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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surgical therapy for reflux esophagitis remains controversial. Sixty-five patients who underwent posterior gastropexy between November, 1970 and February, 1976 are presented. Indications for surgery were: esophagitis, 43 patients; esophagitis with stricture, 12 patients; paraesophageal hernia seven patients; incapacitating postfundoplication syndrome, three patients. The average follow-up was 15.6 months. Eighty-two per cent of the patients had a good to excellent result. Twenty-three per cent of the patients developed radiographically recurrent hiatus hernia; however, the incidence of recurrent esophagitis was only nine per cent. Two patients developed postoperative strictures (one de novo, one recurrent). Two patients ultimately required a fundoplication for control of their esophagitis; one patient required a Thal-Nissen procedure. Lower esophageal sphincter pressure on patients with satisfactory results increased from 6.3 +/- 1.3 cm H2O SEM preoperatively, to 17.4 +/- 3.0 cm H2O SEM postoperatively. This increase achieved a statistical significance of p less than 0.001. In patients who had an unsatisfactory result, postoperative sphincter pressures were unchanged from preoperative values. All unsatisfactory results were obtained in patients with complicated esophagitis, i.e., Barrett's ulcer or stricture, alkaline esophagitis, or previous hiatal surgery. Posterior gastropexy appears to constitute effective therapy in the treatment of uncomplicated reflux esophagitis and paraesophageal hiatus hernia without the distressing morbidity associated with the postfundoplication syndrome.
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PMID:An analysis of recurrent esophagitis following posterior gastropexy. 63 76

Luminal and mucosal pH were measured endoscopically in patients with reflux esophagitis and antral gastritis and in control subjects. In all subjects, significant lumen-to-mucosa gradients were observed in the esophagus, stomach and acidified proximal duodenum. In the reflux patients luminal pH was lower in the fundus (mean +/- SEM, control vs. reflux esophagitis: 2.01 +/- 0.17 vs. 1.32 +/- 0.18; p less than 0.02) and antrum (3.51 +/- 0.35 vs. 2.13 +/- 0.24; p less than 0.01) and, in the gastritis patients, in the fundus (2.01 +/- 0.17 vs. 1.3 +/- 0.17; p less than 0.02). In both patient groups, mucosal pH was lower in the fundus (control vs. reflux vs. gastritis: 4.84 +/- 0.37 vs. 3.37 +/- 0.61 vs. 3.12 +/- 0.6; p less than 0.05) and acidified duodenal cap (6.74 +/- 0.13 vs. 6.09 +/- 0.24 vs. 5.73 +/- 0.46; p less than 0.03). Mucosal pH profiles at the various sites showed less resistance of the gradient to a highly acidic environment in both the lower esophagus and antrum than in fundus and duodenum, and this was the case in the patient and control groups. Though associated with a more acid environment, neither esophagitis nor antral gastritis exhibits a specific deficit in the 'mucus-bicarbonate barrier', suggesting that the pathogenesis of these disorders may depend more on abnormal 'attack' rather than impaired defense.
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PMID:Studies of luminal and mucosal pH in reflux esophagitis and antral gastritis. 161 9

Gastric transplants using the Akiyama method were used to treat esophageal carcinoma in 12 patients. Endoscopic examination, prolonged manometry (greater than 30 min), and 24 h pH monitoring were performed postoperatively to evaluate functional results. All patients could swallow without difficulty at the time of examination and had no dysphagia, regurgitation, heartburn, or sensation of abdominal fullness. Histologic examinations of residual esophagus showed microscopic esophagitis in 5 patients. Percentage of time that pH less than 4 was 42.6 +/- 10.9% (mean +/- SEM) and median pH was 4.3 +/- 1.0. The manometric examination showed no 'esophageal-like' peristaltic waves, but synchronous contractions were demonstrated in 9 patients, gastric type activity in two patients, and no activity was detected in one patient. We conclude that retained gastric peristaltic function is not a prerequisite for a good clinical outcome for swallowing and that despite vagotomy, the stomach continues to produce enough acid to maintain an acidic pH.
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PMID:Functional evaluation of gastric transplants used in esophageal reconstruction. 264 Jan 79

