Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reflux esophagitis and its complications are not only common clinical problems but also problems that can be accurately defined by careful history taking and a knowledge of the pathophysiology of the various manifestations. An element of objective assessment, however, is required to define and substantiate fully an individual patient's problem. Only when disabling subjective and intractable objective complications persist after good medical treatment should surgical intervention be considered. Various antireflux procedures are currently available and all can be effective. Surgeons should review their own experiences and make alterations that they perceive will correct the types of problems encountered. In our current technique for the surgical management of gastroesophageal reflux in the common clinical setting, normal esophageal peristalsis is present, the fundus is adequate for plication, and sufficient esophageal mobilization can be effected to permit reduction of the entire stomach and fundoplication below the diaphragm. In addition, the procedure should be restricted to patients who do not have stenosis or have stenosis that can be readily dilated to 50 French.
 ...
PMID:Reflux esophagitis. 358 99

Reflux esophagitis was first described 50 years ago, and understanding of abnormal gastroesophageal reflux, its complications, and treatment have been recent additions to medical and surgical knowledge. The process by which this information has been acquired, current techniques for measuring abnormal reflux and its complications, mechanisms by which reflux is controlled normally and after antireflux surgery, and the relationship between hiatal hernia and gastroesophageal reflux are the subjects of this presentation.
 ...
PMID:Pathophysiology of gastroesophageal reflux. 405 3

The etiology, pathogenesis, diagnosis, and treatment of reflux esophagitis are reviewed. Reflux esophagitis is the subjective or objective response to gastroesophageal reflux (GER), which is defined as the entrance of gastroduodenal contents into the esophagus not associated with vomiting or belching. The pathogenesis of reflux esophagitis may involve a number of mechanisms, including changes in lower esophageal sphincter pressure, gastric volume, composition of the refluxate, esophageal acid clearance, and esophageal tissue resistance. The most common symptom of reflux esophagitis is heartburn. Regurgitation of fluid into the mouth, usually after bending or during the night, is an unequivocal symptom of GER. Treatment can be divided into three phases. Phase 1 involves the avoidance of certain foods and habits, elevation of the bed head, antacid, and alginic acid-antacid therapy. Phase 2 involves drug therapy with agents not yet approved by the FDA for this indication: bethanechol chloride, cimetidine, and metoclopramide hydrochloride. Bethanechol chloride 25 mg is generally given four times daily. Cimetidine is given in doses of 300-400 mg after meals and at bedtime. Metoclopramide hydrochloride is administered in doses of 10 mg before meals and at bedtime. Phase 3 is antireflux surgery. Clinical experience has shown that phase 1 therapy is successful for about 75% of all patients. Of the 25% that do not respond to phase 1 therapy, about 90% will respond to phase 2 therapy, leaving only 5-10% of all patients with this disorder who will require phase 3 treatment. Current data favor cimetidine and bethanechol over metoclopramide. The least proof of efficacy and the most frequent adverse side effects are seen with metoclopramide. Cimetidine and bethanechol appear to have similar efficacy and relatively infrequent side effects. Evidence confirming the superiority of cimetidine over bethanechol is lacking. Further research is needed to determine the optimal pharmacologic combinations and treatment regimens.
 ...
PMID:Current concepts in the pathogenesis and treatment of reflux esophagitis. 636 Apr 95

Eighty-eight patients with bleeding esophageal varices due to portal hypertension underwent splenectomy and devascularization of the upper half of the stomach and the abdominal esophagus. A Hegar dilator no. 17 was introduced into the esophagus through a gastrotomy. A ring of separated stitches was applied at cardia level, the needle being inserted as far as the metallic surface so as to include the entire wall of the esophagus. Complete interruption of all gastroesophageal vascular communication was thus obtained. After suture of the gastrotomy, a Nissen or Lind's fundoplication was performed. In 62 (70.45%) patients, the immediate postoperative course was uneventful, 21 had non-lethal complications, 13 had abdominal evisceration, six pulmonary complications, four subphrenic abscesses, five patients died, two in hepatic coma, two after reoperation for subphrenic abscess and one after massive hemorrhage due to an acute gastric ulcer. Forty-three patients (48.8%) developed transient ascites which disappeared before they were discharged from the hospital. In thirteen patients (15.6%), the hemorrhage recurred. Of the 32 patients operated one to two years ago, only one rebled. Of the 35 patients operated three to five years ago, nine rebled and three, of the 16 patients operated from five to seven years ago, rebled. With radiological and endoscopic investigations, reduced varices were seen above the suture line, in many cases, passively filled up with blood returning from the azygos vein. Reflux esophagitis was observed in 17 patients who had had a Lortat-Jacob procedure to reduce the His angle; of these, eight rebled later. No gastroesophageal reflux was seen after Nissen or Lind's fundoplication. No fistulae, dysphagia or stenosis was observed.
 ...
PMID:A new procedure for the treatment of bleeding esophageal varices by transgastric azygo-portal disconnection. 660 5

