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)

Gut motility disorders and altered pain perception were reported in patients with irritable bowel syndrome (IBS). To verify foregut involvement in IBS, we studied 30 patients using esophageal manometry and 24-hr pH monitoring of the distal esophagus. Two subgroups of patients underwent esophageal provocative tests (bethanechol 50 micrograms/kg subcutaneously and esophageal balloon distension test). Twelve healthy volunteers formed a control group. A pain threshold on esophageal distension significantly lower than in healthy subjects (11.5 +/- 1 ml vs 22.2 +/- 1.7 ml, P < 0.01) was found in IBS patients. On the other hand, no differences between patients and controls were detected in lower esophageal sphincter pressure and length, esophageal body motility, or GER pattern; furthermore, bethanechol stimulation elicited similar esophageal body motility changes. Our study could confirm no detectable basal or bethanechol-induced esophageal motility disorders in IBS patients, nor enhanced GER. Esophageal involvement in IBS consists of a lower pain threshold on esophageal distension, possibly reflecting an altered visceral receptor sensitivity or modulation throughout the gut.
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PMID:Altered esophageal pain threshold in irritable bowel syndrome. 809 69

Sodium alginate (Gaviscon) is used in the management of gastro-oesophageal reflux in infants. No digestive disadvantages have as yet been reported with the use of the Gaviscon formula available in France, which contains neither aluminium hydroxide nor thickener. Twenty-two healthy neonates were prospectively studied before and after Gaviscon treatment in order to characterize their whole gut transit time with the use of a carmine index. The head of the marker appeared within the same time in both experiments but the appearance of the tail was earlier in the treated infants (P < 0.05), without any subsequent clinical consequences. The slight increase shown in the rate of the clearance of the marker from the gut, is likely to be related to a less proximal to distal dispersion of the marker, subsequently to physical changes occurring in the viscous alginate. Frequency and consistency of the stools were unmodified by treatment and accordingly Gaviscon can be regarded as having no deleterious effect on transit time in neonates.
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PMID:[Influence of sodium alginate on the intestinal transit in low birth weight newborn infants]. 824 49

Cholecystokinin (CCK) belongs to the group of substances known as brain-gut peptides: it functions both as a neuropeptide and a gut hormone. The peptide and its synthetic derivatives (like for instance CCK-8 and the amphibian counterpart caerulein) significantly delay emptying of gastric contents in both animals and humans. The fact that CCK, in doses mimicking postprandial plasma levels, strongly affects emptying rate suggests the peptide to be a physiologic regulator of gastric emptying. Unfortunately, clear definition of the role of CCK in the physiology of gastric motor activity has long been hampered by the lack of specific and potent non-peptide antagonists of CCK-receptors. The availability of such compounds has stimulated a broad array of investigations into the physiological actions of this hormone and examination of its putative role in certain diseases. This paper summarizes the available data concerning the effect of CCK and its antagonists on gastric emptying. The use of selective CCK-antagonists has allowed to establish that the gastric motor effect of the peptide is direct and mediated through the stimulation of CCK-A receptors. As a consequence, CCK-A antagonism results in acceleration of emptying rate under certain experimental and clinical conditions. This peculiar pharmacologic effect of CCK-A antagonists, which could be useful in the treatment of functional dyspepsia (idiopathic or diabetic), gastroparesis and gastro-esophageal reflux disease (where patients often display a delayed emptying rate of solid food) needs to be further investigated, in order to fully explore their potential as gastrokinetic drugs.
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PMID:Effect of CCK and its antagonists on gastric emptying. 829 6

Basal and postprandial levels of the foregut hormones gastrin, cholecystokinin (CCK), motilin, and pancreatic polypeptide, and the distal gut hormones neurotensin and peptide YY were measured in 20 patients with gastroesophageal reflux disease (GERD). GERD was defined by abnormal esophageal exposure to pH less than 4. Ten GERD patients had decreased lower esophageal sphincter (LES) pressure (mean: 4.5 mm Hg, range: 0.8 to 6.8 mm Hg), and 10 patients had normal LES pressures (mean: 14.1 mm Hg, range: 9.7 to 22.4 mm Hg). Eight age-matched healthy subjects were also studied. Basal levels of peptide YY were moderately decreased in GERD patients compared with controls irrespective of LES pressure. In patients with abnormal LES pressure, basal levels of motilin and the postprandial response of CCK were significantly decreased compared with controls; and basal levels of neurotensin and the postprandial response of gastrin were significantly increased compared with controls. Pancreatic polypeptide levels were similar in all groups. These gut hormone changes, which are more marked in patients with poor LES pressure, may reflect primary or secondary abnormalities in GERD.
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PMID:Gastroesophageal reflux disease is associated with enteric hormone abnormalities. 831 Nov 31

A child is described with a previously unreported probable trisomy for a segment of the long arm of chromosome 17 responsible for some distinct clinical features. These include craniofacial and skin abnormalities, failure to thrive, partial malrotation of the gut, malabsorption, gastro-oesophageal reflux, neurodevelopmental delay, autonomic disturbance, and cardiac and CNS abnormalities. The coexistence of Klinefelter's syndrome (47,XXY) is of minor significance in relation to this child's phenotype.
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PMID:Probable de novo 17q duplication (q11.2-->q21.1): a newly recognised chromosomal syndrome in a child with Klinefelter's syndrome. 832 Jul 13