Zinc and vitamin A are known to interact, and deficiencies have been associated with carcinogenesis in experimental animals and humans. Since we previously have demonstrated decreased plasma zinc and vitamin A levels in patients with esophageal cancer, we wished to examine endoscopically obtained epithelial tissue for vitamin A and zinc content. This was not feasible for vitamin A, but using newly developed techniques for zinc analysis of small tissue samples, we measured esophageal epithelial zinc as well as plasma zinc and plasma vitamin A in 21 patients with esophageal cancer, 17 patients with esophagitis, and 12 normals. Mean plasma zinc in the esophageal cancer group (56 +/- 3 micrograms/dl) (mean +/- SEM) was significantly less than in the esophagitis group (72 +/- 5 micrograms/dl) and the normals (78 +/- 5 micrograms/dl). Mean plasma vitamin A in the esophageal cancer group (32 +/- 3 micrograms/dl) was significantly less than the esophagitis group (57 +/- 4 micrograms/dl) or the normals (58 +/- 5 micrograms/dl). There was no significant difference in tissue zinc content (measured as micrograms zinc/g wet weight of tissue, mean +/- SEM) among cancerous tissue (57 +/- 5 micrograms/g) and adjacent normal tissue (61 +/- 4 micrograms/g), esophagitis tissue (66 +/- 6 micrograms/g) and adjacent normal tissue (61 +/- 6 micrograms/g), or normal esophageal tissue (59 +/- 6 micrograms/g). We conclude that deficiencies of zinc or vitamin A may be cofactors in the induction of human esophageal cancer, but a mechanism cannot be accounted for by differences in epithelial zinc content.
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PMID:Esophageal zinc content in human squamous esophageal cancer. 358 28

This study evaluated the effect of the 270 degrees Belsey Mark IV fundoplication on 24 hour ambulatory pH metry variables. Thirty seven patients with confirmed gastro-oesophageal reflux disease who had a Belsey Mark IV antireflux procedure were evaluated preoperatively and three to six months postoperatively including endoscopy, lower oesophageal sphincter manometry, and 24 hour ambulatory pH metry. In 30 of 37 patients the Belsey Mark IV fundoplication was judged successful based on symptom relief and healing of oesophagitis. In these 30 patients percentage reflux for total, upright, and supine time (median and range) decreased significantly (p < 0.001) from 10.0% (2.7-35.3%), 10.8% (3.2-39.9%), and 6.7 (0.0-33.0%) respectively to 0.5% (0.0-7.4%), 0.6% (0.0-13.7%), and 0.1% (0.0-4.9%) after operation. This decrease in reflux time resulted predominantly from a significant (p < 0.001) reduction in the number of reflux episodes from 98 (23-231) to 14 (0-82) postoperatively. Normalisation of total reflux time (upper limit of normal for time with pH below 4:4%) was found in 89% and normalisation of total and upright and supine reflux in 64% of successfully operated patients with confirmed abnormal acid reflux before operation. A successful antireflux procedure was associated with significant (p < 0.001) increases in lower oesophageal sphincter pressure from 7.8 (0.6) mm Hg to 14.5 (0.7) mm Hg mean (SEM). In seven patients with a failed antireflux operation basal lower oesophageal sphincter pressure did not change significant;y (preoperative value 5.7 (1.3) mm Hg; postoperative value 7.8 (0.8) mm Hg). In these patients reflux time did not decrease after the operation and remained in the abnormal range in all patients. It is concluded that a successful, in contrast with a failed, Belsey Mark IV fundoplication is associated with significant decreases in total, upright, and supine reflux time. Normalisation of pH metry variables is not a prerequisite for successful antireflux surgery. A surgery. A successful 270 degree Belsey Mark IV fundoplication was associated with a significant increase in basal lower oesophageal sphincter pressure, in contrast with the failure group. Restoration of a sufficient lower oesophageal sphincter barrier is an important aim in antireflux surgery.
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PMID:Prospective evaluation of 24 hour ambulatory pH metry in Belsey Mark IV antireflux surgery. 782 67

