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 fear of aspiration of gastric contents and its life-threatening consequences in patients(aspiration pneumonitis and respiratory failure), has caused many medical practitioners, particularly anaesthetists, to rigidly follow conservative (i.e. prolonged) preoperative fasting standards. This is the nil per os (NPO) order for clear fluids/liquids and solids overnight or six to eight hours preceding the induction of anaesthesia. This practice neither takes into account the differences in the rate of gastric emptying for solid food (which may exceed six hours) and clear liquids (which is one to two hours), nor the differences in scheduled times of surgery. Long-term prospective studies and retrospective reviews have shown that the incidence of significant clinical aspiration is low: 1.4-6.0 per 100,00 anaesthetics for elective general surgery. Risk factors for pulmonary aspiration include: a high American Society of Anaesthesiologists (ASA) physical status score; emergency surgery; difficult airway management; increased gastric volume and acidity; increased intra-abdominal pressure; gastro-oesophageal reflux; oesophageal disease; head injury with impaired consciousness and extremes of age. Experimental studies and reviews have consistently shown the safety of clear liquid ingestion up to two hours before induction of anaesthesia in healthy patients without risk factors, and the fact that a longer fluid fast does not necessarily offer any added protection against pulmonary aspiration. The conservative pre-operative fasting standard causes discomfort and in some cases, suffering of patients and is therefore unnecessary for patients without risk factor(s). Anecdotal reports at the University Hospital of the West Indies (UHWI) have shown that application of the liberalized guidelines for preoperative fasting and fluid intake has not resulted in increased pulmonary aspiration, morbidity or mortality. Instead it has resulted in decreased irritability, anxiety, thirst and hunger in the peri-operative period. Patients, especially children are more comfortable and the perioperative period is better tolerated. It is therefore time that all medical personnel adopt the liberalized guidelines.
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PMID:Preoperative starvation and pulmonary aspiration. New perspectives and guidelines. 1263 41

Recently, we developed a disposable acid exposure sensor whose in vitro response to acid below pH 4 is linearly determined by the duration of exposure and the degree of acidity. The aim of the present study was to compare the SR to simultaneous esophageal pH and duodenogastroesophageal reflux (DGER) monitoring (Bilitec) in patients investigated for presumed gastroesophageal reflux disease (GERD). Twenty-six patients (16 men, mean age 46 +/- 2 years) with symptoms suggestive of GERD underwent 24-hr ambulatory pH monitoring and SR monitoring at 5 cm proximal to the LES. DGER monitoring was performed in 21 patients. Exposure of the esophagus to acid and to DGER were analyzed. These data were compared to SR. A significant correlation was found between the exposure of the distal esophagus to acid and SR (R = 0.85; P < 0.0001). Similarly, the area below a cutoff pH 4 was significantly correlated to SR (r = 0.81; P < 0.0001). SR was not correlated to DGER (r = 0.16; NS). At a cutoff of 50, the sensitivity and specificity of SR to predict esophageal acid exposure > 5% of time were 91% and 93%, respectively conclusion, the response of the acid exposure sensor is strongly correlated with the results of simultaneous esophageal pH monitoring. The sensor seems able to reliably predict pathological esophageal acid exposure. These findings warrant larger studies of the clinical potential of the acid exposure sensor in the diagnosis and quantification of GERD.
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PMID:Validation of a new method of measuring esophageal acid exposure: comparison with 24-hour pH monitoring. 1264 85

Most patients with peptic ulcer or gastro-oesophageal reflux disease develop nocturnal pain (epigastric and retrosternal pain from midnight to early morning), which often disappears before breakfast. Such pain may be related to a disturbance of the circadian rhythm of gastric acid secretion. Helicobacter pylori is a known aetiological agent of peptic ulcer disease and patients with gastritis or ulcers now undergo infection eradication therapy. However, this can result in the onset or exacerbation of gastro-oesophageal reflux disease. There has been a marked increase in the number of patients with oesophagitis rather than peptic ulcer and because most are negative for H. pylori, attention has centred on the status of their gastric acid secretion. Some patients with oesophagitis complain of nocturnal pain despite treatment with a proton pump inhibitor, and in those cases a short course of an H2 blocker can be very effective. We used a portable pH meter to study, in a cross-over fashion, the changes in the circadian rhythm of gastric acid secretion caused by two H2 blockers, laftidine and famotidine, in 10 H. pylori-negative subjects. There was a significant difference in the rhythm between baseline (no treatment) and when laftidine or famotidine were administered, with mean values for amplitude of 28.1, 13.80 and 10.82, respectively; for the midline estimating statistic of rhythm (MESOR), 22.7, 10.80, and 11.54; and for acrophase, 324.0. 312.3, and 274.5 (p < 0.001). The H2 blockers suppressed the normal circadian rhythm of intragastric acidity, which rises in the evening until the middle of the night and then drops in the morning.
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PMID:Effect of H2 blockers on the circadian rhythm of intragastric acidity. 1265 92

