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 36-year-old woman suffered from bone pain, muscle weakness, and renal stones after prolonged ingestion of antacids for esophageal reflux. Investigation disclosed hypophosphatemia, hypercalciuria, and osteomalacia by bone biopsy. All symptoms and abnormal laboratory findings reversed with a regimen of oral phosphate supplementation and cessation of antacid intake.
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PMID:Antacid-induced osteomalacia and nephrolithiasis. 64 54

A randomized prospective trial was designed to evaluate the preventive treatment of esophagitis in 31 intensive care patients who had a nasogastric feeding tube for at least 10 days. Fourteen patients (group B) received no preventive treatment while 17 patients (group A) received 300 mg of cimetidine every 6 h intravenously and 11 g of colloidal aluminium phosphate every 4 h per os. All patients were fed a standard diet through their nasogastric tube at a constant rate of 30 Kcal/kg/day. Endoscopic controls at day 1 and 10 showed that the number of initial and final esophagitis was not different in groups B and A: 7 and 8 at day 1, 11 and 10 at day 10, respectively. The inefficiency of this preventive treatment suggested that acid gastroesophageal reflux is not a major factor in the occurrence of nasogastric feeding tube-induced esophagitis. However as esophagitis is associated with a more severe Knaus index and a greater number of gastric stress ulcer risk factors, it is suggested that decreased defense of the mucosa may be a key factor in the occurrence of this type of esophagitis.
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PMID:[Attempt at preventive treatment of esophagitis caused by intubation during intensive care]. 355 57

Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
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PMID:Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. 1040 Apr 1

Gastroesophageal reflux is a common problem in the newborn and preschool periods. Recent research suggests that it may be related to eustachian tube dysfunction and otitis media with effusion. The purpose of this experiment was to investigate the relationship between simulated gastroesophageal reflux and eustachian tube dysfunction. Rat middle ears were repeatedly exposed (transtympanically) to pepsin in hydrochloric acid or to phosphate-buffered saline solution. Their eustachian tube function was evaluated by assessing passive opening and passive closing pressures, and active clearance of positive and negative pressure. The passive pressure function tests showed variable results. The rats exposed to pepsin in hydrochloric acid had an impaired ability to clear positive and negative pressure from the middle ear as compared to the rats exposed only to phosphate-buffered saline solution. The results demonstrate that multiple middle ear exposures to pepsin in hydrochloric acid leads to eustachian tube dysfunction in rats.
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PMID:Transient inflammation and dysfunction of the eustachian tube secondary to multiple exposures of simulated gastroesophageal refluxant. 1164 25

A 3-year-old boy was found to have a mixed tubulopathy with hypokalemia (1.9 mmol/l), alkalosis (blood pH 7.51, plasma carbon dioxide pressure 46 mm Hg, plasma bicarbonate 35.7 mmol/l) and hypophosphatemia (1.21 mmol/l). An electrocardiogram disclosed a prolonged heart rate corrected QT interval of 490 ms. The boy was put on potassium chloride, phosphate and nonsteroidal anti-inflammatory agents. With this treatment plasma phosphate normalized and plasma potassium increased up to 3.0-3.3 mmol/l. Three years later the child, who did not have history of gastroesophageal reflux or epileptic convulsions, suddenly died during sleep. The cause of death could not be determined through gross examination of the body. The history of hypokalemia, the QT-prolongation, the sudden death and the failure to assess the cause of death through gross examination of the body suggest that death was caused by an arrhythmia secondary to hypokalemia.
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PMID:Electrocardiographic QT prolongation and sudden death in renal hypokalemic alkalosis. 1213 87

