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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 prospective multifactorial study of symptoms and disturbance of gastrointestinal function has been undertaken in 50 patients with non-ulcer dyspepsia. Objective tests including solid meal gastric emptying studies, gastric acid secretion, E-HIDA scintiscan for enterogastric bile reflux, and hydrogen breath studies were carried out in all patients and validated against control data. Gastroscopy and biopsy were carried out in non-ulcer dyspepsia patients only. Non-ulcer dyspepsia patients were categorised on the basis of predominant symptoms as: dysmotility-like dyspepsia (n = 22); essential dyspepsia (n = 14), gastro-oesophageal reflux-like dyspepsia (n = 11); and ulcer-like dyspepsia (n = 3). In the total non-ulcer dyspepsia population, solid meal gastric emptying was delayed (T50 mean (SEM) = 102 (6) minutes (patients) v 64 (6) minutes (controls), (p less than 0.01) and high incidences of gastritis (n = 26) and Helicobacter pyloridis infection (n = 18) were found. An inverse correlation was observed between solid meal gastric emptying and fasting peak acid output (r = -0.4; p less than 0.01). Indeed gastric emptying was particularly prolonged in eight patients (T50 mean (SEM) = 139 (15) minutes) with hypochlorhydria. In the non-ulcer dyspepsia population oral to caecal transit time of a solid meal was delayed (mean SEM = 302 (14) minutes (patients) v 244 (12) minutes (controls) (p less than 0.01]. Seven patients had a dual peak of breath hydrogen suggestive of small bowel bacterial overgrowth. No association was observed between symptoms and any of the objective abnormalities. This multifactorial study has shown that hypomotility, including gastroparesis and delayed small bowel transit, is common in non-ulcer dyspepsia and may be related to other disorders of gastrointestinal function. No relation between symptoms and disorders of function, however, has been shown.
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PMID:Evidence for hypomotility in non-ulcer dyspepsia: a prospective multifactorial study. 201 18

Surveys of athletes, primarily runners, have shown that digestive disorders are common, associated both with training and racing. Women, in particular, seem to suffer most commonly. Nearly half have loose stools and nausea and vomiting occur frequently after hard runs. Diarrhoea, incontinence and rectal bleeding occur with surprising frequency. Runners may use medications prophylactically to minimise some of these symptoms. Upper digestive symptoms seem to occur more commonly in multisport events such as triathlons or enduro. The published literature is difficult to analyse and the basic intestinal physiology not well studied. Most gastroenterologists are accustomed to evaluating the fasting patient at rest and exercise physiologists are seldom experienced with digestive techniques. Digestive symptoms occurring with exercise referable to the oesophagus include chest pain, gastro-oesophageal reflux symptoms, or symptoms related to alterations in motility. While little is known of the oesophageal physiology during exercise, it is believed that only minimal changes occur in most subjects. Gastro-oesophageal reflux occurs more frequently with exercise than at rest and may produce symptoms of chest pain suggestive of ischaemic disease. Acid exposure may be reduced by pretreatment with histamine H2-receptor antagonists. Oesophageal symptoms, though common, are rarely disabling to the athlete, and the clinical importance lies in confusion with ischaemic disease. Cases of acute gastric stasis following running have been reported and gastric physiology during exercise, particularly bicycling, has been more actively investigated. Gastric emptying during exercise is subject to a number of factors including calorie count, meal osmolality, meal temperature and exercise conditions. However, it is generally accepted that light exercise accelerates liquid emptying, vigorous exercise delays solid emptying and has little effect upon liquid emptying until near exhaustion. Gastric acid secretion probably changes little with exercise although some have postulated that ulcer patients may increase secretion with exercise. Some exercise-associated digestive symptoms, such as diarrhoea and abdominal pain, have been attributed to changes in intestine function. Small bowel transit is delayed by exercise when measured by breath hydrogen oral caecal transit times and motility may be reduced as well. Intestinal absorption during exercise has not been well evaluated but probably changes little in ordinary circumstances. Passive absorption of water, electrolytes and xylose are not affected by submaximal effort. Colonic transit and function is even more difficult to evaluate and published results have been conflicting. However, it is likely that many of the lower digestive complaints of runners such as diarrhoea and lower abdominal cramps are due to direct effects of exercise upon the colon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of exercise on the gastrointestinal tract. 218 30

