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)

The contractile activity of the oesophageal body and of the upper and lower oesophageal sphincter (LOS) can reliably be portrayed by means of low compliance recording systems, either pneumohydraulic or with strain gauge force transducers, and at least two pressure sensors. LOS resting pressure can be assessed by both station and rapid pull-through techniques, or by the sleeve method. States of disordered LOS function, such as achalasia, can be diagnosed dependably only by manometric means. Manometry is of high diagnostic yield for motor disorders of the oesophageal body as well, although generally accepted diagnostic criteria are still lacking. In patients with angina-like chest pain, provocation tests can prove that oesophageal contraction abnormalities cause the symptoms. Edrophonium has been shown to be the most effective and best tolerated provocative agent. Transport of swallowed material through the oesophagus can reliably be recorded by radionuclide transit studies. Such studies are valuable in identifying patients with absent or impaired peristalsis and in evaluating treatment effects, e. g., the effects of mechanic dilatation in achalasia. Gastrooesophageal reflux should be recorded not only qualitatively but also quantitatively, although a definition of what is pathological and what is not has not been generally agreed upon. Recording of oesophageal intraluminal pH over longer periods of time, preferably 24 h, may have the best diagnostic yield. The advent of computer-aided analysis techniques will replace the cumbersome handscoring of motor and pH tracings and, hopefully, contribute to a better understanding and classification of oesophageal pathophysiology.
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PMID:[Methods for measuring the motor activity of the esophagus and gastroesophageal reflux]. 377 64

The human lower esophageal sphincter (LES) is believed to be innervated by nonadrenergic, noncholinergic inhibitory nerves, and cholinergic excitatory nerves. In idiopathic achalasia, LES relaxation is abnormal because the inhibitory nerves to the sphincter are either absent or functionally impaired. The integrity of cholinergic excitatory nerves to the LES, however, has not been thoroughly evaluated. In 27 patients with untreated idiopathic achalasia, and 21 healthy volunteers, we investigated the hypothesis that postganglionic cholinergic nerves to the LES are functionally intact in achalasia. The LES responses to atropine, edrophonium, methacholine, amyl nitrite, and pentagastrin were assessed. In 2 achalasia patients, patterns of fasting motor activity in the LES were investigated during overnight manometric studies. Resting LES pressure was significantly greater in the achalasia patients, 41 +/- 4 mmHg (mean +/- SE), than in the normal subjects, 20 +/- 2 mmHg. Atropine significantly reduced LES pressure in both groups by 30%-75%. Edrophonium increased LES pressure in the achalasia patients but had negligible effect on the normal subjects. The LES in achalasia patients exhibited an increased sensitivity to both methacholine and pentagastrin compared with the normal subjects. In both patients who underwent an overnight manometric study, the LES exhibited cyclic phasic contractile activity synchronous with gastric contractions during the migrating motor complex. We conclude that the study findings support the hypothesis that postganglionic cholinergic LES innervation in achalasia patients is either normal or only minimally impaired, in contrast to the marked impairment of the inhibitory nerves governing LES relaxation.
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PMID:Integrity of cholinergic innervation to the lower esophageal sphincter in achalasia. 394 20

Thirty-four consecutive patients referred to a gastroenterology clinic with suspected esophageal motility abnormality as a cause of their chest pain or dysphagia, or both, were prospectively studied in an 18-mo period. Peristaltic response to 10 wet (5 ml H2O) swallows was recorded in all studies with a low-compliance infusion system. To provoke symptoms and motility abnormalities after baseline evaluation, all patients had acid infusions (0.1 N HCl) and administration of edrophonium (80 micrograms/kg i.v.), pentagastrin (6 micrograms/kg s.c.), and bethanechol (40 micrograms/kg s.c.). Tracings were coded, read, and interpreted blindly. Baseline tracings were abnormal in 23 of 34 patients (68%), including increased amplitude peristaltic contractions ("nutcracker esophagus") in 10 and nonspecific esophageal motor disorders in 13. Acid infusion produced substernal burning in 3 of 33 patients, in motility change in 1 patient. Edrophonium produced chest pain with manometric changes in 6 of 34 (18%) patients. Pentagastrin produced chest pain with manometric change in 1 patient. Bethanechol produced chest pain with manometric change in 2 patients. One patient with low amplitude had elevation of esophageal baseline and multiple simultaneous contractions but no chest pain (subsequently developed achalasia). It was concluded that (a) abnormal motility is a common finding in a symptomatic group of patients with presumed esophageal motility disorder, (b) the "nutcracker" esophagus is the most frequent defect, and (c) attempted provocation of symptoms with acid or drugs is not generally effective; however, edrophonium is the best tolerated and most effective of currently available drugs.
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PMID:Prospective manometric evaluation with pharmacologic provocation of patients with suspected esophageal motility dysfunction. 683 64