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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastroesophageal reflux disease affects more than 40% of Americans, causing heartburn and reflux of gastric contents into the esophagus when bending or lying down. Lifestyle modification, such as weight loss and a diet rich in protein and low in fat and glucose, should increase the patient's resting lower esophageal sphincter pressure. Avoiding exacerbating substances, such as mint, chocolate, alcohol, and tobacco, also may reduce symptoms. Medications may be prescribed to reduce persistent symptoms, although no medication currently available cures the disease process. Patients who need antireflux medication regularly for four to six weeks or more may be candidates for laparoscopic Nissen fundoplication. Patients who do not want to take antireflux medication for the rest of their lives, cannot afford the medication for an extended period of time, or suffer significant side effects from the medication also are candidates. This article describes performing Nissen fundoplication laparoscopically on an outpatient basis. The average length of hospital stay has been decreased to two to three hours when performed laparoscopically on an outpatient basis from 10 days for the open procedure and two to three days when performed laparoscopically on an inpatient basis. The incidence of recurrent heartburn is less than 2% when the procedure is performed laparoscopically and does not appear to be clinically significant.
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PMID:Outpatient laparoscopic Nissen fundoplication. 1206 45

Some athletes suffer from exercise-induced gastrointestinal (GI) disturbances. We developed a profile of GI parameters in 10 symptomatic and 10 asymptomatic athletes both at rest and during exercise. Exercise included 90 min of cycling and running at 70% of maximal power. We measured oesophageal motility, gastro-oesophageal reflux, gastric emptying, orocaecal transit time (OCTT), intestinal permeability and intestinal glucose absorption. During cycling the number and duration of refluxes were increased, whereas gastric emptying showed no differences between rest, cycling and running. The OCTT was increased in the running trial, compared to rest (P=0.005). Also, intestinal permeability was higher in the running trial, compared to rest (P=0.008). There were no differences in intestinal glucose absorption between rest and exercise. Compared with asymptomatic athletes the symptomatic subjects had a higher intestinal permeability (P=0.001), more reflux episodes (P=0.03) and a longer duration of reflux (P<0.05) during cycling. No differences were observed at rest. In conclusion, there is no difference in GI profile between symptomatic and asymptomatic athletes at rest. During exercise, symptomatic subjects have a longer OCTT and a higher intestinal permeability, which is more pronounced during running than during cycling.
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PMID:Gastrointestinal profile of symptomatic athletes at rest and during physical exercise. 1463 26

Acute changes in blood glucose concentration have major effects on gastrointestinal motor function. Patients with diabetes mellitus have an increased prevalence of gastroesophageal reflux. Transient lower esophageal sphincter (LES) relaxation (TLESR) is the most common sphincter mechanism underlying reflux. The aim of this study was to investigate the effect of acute hyperglycemia on triggering TLESRs evoked by gastric distension in healthy volunteers. TLESRs were stimulated by pressure-controlled and volume-controlled (500 ml) gastric distension using an electronic barostat and performed on separate days. On each day, esophageal manometry was performed in the sitting position during gastric distension for 1 h under euglycemia (5 mM), and either marked hyperglycemia (15 mM) or physiological hyperglycemia (8 mM) in randomized order was maintained by a glucose clamp. Marked hyperglycemia doubled the rate of TLESRs in response to both pressure-controlled [5 (3-10.5, median or interquartile range) to 10 (9.5-14.5) per hour, P < 0.02] and volume-controlled [4 (2.5-7.5) to 10.5 (7-12.5) per hour, P < 0.02] gastric distension but had no effect on basal LES pressure. Physiological hyperglycemia had no effect on the triggering of TLESRs or basal LES pressure. In healthy human subjects, marked hyperglycemia increases the rate of TLESRs. Increase in the rate of TLESRs is independent of proximal gastric wall tension. Mechanisms underlying the effect remain to be determined. Hyperglycemia may be an important factor contributing to the increased esophageal acid exposure in patients with diabetes mellitus.
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PMID:Effect of hyperglycemia on triggering of transient lower esophageal sphincter relaxations. 1506 63