Recent studies suggest that gastroesophageal reflux disease (GERD) may be a major cause of globus sensation. However, the incidence and severity of GERD in patients with globus sensation without reflux symptoms are unknown. In order to establish the relationship between globus sensation in the jugular fossa and GERD, 20 patients attending our ear, nose and throat (ENT) outpatient clinic with globus sensation were investigated with 24-h pH monitoring. A four-channel pH catheter was used with the pH electrodes spaced 5 cm apart in order to detect reflux along the whole length of the esophagus. Fifteen patients complained about globus sensation only; five patients complained additionally about classical reflux symptoms. Thirteen patients showed pathologic reflux measurements. Most of the patients had reflux limited to the distal one-third of the esophagus. Patients with pathologic pH measurements were treated with proton pump inhibitors. Ten out of 13 patients improved with treatment. This study suggests that globus may be associated with reflux, and acidity does not have to reach the pharynx to produce globus sensation.
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PMID:Globus sensation and gastroesophageal reflux. 1275 Sep 18

Gastroesophageal reflux disease is a common, usually lifelong, disorder resulting from chronic abnormal exposure of the lower esophagus to gastric contents. Motor dysfunction of the lower esophageal sphincter is the primary cause of this disease. At this writing, no medical therapies can completely resolve abnormal lower esophageal sphincter function; therefore, the treatment of gastroesophageal reflux disease centers on suppression of intragastric acid secretion. Available acid-suppressant medications include proton pump inhibitors, H2-receptor antagonists, and antacids. Of these, the proton pump inhibitors are recognized generally as the mainstays of both short-term and long-term therapy for gastroesophageal reflux disease. All have a low incidence of side effects and are well tolerated by most patients. Five proton pump inhibitors are available currently for patients with gastroesophageal reflux disease. Of these, esomeprazole has shown greater efficacy in controlling intragastric acidity than the others. For patients with erosive esophagitis, esomeprazole has demonstrated higher healing rates and more rapid sustained resolution of heartburn than omeprazole or lansoprazole after up to 8 weeks of once-daily treatment. Because new therapies for gastroesophageal reflux disease are highly effective, patients can be reassured that their disease will be well controlled and their symptoms resolved with a safe and appropriate treatment.
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PMID:Gastroesophageal reflux disease: current treatment approaches. 1467 9

Transient relaxations of the lower esophageal sphincter (tLESRs), but not delayed gastric emptying, are major mechanisms of gastroesophageal reflux in premature infants. These findings are similar to those seen in older children and adults with gastroesophageal reflux disease. Newer antireflux therapies should be developed that target the reduction of gastric acidity or reduction in the number of tLESRs.
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PMID:The role of lower esophageal sphincter function and dysmotility in gastroesophageal reflux in premature infants and in the first year of life. 1468 73

Duodenogastric reflux is the retrograde flow of duodenal contents into the stomach that then mix with acid and pepsin. These agents can reflux into the esophagus (ie, duodenogastroesophageal reflux ) and cause gastroesophageal reflux disease (GERD) and its complications, including stricture, Barrett's esophagus, and adenocarcinoma of the esophagus. Medical and surgical treatments of DGER can be difficult. Best medical treatment is proton-pump inhibitors, which decrease DGER by inhibiting both gastric acidity and volume, making less gastric contents available to reflux into the esophagus. The addition of the gamma-aminobutyric (GABA(B)) receptor agonist baclofen may further reduce DGER in patients not responding to proton-pump inhibitors. Bile acid-binding agents (aluminum-containing antacids, cholestyramine, sucralfate, urosodeoxycholic acid) have physiologic rationale, but their efficacy is unproven. Prokinetic agents can reduce DGER and its upper gastrointestinal symptoms by promoting increased gastric emptying. In patients with medically refractory symptoms, a Roux-en-Y diversion or duodenal switch operation may be helpful.
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PMID:Duodenogastric Reflux-induced (Alkaline) Esophagitis. 1472 38