Five isonitrogenous diets (1-5) with 40% protein using oilcakes as protein sources were formulated and fed to Cirrhinus mrigala fingerlings maintained both under laboratory and field conditions. Water soaking of oilcakes for 24 h before incorporation in the diets helped in the reduction of antinutrient factors (phytase and tannins). Live weight gain in fish fingerlings fed on a diet containing groundnut oilcake (GNOC) was significantly (P < 0.05) enhanced in comparison to the other dietary treatments when examined at the end of a feeding schedule. Laboratory studies have further revealed that APD, PER, GPR and GER values were significantly (P < 0.05) enhanced, while those of feed conversion ratio were significantly (P < 0.05) reduced in fish fed on diet 1 containing GNOC. An analysis of water samples collected at two hourly interval from the aquaria revealed low levels of total ammonia (N-NH4+) excretion and reactive phosphate (O-PO4) production in fish fed on diet 1. Proximate carcass composition also revealed high accumulation of protein, fat, energy and phosphorus in fingerlings fed on a diet containing GNOC. Even in field studies a significant (P < 0.05) increase in mean fish weight gain and specific growth rate (SGR% d(-1)) was observed in fingerlings fed on diet 1, followed by canola (2), sunflower (3), mustard oilcake (4) and sesame (5). Water and sediment quality characteristics also correlated well with fish growth.
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PMID:Oilcakes as protein sources in supplementary diets for the growth of Cirrhinus mrigala (Ham.) fingerlings: laboratory and field studies. 1268 72

Pathogenicity of five isolates of Steinernema carpocapsae (GER: Germany, BUW: Becker Underwood, KOP: Koppert, CZ: Czech Republic, BEL: Belgium) were tested against the fourth instar larvae of the cotton leaf worm, Spodoptera littoralis and the beet armyworm, Spodoptera exigua (Lepidoptera: Noctuidae) at different concentrations (0, 5, 10, 25, and 50 infective juveniles/cm2) in Petri dishes (9 cm dia.) lined with filter paper. Results obtained after 48 h exposure indicated that the pathogenicity varied in time, dose of application and host species. On S. littoralis, KOP, BUW, CZ and GER were more virulent than BEL, whereas all isolates showed 100% control of S. exigua after 72 h. The LC50 values of all five isolates were lower for S. exigua than for S. littoralis. Among the isolates tested, KOP showed the lowest LC50 value in both S. exigua (3.84) and S. littoralis (4.44 infective juveniles). To further check the pathogenicity, the symbiotic bacterium of S. carpocapsae, Xenorhabdus nematophilus, was isolated from Galleria mellonella 30 h after its infection with the nematode. Ten microlitres of 50 mM phosphate buffer containing 0, 10, 100, 1000, or 10,000 cfu were injected into the haemocel of fifth instar larvae of S. exigua. Significant differences in mortality of S. exigua larvae were observed 96 h post-injection with different bacterial doses. Cell-free filtrates of X. nematophilus were isolated from a bacterial suspension; 10 microlitres of filtrates were injected into fifth instars of S. exigua. All larvae had died 72 h post-injection. To check the insecticidal capability of X. nematophilus via oral uptake, suspensions of bacteria at concentrations of 0, 1010, 109, and 108 cfu/ml were sprayed onto tomato leaves cv. Moneymaker infected with fourth instar larvae of S. exigua. None of the larvae were killed after 24 h. Finally, we tested the virulence of selected isolates of S. carpocapsae (KOP, BUW, and BEL) in the glass-house on tomato plants infested with S. exigua or S. littoralis larvae. Nematodes were sprayed at a concentration of 2.5 billion/ha. After 48 h isolate KOP caused higher mortality (99% and 85% on S. exigua and S. littoralis, respectively), than other tested isolates. S. carpocapsae isolates BUW and BEL caused 61-65% mortality on S. exigua and S. littoralis, respectively. As most of the isolates had the same origin, viz. the ALL strain, these results demonstrate differences in pathogenicity of the production.
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PMID:Diversity in pathogenicity of Steinernema carpocapsae and its symbiotic bacterium for Spodoptera spp. 1739 Aug 10

Osteoclasts degrade bone through the creation of an enclosed, acidic extracellular microenvironment adjacent to the bone surface. Membrane bound proton pumps in the osteoclast cell membrane function to create this acidified environment. Accordingly, this H(+) ion transport mechanism provides a potential target for a specific class of drugs, proton pump inhibitors (PPI), with a view to controlling osteoclast mediated bone resorption. Self setting calcium phosphate cements are common bone graft materials that are degraded by osteoclastic activity. We have already shown that incorporation of bafilomycin, a non-regulated PPI, within these cements prevents or delays osteoclast mediated resorption of the cement. We demonstrate here that two regulated proton pump inhibitors, Pantaprazole and Omeprazole, currently used clinically to treat gastroesophageal reflux disorders, are effective in inhibiting osteoclast mediated resorption in-vivo when delivered to a bony defect in self setting calcium phosphate cements. As determined by qualitative histology, Pantaprazole at a dose of 0.5mg/ml produced a delay in osteoclast resorption whilst this effect was not as evident using Omeprazole at an equivalent dose, but higher doses of Omeprazole (40mg/ml) did delay cement resorption. These data demonstrate, for the first time, the functional effect of blocking the H(+)/K(+) ATPase pump in-vivo on the capacity of osteoclasts to resorb bone and the potential of this strategy to modulate osteoclast mediated resorption of calcium phosphate biomaterials.
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PMID:Use of gastrointestinal proton pump inhibitors to regulate osteoclast-mediated resorption of calcium phosphate cements in vivo. 1945 Feb 26