We used a simple questionnaire to determine the presence or absence of symptoms of gastroesophageal reflux disease (GERD) among control (n=531) and diabetic patients (n=629). Of 531 controls, 24.3% reported having symptoms, while 24.9% of 629 diabetic patients had symptoms. Symptomatic diabetic patients (n=157) were then asked to complete a supplemental questionnaire (QUEST) to determine the frequency, severity, and duration of GERD symptoms; a total diagnostic score > or =4 was considered to be positive for GERD. Diabetic patients whose QUEST score was > or =4 had a significantly higher BMI (26.9+/-0.4* vs. 24.4+/-0.4), higher HbA1c (7.5+/-0.2* vs. 7.2+/-0.1), longer duration of diabetes (113.5+/-8.7* vs. 94.0+/-10.6 months), and a higher prevalence of diabetic complications (retinopathy, 24.8%* vs. 21.3%; nephropathy, 32.6%* vs. 19.4%; neuropathy, 30.4%* vs. 23.6%) than diabetic patients whose QUEST score was <4 (*p<0.05). In diabetic patients with GERD, therapy should include not only proton pump inhibitor therapy and other specific measures for GERD, but also appropriate therapy for the diabetes, particularly blood glucose control and weight reduction.
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PMID:Symptoms of gastroesophageal reflux in diabetes patients. 1790 82

In patients undergoing total arch replacement with protruding or mobile atheroma in the proximal aorta, we isolate cerebral circulation from systemic one by starting selective cerebral perfusion (SCP) before systemic arterial perfusion to prevent aortogenic embolic stroke. We disclose the safety of this isolation technique by measuring cerebral oxygenation and metabolism. Sixty-six patients underwent total arch replacement using SCP since 1998. The isolation technique was applied in sixteen patients. Jugular venous oxygen saturation (SjO(2)) was monitored in nine patients undergoing isolation technique (isolation-group) and in thirteen patients of the rest (conventional-group). Oxygen, glucose, and lactate extraction ratio (OER, GER, and LER) were measured at seven time points peri-operatively. The isolation-group had significantly longer SCP time (isolation: 185+/-52 min vs. conventional: 140+/-43 min, P<0.01). During cooling, SjO(2) was kept comparable between groups. OER was minimum at the end of cooling and comparable between groups (isolation: 3.8+/-7.7% vs. conventional: 11.7+/-13.8%, P=0.37). There were no significant differences in GER and LER between groups. There were neither in-hospital death nor stroke. Temporary neurological dysfunction was observed only in conventional-group (n=3, 23%, P=0.12). Isolation technique for total arch replacement could be performed safely and may provide acceptable results in patients at high risk for embolic stroke.
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PMID:Metabolic relevance during isolation technique in total arch repair for patients at high risk with embolic stroke. 1796 10

Adding pectin to an elemental formula increases its viscosity through gelatinization, thus presumably preventing gastro-oesophageal reflux and aspiration pneumonia. We investigated the influence of the viscosity of an elemental formula on gastric emptying. Eleven healthy volunteers underwent three tests at intervals of >1 week. After fasting for >8 h, each subject received a test meal (enteral nutrition solution, enteral solution plus pectin, or water). Then gastric emptying (continuous (13)C breath test), gastro-oesophageal intraluminal pressures, oesophageal pH, and blood levels of glucose, insulin and gastrin were all measured simultaneously. The gastric emptying coefficient was significantly increased by adding pectin to enteral nutrition (3.01 +/- 0.10 vs 2.78 +/- 0.10, mean +/- SE, P < 0.05). The antral motility index was also significantly higher with pectin than without at 45-60 min and 60-75 min after the test meal (526 +/- 237 vs 6.5 +/- 4.6 mmHg s(-1) and 448 +/- 173 vs 2.3 +/- 2.3 mmHg s(-1) respectively; P < 0.05). Plasma glucose was significantly higher with pectin than without it at 60 min after ingestion (141.5 +/- 6.03 vs 125.8 +/- 4.69 microM mL(-1), P < 0.05). In healthy individuals, pectin increased the viscosity of enteral nutrition and accelerated gastric emptying.
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PMID:High-viscosity liquid meal accelerates gastric emptying. 1797 39