The role of motility tests in the evaluation of some common disorders in which motility has been assumed to play a role is reviewed. Three separate areas, non-cardiac chest pain, constipation and the irritable bowel syndrome are discussed. In each area, considerable difficulty in the clinical definition of these disorders persists and presents a major obstacle to the evaluation of diagnostic tests. With regard to non-cardiac chest pain, it is apparent that gastro-oesophageal reflux and sensory/perception abnormalities, rather than dysmotility, are the predominant factors, and investigations should take account of this. While studies of colonic and small intestinal motility have demonstrated various abnormal patterns in patients described as suffering from the irritable bowel syndrome, the specificity of any of these motor 'abnormalities' remains uncertain, and manometry cannot be recommended as a diagnostic tool in this context. Considerable advances have been made in our understanding of gut motor physiology and in our ability to accurately record motor function in man, the basic pathophysiology of many 'functional' gut syndromes remains unclear, and the role of dysmotility, in particular, poorly defined.
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PMID:Gastrointestinal motility testing--a personal perspective. 857 21

The term 'functional disorder' has two main meanings in the clinical realm, neither mutually exclusive: (i) a demonstrable disorder of function that readily explains the symptoms (the common wisdom in the accepted biomedical model of disease); and (ii) a variable combination of chronic or recurrent symptoms not explained by structural or biochemical abnormalities. This is a broader view that incorporates the concepts of illness as well as disease, and one which recognizes that symptoms and behavior may be out of proportion to the objective evidence of abnormality. The challenge is to reconcile these two apparently different views of a patient presenting with symptoms. In this way, investigation and management of a patient's symptoms can be directed not only to the underlying motor and sensory disorders, but also to all of the other psychosocial and cognitive-behavioral factors that impact on the gut through the brain-gut axis and on patient behavior. These numerous aspects of functional gut disorders will be illustrated by a discussion of the factors involved in the pathophysiology of gastroesophageal reflux disease and of the behavior of individuals with this disorder.
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PMID:Overview of functional gut disorders: a challenge. 857 38

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

The aetiopathogenesis of ventilator-associated pneumonia (VAP) requires abnormal oropharyngeal and gastric colonization and the further aspiration of their contents to the lower airways. VAP develops easily if aspiration or inoculation of microorganisms occur in patients with artificial airways, in whom mechanical, cellular and/or humoral defences are altered. Well-known risk factors for gastric colonization include: alterations in gastric juice secretion; alkalinization of gastric contents; administration of enteral nutrition; and the presence of bilirubin. However, the role of the colonized gastric reservoir in the development of VAP remains debatable. Evidence in favour of the role of the stomach in the development of VAP comes mainly from randomized, controlled trials of selective gut decontamination and stress ulcer prophylaxis in the intensive care unit (ICU), in which reducing the bacterial burden of the stomach decreases the incidence of nosocomial respiratory infections. However, at least three studies of flora have found an absence of stomach origin of pneumonia occurring during mechanical ventilation. Prophylactic measures suggested to prevent VAP in relation to the gastric reservoir include: treatment for stress ulcers with sucralfate; prevention of duodenal reflux with metoclopramide; reduction of gastric burden and bacterial translocation by selective digestive decontamination; acidification of enteral feeding; and jejunal feeding. Gastro-oesophageal reflux can be prevented by using small bore nasogastric tubes and jejunal feeding. The aspiration of gastric contents can be reduced by positioning patients in a semirecumbent position, checking the patency of the tube cuff, and aspiration of subglottic secretions. The role of the stomach as a reservoir for microorganisms causing ventilator-associated pneumonia is still controversial but despite the debate, there is major evidence in the literature in favour of the gastric origin of part of these pulmonary infections.
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PMID:Stomach as a source of colonization of the respiratory tract during mechanical ventilation: association with ventilator-associated pneumonia. 886 1

Repeated oesophageal acidification is a definitive feature of gastro-oesophageal reflux disease, which in turn is caused by relaxation of the lower oesophageal sphincter (LOS). This study in anaesthetised ferrets investigates the reflex pathways involved in effects of oesophageal acidification on motor function of the LOS, with particular focus on the role of tachykinins. LOS pressure was monitored with a perfused micromanometric sleeve assembly. Oesophageal acidification reduced LOS pressure by 48 +/- 5% until washout with saline. This reduction became larger with repeated tests, and was unaffected in amplitude by acute bilateral vagotomy, although the response became slower in onset. Intra-oesophageal capsaicin (0.5% solution) caused a 68 +/- 17% decrease in LOS pressure which remained unchanged with repeated tests. The NK-1 receptor antagonist CP96,345 (1-5 mg/kg intravenous (i.v.) blocked the post-vagotomy LOS responses to both intra-luminal acid and capsaicin. Close intra-arterial (i.a.) injections of capsaicin (1-100 micrograms) gut induced LOS relaxation which was neither vagally nor NK-1 receptor-mediated. Substance P or the selective NK-1 receptor agonist [Sar9, Met(O2)11] substance P (25-500 ng close i.a.) caused a biphasic LOS response, consisting of initial brief contraction followed by prolonged, dose-dependent relaxation. Tetrodotoxin (10 micrograms/kg close i.a.) changed the biphasic response to substance P to excitation only. The neurokinin-1 (NK-1) receptor antagonist CP96,345 (0.3-10 mg/kg i.v.) dose-dependently reduced the inhibitory response to substance P. The excitatory phase of the response to substance P was larger and prolonged after guanethidine (5 mg/kg, i.v.), or propranolol (1 mg/kg, i.v.). L-NAME (100 mg/kg i.v.) reduced the inhibitory phase. The selective NK-2 receptor agonist [beta-Ala8] neurokinin A(4-10) caused LOS excitation only. These data indicate that intra-oesophageal acid causes substance P release from extrinsic afferent nerve endings which activates local inhibitory pathways to the LOS via NK-1 receptors.
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PMID:Lower oesophageal sphincter responses to noxious oesophageal chemical stimuli in the ferret: involvement of tachykinin receptors. 940 24


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