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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For centuries it was recognized that the stomach produces a juice, which has acidic properties, however, it was not until 1824 when Prout demonstrated the presence of hydrochloric acid in gastric juice. At the same time experiments on a patient with gastric fistula began by W. Beaumont showing alterations of acid secretion after meals and under various psychological conditions. After the discovery by L. Popielski in 1920 that histamine is a direct stimulant of oxyntic glands, histamine started to be used in the 1930s in gastric secretory tests. Then in 1949 the dose of histamine was established by K. Kowalewski to induce in humans maximal gastric secretion and in 1953 Kay from UK, using a similar dose of histamine (0.04 mg/kg), introduced augmented histamine test to determine maximal acid output. The digestive period of gastric secretion can be divided into 3 phases: cephalic phase, gastric phase, and intestinal phase. When an acidified meal reaches the antrum or proximal part of the small intestine, the inhibitory autoregulatory mechanisms are triggered. Using a peptone meal as a physiological stimulant of gastric secretion, Fordtran and Walsh designed in 1973 the intragastric titration method. Histamine stimulates H1 and H2 receptors, producing some side effects so Betazole (Histalog), an analogue of histamine was introduced, because of smaller side effects than with histamine. In 1967, pentagastrin, which contains a C-terminal amino-acid sequence of gastrin and does not exert serious side effects, was applied first in Poland as a stimulant of gastric acid secretion instead of histamine. At the present time, a 12 or 24 h pH-metry with a magnetic recording of gastric acidity using the Digitrapper was found to have a greater diagnostic value in assessment of gastric acid secretion under natural conditions including meal than classic gastric secretory tests. This technique has been widely used in detecting the duodeno-gastric or gastro-esophageal reflux (GERD) and testing various drugs affecting gastric acid secretion and healing acid-pepsin disorders.
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PMID:Gastric analysis with fractional test meals (ethanol, caffeine, and peptone meal), augmented histamine or pentagastrin tests, and gastric pH recording. 1507 65

Achalasia surgical treatment alters the esophagogastric junction anatomy (cardiomyotomy plus fundoplication or esophagectomy and gastric pull-up), thus favoring a certain degree of gastroesophageal reflux. Gastric secretory and hormonal functioning is not completely known in chagasic patients. The aim of this study was to evaluate the gastric secretory and hormonal response in patients with end-stage chagasic achalasia compared with normal subjects. Gastric secretion and hormonal response were assessed by estimation of gastric acid secretion (GAS) in basal condition and after pentagastrin stimulation, basal serum gastrin, and serum pepsinogen (SP) in basal condition and after betazole hydrochloride (Histalog; Eli Lilly and Company, Indianapolis, IN, USA) stimulation in 27 patients with chagasic achalasia. The results were then compared with those of 24 normal subjects. In the chagasic group, the mean basal and stimulated GAS were significantly lower than in the control group (basal: 1.277 vs. 3.13, P = 0.002; stimulated: 15.9 vs. 35.8, P = 0.0001). Chagasic patients' SG levels showed a significantly higher basal value than the control group (83.3 vs. 36.8, P = 0.0001). There was a significant increase of SP after stimulation compared with the basal levels in both chagasic and control groups. Although the chagasic patients' SP values were higher than the controls, this difference was not statistically significant, either in basal and stimulated conditions (basal: 122.0 vs. 108.9, stimulated 120 min: 177.1 vs. 158.9). In patients with chronic Chagas' disease (ChD), although autonomic denervation does not suppress the strength of the gastric mucosal cells' secretory response to stimulation, it reduces GAS (parietal cell) without, however, affecting SP production (chief cells). On the other hand, the gastrin-producing cells have continuously been stimulated by low GAS.
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PMID:Gastric secretory and hormonal patterns in end-stage chagasic achalasia. 1930 18