Omeprazole is a powerful inhibitor of gastric acid and may suppress Helicobacter pylori by effecting the pKa of H pylori urease, by altering the pattern of infection, or by promoting overgrowth of other bacteria. At routine endoscopy H pylori was detected by histology and culture before and after four weeks' treatment with omeprazole, 40 mg each morning. A 13C-urea breath test was also done at t = 0, 2, 4, and 6 weeks. Thirty nine patients with duodenal ulcer (n = 25) or reflux oesophagitis (n = 14) were studied, of whom 29 of 39 had H pylori infection. During omeprazole treatment, 13C-urea breath test values fell significantly--mean (SEM) values before treatment and at four weeks were 23.0 (2.1) and 15.5 (2.7) per mil respectively, p < 0.001. Before treatment H pylori was seen in 28 of 29 antral, 29 of 29 corpus, and 28 of 29 fundic biopsy specimens. After four weeks of omeprazole treatment, the histological density of H pylori in the antrum and corpus was reduced (p < 0.001), while that in the fundus was increased. The migration of H pylori from the antrum to the fundus was associated with a corresponding decrease in the activity of antral gastritis. H pylori was not seen in antral biopsy specimens from 12 of 29 patients whose median excess delta 13CO2 excretion fell from 23.0 to 9.9 per mil. In the body mucosa, 26 of 29 specimens were still positive for H pylori and there was no significant change in the gastritis type. Two weeks after finishing treatment, the mean (SEM) excess delta 13CO2 excretion returned to levels before treatment. Omeprazole decreases antral H pylori colonisation but increases that in the fundus. The changes in the intragastric distribution of the organism are associated with concomitant changes in the activity of gastritis and are matched by a progressive fall in the excretion of delta 13CO2.
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PMID:Changes in the intragastric distribution of Helicobacter pylori during treatment with omeprazole. 789 Feb 14

Gastric acid suppression could improve heartburn by healing oesophagitis or by reduction of oesophageal sensitivity to acid. To independently assess changes in oesophageal sensitivity, it would be necessary to study patients with reflux disease but no oesophagitis. The aim of this study was to investigate the effect of acid suppression on oesophageal sensitivity and to assess the time course of any measured effect. Twenty seven patients were recruited, of whom 25 completed the study (14 men and 11 women, mean (SD) age 50 (15) years). All had classic symptoms of gastro-oesophageal reflux but normal results of upper gastrointestinal endoscopy and oesophageal mucosal histological tests. Each had abnormal 24 hour pH studies and a positive acid perfusion tests. Subjects were assigned double blind to placebo (n = 11) or famotidine 40 mg twice daily (n = 14) for four weeks. Acid perfusion tests were carried out at 0, 4, 5, and 8 weeks and time to heartburn recorded. Time to heartburn (mean (SEM)) was 124 (78) seconds in the famotidine and 187 (154) in the placebo group at week 0 (NS). Compared with baseline, significant increases in time to heartburn was found with famotidine at weeks 4 (383 (102), p < 0.01) and 5 (344 (92), p < 0.01) but not week 8 (336 (90) seconds). No significant effects were found with placebo (219 (41), 146 (23), and 144 (25) seconds for weeks 4, 5, and 8). Heartburn symptom score decreased significantly with famotidine (mean scores 3.6, 1.9, 2.1, and 2.6 at weeks 0, 4, 5, and 8 (p=0.001)) and showed a significant negative correlation with time to heartburn (r(s)=-0.60; p<0.0001). It is concluded that oesophageal sensitivity to acid is reduced by famotidine independent of and effect on oesophagitis; the effect wanes one to four weeks after the end of treatment and correlates with change in heartburn score.
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PMID:Effect of famotidine on oesophageal sensitivity in gastro-oesophageal reflux disease. 817 79

