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)

A 14-year-old boy presented with regurgitation, malnutrition, and chronic lung insufficiency with a history of successful repair of esophageal atresia and tracheoesophageal fistula in the newborn period. Barium swallow and manometry results showed achalasia. Hellar operation with antireflux procedure resulted in complete symptomatic relief. Histology and immunohistochemistry including PGP9.5, MAP5, cKit, and nNOS of myotomy specimen showed intact innervation. Although esophageal dysmotility after esophageal atresia repair usually is caused by gastroesophageal reflux and incoordination of peristalsis, the possibility of achalasia should also be considered, because a casual relationship between esophageal atresia and achalasia may exist.
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PMID:Esophageal atresia and achalasialike esophageal dysmotility. 1548 12

The purpose of the present study was to determine the effect of chronic alcohol consumption on reactivity of esophageal tunica muscularis mucosae (TMM) and lower esophageal sphincter (LES) smooth muscle. Six male rats in alcohol-fed group received ethanol (7.2% v/v) in a modified liquid diet for 4 weeks. Two control groups were used; six rats in the standard diet-fed group received rat chow and water for 4 weeks. Six rats in sucrose-fed group were given sucrose and received a liquid diet. The smooth muscle reactivity of TMM and LES strips from ethanol-fed and control animals was evaluated in organ chambers. Also histologic study was undertaken to show effects of chronic alcohol consumption. Maximum contractile responses of TMM to KCl and carbachol were decreased in the ethanol-fed group compared to the control groups. Relaxant responses to serotonin were decreased in the ethanol-fed group compared to the control groups. In TMM, isoproterenol- and papaverine-induced relaxant responses were similar in the ethanol-fed and control groups. In LES smooth muscle, relaxant responses to papaverine or isoproterenol were similar in the control groups and the ethanol-fed group. There was no change in agonist potency among the groups. The relaxation response elicited by nicotine and sodium nitroprusside (SNP) or contractile response elicited by carbachol and 80 mM KCl was decreased with maximum responses and pD(2) values, in the ethanol-fed group compared to that of the control groups in LES. Decreased nNOS immunoreactivity in myenteric plexus was found in alcohol-exposed group compared to control groups. Our findings suggest that chronic alcohol consumption impairs relaxant and contractile responses of both TMM and LES smooth muscle and it may contribute to gastroesophageal reflux commonly seen after alcohol binges.
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PMID:Effects of chronic ethanol consumption on rat upper gastrointestinal system: functional and histologic findings. 2281 4

Obesity is highly prevalent worldwide and is associated with significant morbidity and mortality. The focus of this review is to delineate the changes in gastrointestinal motility observed in obesity. A systematic review of the published literature on obesity and gastrointestinal motility was performed. Here, we describe the current understanding of the changes in obesity in the esophagus, stomach, small intestine and colon. Major findings include supportive evidence for increased gastroesophageal reflux disease and esophageal motility disorders in obesity, and a rapid gastric emptying time seen in obese individuals. The proximal small intestinal transit seems to be increased in obesity and this may be secondary to efficient nutrient absorption and subsequent lack of nutrient-induced satiety signals conveyed from the small intestine. In obesity, there is some evidence for delayed colonic transit as well as a reduction in colonic serotonin availability. The molecular mechanisms underlying altered motility in obesity could be secondary to reduced cannabinoids or its receptor cannabinoid receptor 1 (CB1) expression as well as due to loss of neuronal nitric oxide synthase (nNOS) neurons. The interactions of diet and obesity and the alteration of microbiota in this setting are just being explored and may offer novel insights into the changes of gastrointestinal motility in obesity.
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PMID:Effect of high fat-diet and obesity on gastrointestinal motility. 2443 1

The 2007 Consensus Statement for Standard of Care in Spinal Muscular Atrophy (SMA) notes that patients suffer from gastroesophageal reflux, constipation and delayed gastric emptying. We used two mouse models of SMA to determine whether functional GI complications are a direct consequence of or are secondary to survival motor neuron (Smn) deficiency. Our results show that despite normal activity levels and food and water intake, Smn deficiency caused constipation, delayed gastric emptying, slow intestinal transit and reduced colonic motility without gross anatomical or histopathological abnormalities. These changes indicate alterations to the intrinsic neural control of gut functions mediated by the enteric nervous system (ENS). Indeed, Smn deficiency led to disrupted ENS signaling to the smooth muscle of the colon but did not cause enteric neuron loss. High-frequency electrical field stimulation (EFS) of distal colon segments produced up to a 10-fold greater contractile response in Smn deficient tissues. EFS responses were not corrected by the addition of a neuronal nitric oxide synthase inhibitor indicating that the increased contractility was due to hyperexcitability and not disinhibition of the circuitry. The GI symptoms observed in mice are similar to those reported in SMA patients. Together these data suggest that ENS cells are susceptible to Smn deficiency and may underlie the patient GI symptoms.
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PMID:SMN deficiency disrupts gastrointestinal and enteric nervous system function in mice. 2622 59

Development of infantile hypertrophic pyloric stenosis during postoperative period in EA with TEF is rare. Postoperative vomiting or feeding intolerance in EA is more common which is due to esophageal stricture, gastroesophageal reflux and esophageal dysmotility. A typical case of IHPS also presents with non-bilious projectile vomiting at around 3-4 weeks of life. The diagnosis of infantile hypertrophic pyloric stenosis in this subset is usually delayed because of its rarity. We report a case of IHPS in postoperative EA and emphasize on high index of suspicion to avoid any delay in diagnosis with its metabolic consequences.
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PMID:Infantile Hypertrophic Pyloric Stenosis in Postoperative Esophageal Atresia with Tracheoesophageal Fistula. 2629 Aug 14