Alkaline gastroesophageal reflux.
ABSTRACT Twenty-four hour monitoring provides a continuous record of the pH of the lower esophagus in a near physiologic setting. The upper level of physiologic reflux was determined from the percentage of time and the number of episodes that the pH was less than 4 or more than 7 and the mean duration of each episode in fifteen asymptomatic subjects. One hundred patients with symptoms of gastroesophageal reflux were divided into four groups on the basis of twenty-four hour pH monitoring: those with abnormal acid but normal alkaline reflux, termed acid refluxers (51 patients); those with both abnormal acid and alkaline reflux, termed acid-alkaline refluxers (25); those with normal acid and abnormal alkaline reflux, termed alkaline refluxers (6); and those with both normal acid and alkaline reflux, termed nonrefluxers (18).Nonrefluxers had a similar incidence of heartburn, regurgitation, and dysphagia as acid and acid-alkaline refluxers, proving the inaccuracy of symptoms for detecting reflux. Alkaline refluxers had a lesser incidence of heartburn but a greater incidence of regurgitation, and four alkaline reflux patients presented with severe pulmonary disease secondary to aspiration. Similar incidence and degree of esophagitis was seen in acid, acid-alkaline, and alkaline refluxers. All three groups of symptomatic refluxers had a mean distal esophageal sphincter pressure significantly lower than that of the control asymptomatic subjects. There was no difference in the distal esophageal sphincter pressure between controls and symptomatic nonrefluxers.Nine of the patients with acid-alkaline reflux and one of the patients with alkaline reflux underwent an antireflux procedure and were restudied three months postoperatively. All ten patients had a 24 hour pH acid score within normal limits, but two had an abnormal 24 hour pH alkaline score. In both patients, reflux was demonstrated after placing an acid load in the stomach.It is concluded that symptomatic gastroesophageal reflux in patients with an intact gastrointestinal tract is a mixture of both acid and alkaline secretions, with one or both abnormal due to different degrees of acid production and pyloric regurgitation. Patients with alkaline reflux may develop serious complications of reflux in the absence of typical symptoms of heartburn. Twenty-four hour pH monitoring of the esophagus is useful in the identification of these patients and in evaluating the ability of an antireflux procedure to control both abnormal acid and alkaline reflux.
Full-textDOI: · Available from: Jorge A Wernly, May 30, 2015
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ABSTRACT: Duodeno-gastric and gastro-oesophageal reflux are of potential significance in the pathogenesis of dyspepsia and heartburn. However, convincing evidence that duodeno-gastric reflux, in itself, causes symptoms is not yet available, and none of the techniques designed to measure duodeno-gastric reflux has gained broad clinical acceptance. Monitoring of oesophageal pH has become the gold standard, however, for demonstrating gastro-oesophageal reflux disease, and the technique has become fairly standardized. The importance of measuring gastro-oesophageal reflux is not so much to differentiate normal (physiological) reflux from abnormal (pathological) reflux, but rather to assess the effect of treatment and to quantify the relationship between gastro-oesophageal reflux and symptoms. To achieve the latter, a number of indices have been described and tested, with which the temporal association between reflux and symptoms can be expressed quantitatively. It has become clear that troublesome symptoms may be induced by reflux in the absence of oesophagitis and even pathological oesophageal acid exposure. Primary indications for oesophageal pH monitoring are: reflux symptoms in the absence of oesophagitis, atypical symptoms (with or without oesophagitis), non-cardiac chest pain, and an unsatisfactory response to the treatment of gastro-oesophageal reflux disease.Alimentary Pharmacology & Therapeutics 12/1997; 11(s2). DOI:10.1111/j.1365-2036.1997.tb00790.x · 4.55 Impact Factor
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ABSTRACT: The results obtained in a recent study of surgically induced reflux oesophagitis in rats (Kranendonk, 1980) prompted the study presented in this thesis. In the randomized study by Kranendonk (1980) the reflux of pancreatic juice invariably resulted in oesophagitis; admixture of bile and/or gastric juice caused no significant differences in the extent of the oesophagitis. The reflux of bile or gastric juice was not associated with the development of oesophageal lesions. However, the study lacked control data on the composition of oesophageal contents as proof of the supposed reflux. Furthermore Kranendonk (19801 described the development of mural fibrosis starting after 14 days of reflux and progressing with time. The concomitant inflammatory changes, however, made a good interpretation of the presence of fibrosis impossible. It was therefore decided to further study surgically induced reflux oesophagitis in rats in order to prove the supposed reflux and to further study mural fibrosis. Being aware of the anatomical differences between the oesophagus of rats and of the human being 7 the rat was none the less chosen as experimental animal because of the ready avai!ability of a good experimental model. In addition, rats can be kept in relatively large numbers 7 allowing more elaborated experiments with appropriate statistical ·analysis.
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ABSTRACT: Simultaneous 22-h measurements of intraoesophageal and intragastric pH were made in 22 patients with symptoms of gastro-oesophageal reflux (7 with peptic oesophagitis, 8 with peptic oesophageal stricture, and 7 with peptic oesophagitis and previous partial gastrectomy) to determine whether alkaline intraoesophageal pH is a consequence of alkaline gastro-oesophageal reflux. In the three groups of patients intraoesophageal pH was >7 for 16.9 ± 4.8%, 27.5 ± 7.6%, and 21.0 ± 7.7%, respectively, of total recording time (p = NS). Intragastric pH > 7 was recorded only in the patients with partial gastrectomy (10.3 ± 5.3% of recording time; p < 0.01 in comparison with the other groups). Elevations of intraoesophageal pH to >7 never occurred during episodes of alkatinization of intragastric pH. These results suggest that refluxed fluids are unlikely to be the cause of alkaline intraoesophageal pH in patients with peptic oesophagitis.