For centuries it was recognized that the stomach produces a juice, which has acidic properties, however, it was not until 1824 when Prout demonstrated the presence of hydrochloric acid in gastric juice. At the same time experiments on a patient with gastric fistula began by W. Beaumont showing alterations of acid secretion after meals and under various psychological conditions. After the discovery by L. Popielski in 1920 that histamine is a direct stimulant of oxyntic glands, histamine started to be used in the 1930s in gastric secretory tests. Then in 1949 the dose of histamine was established by K. Kowalewski to induce in humans maximal gastric secretion and in 1953 Kay from UK, using a similar dose of histamine (0.04 mg/kg), introduced augmented histamine test to determine maximal acid output. The digestive period of gastric secretion can be divided into 3 phases: cephalic phase, gastric phase, and intestinal phase. When an acidified meal reaches the antrum or proximal part of the small intestine, the inhibitory autoregulatory mechanisms are triggered. Using a peptone meal as a physiological stimulant of gastric secretion, Fordtran and Walsh designed in 1973 the intragastric titration method. Histamine stimulates H1 and H2 receptors, producing some side effects so Betazole (Histalog), an analogue of histamine was introduced, because of smaller side effects than with histamine. In 1967, pentagastrin, which contains a C-terminal amino-acid sequence of gastrin and does not exert serious side effects, was applied first in Poland as a stimulant of gastric acid secretion instead of histamine. At the present time, a 12 or 24 h pH-metry with a magnetic recording of gastric acidity using the Digitrapper was found to have a greater diagnostic value in assessment of gastric acid secretion under natural conditions including meal than classic gastric secretory tests. This technique has been widely used in detecting the duodeno-gastric or gastro-esophageal reflux (GERD) and testing various drugs affecting gastric acid secretion and healing acid-pepsin disorders.
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PMID:Gastric analysis with fractional test meals (ethanol, caffeine, and peptone meal), augmented histamine or pentagastrin tests, and gastric pH recording. 1507 65

Although alteration of airway pH may serve an innate host defense capacity, it also is implicated in the pathophysiology of obstructive airway diseases. Acid-induced asthma appears in association with gastroesophageal reflux after accidental inhalation of acid (fog, pollution, and workplace exposure) and in the presence of altered airway pH homeostasis. Endogenous and exogenous exposures to acids evoke cough, bronchoconstriction, airway hyperreactivity, microvascular leakage, and heightened production of mucous, fluid, and nitric oxide. Abnormal acidity of the airways is reflected in exhaled breath assays. The intimate mechanisms of acid-induced airway obstruction are dependent on activation of capsaicin-sensitive sensory nerves. Protons activate these nerves with the subsequent release of tachykinins (major mediators of this pathway) that, in conjunction with kinins, nitric oxide, oxygen radicals, and proteases, modulate diverse aspects of airway dysfunction and inflammation. The recognition that acid stress might initiate or exacerbate airway obstructive symptomatology has prompted the consideration of new therapies targeting pH homeostasis.
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PMID:Acid stress in the pathology of asthma. 1510 Jun 63

Fifteen-year experience in the treatment of 588 patients with esophageal and gastroduodenal bleedings is analyzed. Surgery was performed in 286 patients, 302 patients were treated conservatively including 71 patients who underwent endoscopic procedures. Principles of differentiated treatment policy are developed. Selective proximal vagotomy in combination with fundoplication (if indicated, with surgeries draining the stomach) is surgery of choice in bleeding reflux-esophagitis and gastroduodenal ulcerous bleedings. These methods eliminate pathogenetic factors of bleeding gastro-esophageal reflux, lower acidity of gastric juice.
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PMID:[Vagotomy in the treatment of bleeding reflux-esophagitis and gastroduodenal bleedings]. 1521 34


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