The management of oesophageal reflux disease can and should be highly individualised, depending on the severity of the disease. Mild occasional symptoms of heartburn can often be controlled with conservative measures or changes in diet and antacids. For patients with erosive or ulcerative oesophageal disease, it is becoming clear that acid plays a crucial role in injury and that suppression of acid enhances healing. Antipeptic dosages of histamine receptor antagonists achieve good relief of symptoms but may not always heal erosive oesophagitis. Healing rates are improved with the use of new hydrogen-potassium adenosine triphosphatase (ATPase) pump inhibitors which suppress virtually all acid production. The recurrence of disease is common after acid suppression therapy is discontinued, suggesting the need for some form of long term maintenance therapy. Promotility drugs, which improve oesophageal motility, have inconsistent results in clinical trials and have been associated with a higher rate of adverse drug effects in comparison with acid-suppressive therapies. Surgical treatment should still be considered for patients with chronic recurrent disease who do not respond well to pharmacological therapies.
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PMID:Treatment approaches to reflux oesophagitis. 219 48

The author examined 30 patients with clinical symptoms of gastroesophageal reflux. The patients suffered of bronchial asthma (19) and chronic obstructive bronchitis (11). Intraesophageal and intragastric proteolysis with subsequent digestion of the protein substrate in solutions with different concentration of hydrogen ions (pH 1.68 and 8.15). Gastroesophageal reflux was observed in 25 and duodenogastroesophageal in 16 patients. The gastric and duodenal contents reached the upper portions of the esophagus in 14 of the 30 patients. The obtained findings indicate frequent effects of proteases on the bronchi.
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PMID:[Gastroesophageal reflux in patients with chronic nonspecific lung diseases]. 220 49

OEsophageal manometry, acid perfusion test and recording of oesophageal pH after gastric filling with 300 ml HCI were carried out in 55 patients with at least one symptom of gastro-oesophageal reflux (GER). None of the patients complained of dysphagia or had a history of haemorrage, but 19 had oesophagitis on endoscopy. pH probe recordings showed evidence of GER in 72% of the patients, and acid perfusion was painful in 44%. The resting lower oesophageal sphincter pressure was below normal in 20%. Thirty-eight p. cent had peristaltic disorders associated with significantly decreased sphincter pressure. In this category of patients, oesophageal pH recordings constitute the best method for diagnosing GER. Apositive acid perfusion test indicates that the clinical symptoms are due to abnormal sensitivity of the mucosa to hydrogen ions. Manometry is useful for a study of motor disorders resulting from GER, but insufficient to determine whether or not GER is present.
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PMID:[Gastro-oesophageal reflux syndrome. Functional exploration of the oesophage in 55 patients (author's transl)]. 742 98

Chronic Esophageal reflux induces reflux esophagitis, which is a common finding in gastroenterological practice. Reflux esophagitis produce symptoms like pirosis, regurgitation and in some cases respiratory complains resembling asthma or angina-like chest pain. The pathophysiology of this disease is based on a multifactorial origin, which usually results in the chronic evolution of the disease. In recent years, there have appeared new evidences pointing out to alterations in the relaxing mechanisms of the lower esophageal sphincter; however, some patients having reflux esophagitis show normal shincteric pressure. The sweep action of esophageal smooth muscle is a key point for sending back to stomach the eventually refluxed material; it has been demonstrated that this sweeping action is impaired in many patients having reflux esophagitis. Incompetence of lower esophageal sphincter seems to be related a local to neural alteration rather than to smooth muscle functional disturbance. Recent findings stablis a link between local nitric oxide release and relaxation of the lower esophageal sphincter. Esophageal mucosaldisplay an intrinsic resistance to HCL, pepsin, bilis and enzymes deleterious action by a blockade of back-defusion of hydrogen ions contained in the refluxed material. Nevertheless, some other luminal and non-luminal factors are involved in this mucosalprotection. When these intrinsic resistance factors are abated, tisular lesions like ersion, ulcer and Barret's mucosal changes can occur; is of particular interest because its potential malignant evolution. Esophageal reflux usually resolves with medical treatmen, but in some particular cases surgical correction is indicated for improving the antireflux barrier.
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PMID:[Reflux esophagitis]. 776 23

