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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 past two decades have seen outstanding contributions to our knowledge of the physiology of the esophagus, particularly of the lower esophageal sphincter. The clinical syndrome of reflux peptic esophagitis has been clearly delineated and is now well recognized. Although the relationship of the lower esophageal sphincter failure, which causes sliding esophageal hiatal hernia, remains obscure, successful hiatal herniorrhaphy by a variety of methods produces satisfactory clinical results in a majority of patients. There is a significant failure rate in all methods and a morbidity clearly related to operative intervention. Additive surgery such as vagotomy and pyloroplasty is not useful in preventing recurrence and is associated with increased morbidity. Peptic strictures with firm, fibrous stenosis can be satisfactorily treated in most cases with the Thal fundic patch to widen the lumen and Nissen fundoplication to prevent further gastroesophageal reflux.
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PMID:Sliding esophageal hiatal hernia and reflux peptic esophagitis. 109 46

Gastroesophageal reflux is not synonymous with sliding hiatus hernia. It should be approached as a condition dependent on the intrinsic strength of the lower esophageal sphincter rather than on the presence of a hiatus hernia. The patient's account of symptoms is probably the most important means of diagnosis, but in addition the patient's history should be supplemented by radiographic evaluation. Initially the treatment of gastroesophageal reflux is one of prevention. If this conservative approach proves ineffective, drugs that restore sphincter strength can be tried. Surgery should be resorted to only if medical treatment fails, and then one of the newer specific antireflux procedures should be the operation of choice.
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PMID:Recent advances in management of gastroesophageal reflux. 110

An obstructing lesion of the lower thoracic esophagus should be evaluated carefully and appropriate surgical therapy planned to correct the abnormal physiology. Gastroesophageal reflux is the most frequent cause of esophageal stricture and usually can be managed effectively by dilatation of the esophagus, restoration of a competent lower esophageal sphincter, and repair of an associated hiatal hernia. Collis gastroplasty and a Belsey herniorrhaphy are useful when the esophagus is excessively shortened. Firm, fixed esophageal strictures may be treated by the Thal procedure accompanied by Nissen's fundoplication or by resection of the stricture and interposition of a colon graft or an achlorhydric tube. The management of other benign strictures secondary to scleroderma, ingestion of caustic substances, or benign neoplasms must be individualized. Most benign strictures may be cared for by dilatation; however, firm, fixed strictures should be resected. Wide surgical resection is indicated for primary malignant lesions of the lower thoracic esophagus that are localized or have limited lymph node metastasis.
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PMID:Surgical management of strictures of the lower thoracic esophagus. 112 68

Resting lower esophageal sphincter pressures and fasting serum gastrin levels were measured in 35 consecutive patients. 28 of these patients were subdivided into Group I, which consisted of 9 patients with symptomatic gastroesophageal reflux and hiatus hernia, and Group II was further subdivided into Group IIA, 5 patients with hiatus hernias, and Group IIB, 14 patients without hiatus hernia. Mean LES pressures for Groups I, IIA, and IIB were 9.7, 36.8, and 25.6 cm H2O, and serum gastrin levels were 129, 74, and 116 pg/ml, respectively. Examination of these data as a whole or as subgroups failed to demonstrate a correlation between these two variables. The remaining 7 patients had abnormal sphincters (3 patients which scleroderma and 2 with achalasia) or abnormal serum gastrin levels (1 patient with pernicious anemia and 1 patient with antrectomy and Billroth II anastomosis). For these patients as well, no correlation between LES pressure and serum gastrin level was found. These results cast doubt on the hypothesis that endogenous gastrin is a major factor in the maintenance of resting LES pressure.
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PMID:Correlation of lower esophageal sphincter pressure and serum gastrin level in man. 114 86

Hiatal hernia should be included in the differential diagnosis of all children with emesis and failure to thrive, since early diagnosis is imperative to prevent the irreversible esophageal damage from long-standing peptic esophagitis. The Nissen fundoplication as described in this paper appears to be far superior to gastropexy in preventing recurrence of gastroesophageal reflux. Colon interposition should be reserved for those cases in which hiatal herniorrhaphy is technically impossible. Successful repair of the hiatal hernia results in rapid improvement in the nutritional status of these children.
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PMID:Surgical management of hiatal hernia in children. 118 64

Serum gastrin concentration was measured in newborns and infants with no gastrointestinal disorders, in the fasting state and after food stimulation. Mean fasting concentration in 14 newborns aged 1 to 12 days (130 . 4 pg/ml +/- 11 . 4 SE) was significantly higher than the mean value in 23 infants aged 1.5 to 22 months (101.4 +/- 6.6 pg/ml). Ingestion of the usual milk meal resulted in a definite rise of the serum gastrin level in the 5 subjects tested (3 newborns and 2 infants). The mean fasting serum gastrin level in 6 babies with hiatus hernia and gastro-oesophageal reflux was found to be no different from the corresponding value in 8 age-matched controls. However, a conspicuously raised fasting gastrin concentration was observed in one infant with lower oesophageal dyskinesia. The results indicate that the release of gastrin and the reactivity of the hormone-producing sites to food stimulation in early life are similar to those in adult humans. No defect of gastrin release was shown in patients with gastro-oesophageal reflux.
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PMID:Serum gastrin level in early childhood. 124 75

