Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Willmen gastric bubble has been used as an adjunct to weight loss in morbidly obese patients. 35 patients with morbid obesity were studied with routine manometry, esophageal 24-h-pH-measurement, and gastric emptying studies before and 4 weeks after bubble placement. During emptying studies blood samples were taken to measure gastrin, PP, CCK, VIP, neurotensin and insulin. No patient developed heartburn or regurgitation after bubble placement. Esophageal motility and LES function remained unchanged. There was no important pathological gastroesophageal reflux before and after gastric bubble. The gastric emptying time of solid food was unchanged by gastric bubble placement and the emptying time of liquids was accelerated up to normal. In patients with fasting gastrin levels less than 20 pg/ml at the beginning of the first test we found no differences in gastrin release before and after bubble insertion. In patients with primary high fasting values gastrin release was significantly increased. CCK, VIP, neurotensin and insulin levels were unchanged. With PP we measured significantly raised fasting levels after gastric bubble. We conclude that esophageal and LES functions are not altered by Willmen gastric bubble placement and that primary retardation of fluids is changed to normal. Bubble induced gastric tension increases fasting PP. In case of high fasting gastrin the bubble leads to an extremely high food response without any clinical signs.
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PMID:[Does the stomach balloon modify the function of the esophagus and lower esophageal sphincter, stomach emptying and release of gastrointestinal peptides?]. 266 61

Twenty patients with gastroesophageal reflux disease (10 with compensated and 10 with decompensated gastroesophageal incompetence) were examined to determine if there was a correlation between the ability of physiological stimuli to tonicize the lower esophageal sphincter (LES) and the response to pentagastrin stimulation (Gastrodiagnost). The pressure of the lower esophageal sphincter as well as blood levels of the hormones/neurotransmitters gastrin, PP and VIP were determined after giving a 300 ml intragastral bolus of either 0.9% NaCl or 20% peptone solution. All patients exhibited per definitionem a positive common-cavity phenomenon on abdominal compression. Intravenous pentagastrin stimulated the LES in patients with compensated gastroesophageal incompetence (GI) but not in those with decompensated GI (p less than or equal to 0.0005). Esophagoscopy revealed a severe esophagitis in 80% of the patients with decompensated GI but in only 10% of the patients with compensated GI. Peptone stimulated the LES in patients with compensated GI (p less than or equal to 0.005) at 5, 10 and 15 minutes, pepton vs. NaCl). Neither NaCl nor peptone increased the tone of the LES in patients with decompensated GI. Peptone but not NaCl caused a significant increase of serum gastrin in all patients: there was no difference between the two groups. Neither NaCl nor peptone influenced VIP levels in peripheral blood. PP levels increased significantly in both groups following peptone. Physiological responsiveness of the LES can be inferred from the manometric data and the results of the pentagastrin test. A negative reaction to pentagastrin is associated with a loss of response to physiological stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Peptone stimulation of the lower esophageal sphincter in patients with reflux disease]. 323 24

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