Liquid esophageal transit and gastric emptying, mouth-to-cecum transit, and whole gut transit of a solid-liquid meal were measured in 14 patients with PSS, 16 control subjects (esophageal transit), and 20 control subjects (gastrointestinal transit), respectively, by using scintigraphic techniques, the hydrogen breath test, and stool markers. In patients with PSS, the glucose hydrogen breath test for detection of small intestinal overgrowth was performed and various gastrointestinal symptoms were determined. Esophageal transit and gastric emptying were significantly prolonged in PSS patients with 11 of 14 PSS patients (79%) disclosing delayed esophageal transit and eight of 14 PSS patients (57%) disclosing delayed gastric emptying. All PSS patients with prolonged gastric emptying also had delayed esophageal transit and there was a significant positive correlation between esophageal transit and gastric emptying (r = 0.696, P < 0.01). No significant differences between PSS patients and controls were detected concerning mouth-to-cecum transit and whole gut transit, but abnormally delayed mouth-to-cecum transit was found in four of 10 PSS patients (40%) and abnormally prolonged whole gut transit was detected in three of 13 PSS patients (23%). Small bacterial overgrowth was diagnosed in three of 14 PSS patients (21%). Delayed esophageal transit and gastric emptying were associated with dysphagia, retrosternal pain, and epigastric fullness, while prolonged whole gut transit was associated with constipation. It is concluded that delayed gastric emptying is frequently associated with esophageal transit disorders in PSS patients and may be one important factor for the development of gastroesophageal reflux disease in these patients.
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PMID:Gastrointestinal transit through esophagus, stomach, small and large intestine in patients with progressive systemic sclerosis. 792 44

Thirty-five patients with gastroesophageal reflux (GER) proved on ambulatory esophageal hydrogen monitoring were surgically treated by a floppy Nissen fundoplication. Postoperatively, reflux and symptoms related to it were almost completely abolished. Transient bloating syndrome was observed in five instances. The operation significantly improved esophagitis (p < 0.01), increased lower esophageal sphincter pressure (p < 0.01) and increased amplitude of esophageal peristalsis (p < 0.01). However, postoperative motility of the esophagus as detected by manometry was still impaired as compared with that for the control group. Delayed esophageal transit did not improve postoperatively, although no dysphagia was accounted. Impaired esophageal motility in GER was associated with delayed gastric emptying, which, however, improved postoperatively. It is concluded that esophageal and gastric motor abnormalities are rather primary disorders in GER. After successful fundoplication, esophageal dysmotility, aggravated by reflux esophagitis, improves to some extent, while gastric emptying is enhanced.
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PMID:The effect of floppy Nissen fundoplication on esophageal and gastric motility in gastroesophageal reflux. 826 74

Gastroesophageal reflux is a common disease. Its chronic course, even if mild, is sometimes complicated by erosive oesophagitis. Drug therapy acts against gastric acidity and motility disorders. Treatment of gastroesophageal reflux disease has three aims: improvement of symptoms and quality of life, healing erosive lesions and prevention of symptomatic and endoscopic relapses. Non-drug measures are always useful, even if their efficacy is not well established. Initial therapy of a symptomatic reflux or mild oesophagitis is most of the time effective (antacids, prokinetics, H2 receptor antagonists). Proton-pump inhibitors are also effective in healing and preventing severe oesophagitis. Questions about long-term treatment adverse events with powerful acid inhibitors, such as hypergastrinemia and the risk of gastric carcinoid tumours seem to be resolved. Studies are requested to define the optimal long-term maintenance treatment with cisapride, H2 receptor antagonists or proton-pump inhibitors at low doses in prevention of symptomatic and mild oesophagitis relapses.
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PMID:[Therapeutic principles in gastroesophageal reflux]. 857 Sep 62

Laryngeal manifestation of gastroesophageal reflux is felt to be prevalent in our society. In general, diagnosis has been based primarily on symptoms. Historically, additional testing included laryngoscopy, barium swallow, manometry, and more recently, single- and double-probe pH monitoring. We evaluated 68 patients who were symptomatically suggestive of having reflux laryngitis. We administered surveys grading their symptoms. All patients underwent standardized videolaryngostroboscopic evaluation and computerized acoustic analysis. Patients then underwent a uniform therapy of dietary restrictions and omeprazole, a hydrogen ion inhibitor, for 12 weeks. Patients were then retested. This regimen demonstrated an 85% success of relieving symptoms. Utilizing the new laryngoscopic grading system, improvement was found to be statistically significant in improvement of all findings except granulomas. In patients with the pretherapy complaint of hoarseness, acoustic measures of jitter, shimmer, habitual frequency, and frequency range all showed significant improvement. The authors conclude that in patients with symptomatic reflux laryngitis, standardized videolaryngoscopy and, if hoarse, acoustic analysis are useful exam techniques to aide diagnosis and monitor therapy. Anti-reflux therapy with omeprazole is effective and improvement can be objectively demonstrated with the techniques described.
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PMID:Subjective, laryngoscopic, and acoustic measurements of laryngeal reflux before and after treatment with omeprazole. 894 45


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