Tracheobronchial aspiration of gastric secretions has been suggested in published reports as a possible cause for idiopathic pulmonary fibrosis. Forty-eight of 131 patients with roentgenographic evidence of pulmonary fibrosis had no established etiologic diagnosis after individualized evaluations. They were prospectively studied by upper gastrointestinal series to determine the incidence of gastroesophageal reflux. The incidence of both hiatal hernia and reflux were statistically higher in the study group than in a group of 270 age-matched controls who had upper gastrointestinal series for the usual indications; (2) a subgroup of 15 patients who had pulmonary fibrosis and serologic evidence which suggested immune-mediated diseases; and (3) a subgroup of 23 patients with pulmonary fibrosis of established etiology. The patients in the study group could be further characterized by clinical and roentgenographic presentations, low maximum-mid-expiratory flow rates, and lung biopsies compatible with interstitial fibrosis. These observations and other cited evidence are supportive of the concept that repeated, small tracheobronchial aspirations of gastric acid secretions over a long period of time may cause interstitial pulmonary fibrosis.
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PMID:Pulmonary fibrosis associated with tracheobronchial aspiration. A study of the frequency of hiatal hernia and gastroesophageal reflux in interstitial pulmonary fibrosis of obscure etiology. 126 17

Seven tests which have been recommended for the diagnosis of gastro-esophageal reflux were applied in 24 healthy controls and in 48 patients with symptoms of reflux disease. The correlation coefficient of test results with the subjective symptoms of the patient decreased in the following order: 1) acid clearance from the distal esophagus (r = 0.558, p less than 0.001), 2) suction biopsy 5 cm above lower esophageal sphincter (LES) with evaluation of granulocytic infiltrates (r = 0.450, p less 0.001), 3) radiological demonstration of hiatal hernia (r = 0.435, p less than 0.001), 4) reflux provocation test (r = 359, p less than 0.01), 5) modified Bernstein test (r = 0.322, p less than 0.01), 6) acid relux test (r = 0.252, p less than 0.05), 7) resting pressure of LES (r = 0.246, p less than 0.05). Results of the Maudsley Personality Inventory were not correlated with subjective symptoms (r = 0.188, p greater than 0.1). By stepwise multiple regression analysis it was shown that optimal diagnosis of reflux is achieved by combination the following 4 procedures: 1) acid clearance, 2) modified Bernstein test, 3) suction biopsy, and 4) radiology.
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PMID:Gastro-oesophageal reflux disease: correlation of subjective symptoms with 7 objective oesophageal function tests. 127 17

From 1980 to 1989, 18 patients with esophageal achalasia had postoperative restricture. Inadequate myotomy was shown in 7 patients, scar constriction in 5, gastroesophageal reflux in 3, and paraesophageal hiatus hernia in 1. Seventeen patients underwent reoperation including modified myotomy (11), esophagastrotomy (4), operation for esophageal hiatus hernia (1), and cardioplasty combined with fundoplication (1). The causes of restricture, diagnostic methods, operative procedure and methods of precaution are discussed.
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PMID:[Reoperation of esophageal achalasia]. 133 48

Gastroesophageal reflux is a common event characterized by orad movement into the esophagus of gastric and/or duodenal contents. Reflux may produce either no damage to the esophageal mucosa or erosions, exudates, ulcerations, strictures, and/or Barrett's (columnar-lined) esophagus. In addition to the esophagus, all the anatomic structures from the pharynx to the lung may be affected by reflux. Numerous factors promote abnormal esophageal mucosal contact time with acid and pepsin. These include incompetent lower esophageal sphincter, impaired esophageal clearance, increased frequency of reflux episodes, delayed gastric emptying, and the presence of a hiatal hernia. The relative contribution of each of these factors in the pathogenesis of esophageal mucosal disease has not been clearly defined. Epidemiologic and clinical data support an association between gastroesophageal reflux and pulmonary disease. Most asthmatic patients, independent of bronchodilator use, have evidence of gastroesophageal reflux, as demonstrated by ambulatory pH testing, endoscopy, and the presence of reflux symptoms. Studies with antireflux agents indicate that partial or complete symptom relief and healing of esophagitis are obtained in about half the patients using H2-receptor antagonists and almost all patients using omeprazole. Preliminary evidence suggests that surgical correction of reflux may lead to improved pulmonary status. Controlled clinical trials are needed, however, to further determine whether effective gastric acid suppression will improve reflux-associated pulmonary disease.
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PMID:Gastroesophageal reflux disease and its consequences. 139 7


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