was normalized. The positive effect of such rehabilitative treatment persisted during 6-8 months.
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PMID:[Rehabilitation of the patients presenting with oesophageal achalasia following balloon cardiodilation]. 2299 59