Protective effect of quercetin and alpha-tocopherol on experimental reflux oesophagitis in rats was investigated. Rats received quercetin, (100 mg/kg), alpha-tocopherol (16 mg/kg), omeprazole (30 mg/kg) given at 1 h prior to surgery. Quercetin and alpha-tocopherol significantly inhibited the oesophagitis index to 1.33+/-0.12 (P<0.001) and 1.83+/-0.14 (P<0.001) respectively, as compare to control group 3.5+/-0.21. Further, acid and pepsin out put of gastric contents were significantly decreased in treated groups. Indeed, quercetin significantly inhibited the lipid peroxidation (from 0.69+/-0.05 to 0.43+/-0.04 nmol of malonyldialdehyde (MDA)/mg protein) (P<0.001) and increased in levels of catalase to 29.5+/-2.7 units of catalase activity/mg protein and superoxide dismutase (SOD) to 92.4+/-10.5 units/mg protein (P<0.001). The alpha-tocopherol and omperazole showed significant inhibition in lipid peroxidation (0.34+/-0.02 and 0.38+/-0.01) (P<0.01) and enhanced the activities of catalase (34.3+/-3.6 and 31.5+/-3.4) (P<0.01) and SOD (87.3+/-9.2 and 76.60+/-6.9) activity. Quercetin and alpha-tocopherol treated group significantly increased the glutathione level to 36.5+/-2.78 (P<0.01) and 32.1+/-2.34 (P<0.05) respectively. However, it altered the elevated levels of sialic acid and hexose contents in oesophageal tissue. Indeed, quercetin significantly decreased the elevated plasma histamine content (P<0.05). Quercetin and alpha-tocopherol significantly attenuated the elevated level of collagen in oesophageal tissue as of the omeprazole. The results suggest that antioxidants could attenuate the severity of reflux oesophagitis and prevent the oesophageal mucosal damage and validate its therapeutic use in gastroesophageal reflux disease.
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PMID:Effect of quercetin, flavonoids and alpha-tocopherol, an antioxidant vitamin, on experimental reflux oesophagitis in rats. 1854 60

Abnormalities of nutrition status are a common problem in children on peritoneal dialysis (PD) and a source of significant morbidity and mortality. The state of decreased body protein mass and fuel reserves (body protein and fat mass) common in PD patients is now better known as protein-energy wasting (PEW). Protein-energy wasting is a slow, progressive process in chronic kidney disease. The correct approach to this problem includes measurement of early, intermediate, and late markers of PEW, and consideration of the risk factors specific to the patient and to PD. The earliest markers of PEW are associated with some symptoms observed clinically: a decrease in dietary intake and an increase in inflammatory markers. The second stage in the development of PEW (patients with established PEW) is characterized by abnormalities in numerous markers: bioimpedance analysis (BIA) and anthropometric indices, other indices of body mass and composition, biochemical parameters, and indices of protein, glucose, and lipid metabolism. When PEW is established, clear clinical signs become evident: patients in this stage are characterized by high rates of hospitalization and an increased risk for morbidity and mortality as compared with patients without cachexia. Risk factors for PEW can already be present in an apparently well-nourished child who initiates PD: glucose absorption from PD fluid, abdominal distension from PD volume, gastroesophageal reflux, and even more importantly, inadequate dialysis dose in relation to decline in residual renal function. Given the complexity of the pathogenesis and clinical picture of PEW, no single measure, but rather panels of nutritional measures are necessary to diagnose the condition. Combined nutrition scores such as the anthropometry-BIA nutrition score may add value to the monitoring of nutrition status in children on PD.
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PMID:Assessment and monitoring of nutrition status in pediatric peritoneal dialysis patients. 1927 Feb 11

Conventional measurement of gastric secretion is invasive and cannot assess the intra-gastric distribution of gastric contents or the effects of secretion on gastric function. This study assessed the effect of gastric secretion on gastric volume responses and emptying (GE) using a validated fast T(1) mapping magnetic resonance imaging (MRI) technique. Twelve healthy participants were studied in the fasted state and after 200 kcal Gadolinium-DOTA labelled glucose meal during intravenous infusion of pentagastrin or placebo in double-blind, randomized order. Total gastric volume (TGV) and gastric content volume (GCV) was assessed by MRI volume scans and secretion by fast T(1) mapping. Data was described by the kappa-coefficient (volume change after meal ingestion), by GE half time (T(50)) and maximal GE rate (GER(max)) derived all from a GE model. Pentagastrin increased GCV and TGV compared to placebo [kappa(GCV):1.6 +/- 0.1 vs 0.6 +/- 0.1; kappa(TGV): 1.6 +/- 0.1 vs 0.7 +/- 0.1; P < 0.001]. T(1) maps revealed a secretion layer above the meal, the volume of which was associated with kappa (R(2) = 83%, P < 0.001). TGV and GCV change were similar in both conditions (kappa; P = ns). T(50) was higher for pentagastrin than for placebo (84 +/- 7 vs 56 +/- 4min, P < 0.001); however, GER(max) was similar (5.9 +/- 0.6 vs 4.9 +/- 0.4 mL min(-1), P = ns). This study shows volume and distribution of gastric secretion can be quantified in-vivo by non-invasive MRI T(1) mapping. Increased GCV drove TGV accommodation without evidence of a direct effect of pentagastrin or excess acid on gastric function. Secretion increases GCV thus prolongs GE as assessed by T(50); however, GE rate is unchanged.
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PMID:The effect of gastric secretion on gastric physiology and emptying in the fasted and fed state assessed by magnetic resonance imaging. 1934 41

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


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