Whether the oesophageal motor response to reflux, as recorded over 24 hours, is impaired in patients with reflux oesophagitis was investigated. Twenty three patients with oesophagitis (Savary-Miller grades I-IV) and 23 control subjects matched for age and sex underwent 24 hour ambulatory pH and pressure monitoring. All contractions occurring in the 2 minute period after the onset of each reflux episode were analysed automatically using dedicated computer algorithms. A total of 2085 reflux episodes occurred--1513 in patients and 572 in controls. Oesophageal acid exposure was greater (p < 0.01) in patients than in controls (mean (SEM) % time pH < 4 13.3 (1.7) and 5.3 (0.9)%, respectively). The mean duration of the supine reflux episodes was longer (p < 0.01) in patients (11.2 (2.8) minutes) than in controls (5.1 (1.8) minutes). In the upright period, no significant differences in the motor response to reflux were found. In the supine period, the patients showed a higher number of reflux induced contractions (4.40 (0.61) v 1.62 (0.31), p < 0.01), a higher contraction amplitude (4.55 (0.42) v 2.99 (0.71) kPa, p < 0.02) and longer contractions (1.86 (0.19) v 1.32 (0.29) seconds, p < 0.05). The percentages of peristaltic and simultaneous contractions that occurred in response to supine reflux did not differ between the two groups. In patients with reflux oesophagitis the motor response of the oesophagus to reflux is not impaired. During the supine period the response is even stronger than in healthy controls.
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PMID:Oesophageal motor response to reflux is not impaired in reflux oesophagitis. 847 77

Endoscopy, esophageal manometry and pH monitoring, gastric emptying test, and heartburn quantification on a visual analog scale were performed in 22 achalasic patients in order to clarify which events are associated with pathological esophageal acidification after successful LES dilatation. Five patients presented pathological acidification. Dilatation reduced LES tone from 38.3 +/- 4.2 to 14.6 +/- 1.1 mm Hg (mean +/- SEM); there was, however, no difference between nonrefluxers and refluxers (14.8 +/- 1.2 vs 13.8 +/- 2.5 mm Hg). The emptying time in achalasic patients was delayed compared to controls (315.9 +/- 20.9 min vs 209 +/- 10.4) due to prolonged lag-phase and reduced slope of the antral section-time curve, but, again, there was no difference between refluxers and nonrefluxers. The acid clearance was delayed in refluxers compared to nonrefluxers (15.9 +/- 4.5 vs 2.5 +/- 1.8 min, P<0.05). Two refluxers presented grade 1 esophagitis; one of them developed an esophageal ulcer. The heartburn score was the same in refluxers and nonrefluxers. Pathological acidification after pneumatic dilatation is associated with persistent problems in esophageal emptying rather than with excessive sphincter divulsion.
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PMID:Pathological esophageal acidification and pneumatic dilitation in achalasic patients. Too much or not enough? 860 84

Pediatric patients who present with symptoms of gastroesophageal reflux and severe eosinophilic esophagitis may be unresponsive to aggressive anti-reflux medical therapy. In order to determine whether the degree of eosinophilia predicts anti-reflux treatment response and possibly distinguishes different etiologies, we reviewed the initial biopsies of patients with esophageal eosinophilia and compared the number of eosinophils with the response to anti-reflux treatment. Over a 1-year period, 102 patients with a biopsy demonstrating at least 1 intraepithelial eosinophil were identified among patients undergoing initial endoscopy for symptoms of reflux. All patients were treated with H2 blockers and prokinetic agents. Treatment response was classified into three categories: improvement, relapse, and failure. There were significant differences between the group who improved (mean eosinophil count [MEC] 1.1 +/- 0.3 SEM) and those who failed (24.5 +/- 6.1 SEM, P < 0.0025) or relapsed 6.4 +/- 2.4 SEM, P < 0.05). A threshold MEC value of > or = 7 provided a sensitivity of 61.3%, a specificity of 95.7%, and a predictive value for treatment failure of 86.1. A MEC value of < 7 provided an 85% predictive value of successful therapy. From these data we made the following conclusions: (1) The number of eosinophils has a predictive value of treatment response with > or = 7 per high power field offering a valuable clinical threshold for predicting outcome of conventional therapy. (2) The variable response to conventional reflux treatment may reflect different etiologies. (3) Alternate medical treatment modalities may be appropriate in the presence of severe eosinophilia, before considering surgical intervention.
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PMID:Severity of esophageal eosinophilia predicts response to conventional gastroesophageal reflux therapy. 984 1


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