Adamowicz and colleagues raised the alert in 2007 about patients with atypical hereditary fructose intolerance (HFI) primarily misdiagnosed as CDG Ix. We describe a girl with neonatal hypertonia, facial trismus, absent swallowing and coughing reflexes, gastro-oesophageal reflux and sporadically elevated Krebs cycle metabolites and lactate. At 14 months microcephaly and hepatomegaly were noted, with hypertransaminasaemia but normal blood coagulation, glucose, phosphate, and absent urinary reducing substances. Neurological impairment persisted. Because of hepatic and neurological abnormalities with developmental delay, Tf IEF was performed and showed a severe type 1 pattern, resulting in a wrong diagnosis of CDG. Subsequently, an aversion to fruits suggested HFI, confirmed by the finding of ALDOB mutations (p.A150P/p.N335K). The girl improved with fructose-free diet, but liver cirrhosis led to hepatic transplantation. She is now 7 years old with good evolution; facial trismus and hypertonia reversed, but microcephaly persists. Transferrin MALDI-TOF MS characterization revealed underoccupation of glycosylation sites and glycan abnormalities, which reversed with dietary treatment. High maternal fructose concentrations might have caused neonatal abnormalities. Although in our patient's mother there is no fructose accumulation at present, it is possible that increased ingestion of fruits and vegetables during pregnancy, together with her heterozygosity, caused an accumulation of fructose that finally affected the fetus. We also describe slightly abnormal transferrin isoelectric focusing and MALDI-TOF MS patterns of intact transferrin and N-glycans in a fructose-1,6-bisphosphatase (FBP1)-deficient patient. While HFI is a well-known cause of secondary CDG, we found no reports of abnormal transferrin isoelectric focusing patterns in FBP1 deficiency and we introduce this condition as a possible secondary cause for altered transferrin isoelectric focusing.
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PMID:Secondary disorders of glycosylation in inborn errors of fructose metabolism. 1976 53

We have focused on understanding the onset of gastroesophageal reflux disease by examining the mucosal response to the presence of acid in the esophageal lumen. Upon exposure to HCl, inflammation of the esophagus begins with activation of the transient receptor potential channel vanilloid subfamily member-1 (TRPV1) in the mucosa, and production of IL-8, substance P (SP), calcitonin gene related peptide (CGRP) and platelet activating factor (PAF). Production of SP and CGRP, but not PAF, is abolished by the neural blocker tetrodotoxin suggesting that SP and CGRP are neurally released and that PAF arises from non neural pathways. Epithelial cells contain TRPV1 receptor mRNA and protein and respond to HCl and to the TRPV1 agonist capsaicin with production of PAF. PAF, SP and IL-8 act as chemokines, inducing migration of peripheral blood leukocytes. PAF and SP activate peripheral blood leukocytes inducing the production of H(2)O(2). In circular muscle, PAF causes production of IL-6, and IL-6 causes production of additional H(2)O(2), through activation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. Among these, NADPH oxidase 5 cDNA is significantly up-regulated by exposure to PAF; H(2)O(2) content of esophageal and lower esophageal sphincter circular muscle is elevated in human esophagitis, causing dysfunction of esophageal circular muscle contraction and reduction in esophageal sphincter tone. Thus esophageal keratinocytes, that constitute the first barrier to the refluxate, may also serve as the initiating cell type in esophageal inflammation, secreting inflammatory mediators and pro-inflammatory cytokines and affecting leukocyte recruitment and activity.
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PMID:Viewpoints on Acid-induced inflammatory mediators in esophageal mucosa. 2110 19


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