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.
 ...
PMID:[Reflux esophagitis]. 776 23

Reflux esophagitis, usually the mild to moderate form, is found endoscopically in less than 50% of patients with classic symptoms of gastroesophageal reflux disease (GERD). These patients tend to have low lower esophageal sphincter pressures, poor esophageal clearance, and hiatal hernias. The endoscopic findings of distal esophageal erosions and ulcerations are a specific, but not very sensitive, marker of GERD. Treatment of reflux esophagitis usually requires H2 antagonists, omeprazole, or antireflux surgery.
 ...
PMID:Severe reflux esophagitis. 781 41

A case of chronic gastric organoaxial volvulus, gastroesophageal reflux, esophagitis, and chronic anemia is presented. Reflux esophagitis and chronic anemia have not been reported previously as clinical signs associated with gastric volvulus in a child. A Meckel's scan is used to diagnose the displaced stomach.
 ...
PMID:Organoaxial gastric volvulus detected by Meckel scan. 792 99

In a prospective study of consecutive patients with reflux esophagitis and/or hiatal hernia and Barrett's esophagus, the prevalence of Helicobacter pylori was assessed. Antral biopsy specimens were studied and a serum sample for detection of IgG antibodies against Helicobacter pylori was taken. As a reference group patients presenting with a normal esophagus, stomach, and duodenum were taken. Reflux esophagitis was diagnosed in 118 patients, hiatal hernia without esophageal inflammation in 109, and Barrett's esophagus in 13. Helicobacter pylori was present in 74 (30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacter pylori was significantly lower in all groups compared with the reference group (P < 0.001). There was no difference when patients with esophagitis, Barrett's esophagus, or hiatal hernia were compared. Patients with esophagitis and Helicobacter pylori in their antrum are significantly older than esophagitis patients without concomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). It is concluded that the prevalence of Helicobacter pylori infection in patients with gastroesophageal reflux disease is significantly lower than in the reference group, irrespective of the severity of esophagitis. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.
 ...
PMID:Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. 900 23

Reflux esophagitis may result from the action of both acid and non-acid agents. The aim of this study was to test a new system able to measure the quantity of the bilirubin contained in the esophageal lumen. The analysis of esophageal reflux composition was conducted in two phases. In the first bile and pancreatic enzyme, concentration of 136 fluid samples obtained with ambulatory esophageal long-term reflux aspiration test were measured. For the second, the total bilirubin content of each sample was measured in vitro with a fiberoptic probe (Bilitec 2000, Synetics Medical Inc., Sweden). Studies were performed on 48 subjects: 43 patients with esophageal reflux and five healthy volunteers. The results of both techniques were then compared. Higher concentration of bile and pancreatic enzymes were found in esophageal fluid samples of patients with endoscopic esophagitis. Bile and pancreatic enzyme concentrations of esophageal fluid samples were higher in patients after gastrectomy compared to patients with intact stomachs. There was a significant correlation between the total bilirubin concentration of fluid specimens and the fiberoptic probe reading of bilirubin (r = 0.72, P < 0.001). The presence of bilirubin and bile acids within the esophageal refluxate can be determined reliably with continuous fiberoptic measurement. The correlation between total bilirubin content and the concentrations of pancreatic enzymes contained in the esophageal refluxate suggests that bilirubin is a good tracer for non-acid, duodenal or intestinal reflux in the esophagus.
 ...
PMID:Assessment of non-acid esophageal reflux: comparison between long-term reflux aspiration test and fiberoptic bilirubin monitoring. 907 69

A case with esophageal anisakiasis accompanied by reflux esophagitis is described. A 38-year-old man visited our hospital with complaints of heartburn and disturbance of food passage about seven hours after eating raw cuttlefish. The first esophagogastroscopy revealed an anisakis larva invading the squamocolumnar junction. Near the anisakis larva, a whitish exudate was demonstrated in the distal esophagus just proximal to the squamocolumnar junction. An anisakis larva was easily extracted from the esophagus by forceps. Reflux esophagitis with whitish exudative mucosal lesions and an area of linear erythema more than 5mm long were noted endoscopically 8 weeks after treatment with lansoprazole and cisapride. After six months the third endoscopic examination clarified that there was neither exudate nor erythema in the distal esophagus. Judging from the clinical course that he complained of newly experienced heartburn about seven hours after eating raw cuttlefish, and that whitish exudative mucosal lesions and an area of linear erythema did not disappear at three months after extraction of the anisakis larva. It was concluded that an anisakis larva enters the stomach first and then returns to the esophagus by gastroesophageal reflux.
 ...
PMID:Esophageal anisakiasis accompanied by reflux esophagitis. 947 45


<< Previous 1 2 3 4 5 Next >>