Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postprandial serum gastrin secretion was studied in 26 patients with X-ray-negative dyspepsia. Seven patients had a normal duodenum while 19 had duodenal anomalies. In patients with an abnormal duodenal loop, the mean postprandial serum gastrin secretion was significantly higher after 45, 60 and 120 min than that of the control group. No significant difference was demonstrated in the basal state. A delay in gastric emptying rate might be the cause of increased postprandial serum gastrin secretion in patients with an abnormal duodenal loop.
 ...
PMID:The influence of an abnormal duodenal loop on basal and food-stimulated serum gastrin concentrations. 72 22

The relationship between different features of gastric mucosal inflammation, intragastric pH and serum gastrin concentration and the distribution and quantity of Helicobacter pylori was studied in a series of 107 dyspepsia patients. H. pylori was identified in 62 cases (59%), and its presence was associated with increased amounts of mononuclear inflammatory cells and neutrophilic and eosinophilic leucocytes in both the antrum and the corpus. The number of H. pylori in the antral mucosa was significantly associated with the quantity of mononuclear inflammatory cells. It was also associated with glandular atrophy in antral mucosa, so that slight and moderate glandular atrophy were significantly more common in cases with abundant H. pylori. Intragastric pH and serum gastrin concentration were inversely related to the number of H. pylori in both the antral and corpus mucosa. H. pylori positive patients were also divided into groups according to proportions of H. pylori in the antral and corpus mucosa. In 5 of these patients (8%) the bacteria were present only in the corpus, and this group had a significantly more pronounced degree of glandular atrophy in the corpus mucosa, higher intragastric pH and a higher serum gastrin concentration than the other H. pylori positive patients. The other patients with a higher corpus H. pylori than antral H. pylori score (n = 25; 34%) also had a significantly higher intragastric pH and serum gastrin concentration than those with a corpus H. pylori score lower than or equal to the antral score, while the latter had more severe inflammation in the antral mucosa and a lower intragastric pH and serum gastrin concentration. The results suggest that inflammation in the antrum forms a favourable environment for H. pylori, while atrophy of the corpus glands, being connected with increased pH, leads to a diminished amount of H. pylori. They thus support the view that proliferation of H. pylori is dependent on acid produced by the corpus mucosa.
 ...
PMID:Helicobacter pylori in dyspeptic patients: quantitative association with severity of gastritis, intragastric pH, and serum gastrin concentration. 175 20

The role of Helicobacter pylori infection in causing chronic dyspepsia is in need of further clarification. More well-designed prospective studies are necessary to ascertain whether and to what extent H. pylori-related chronic inflammation in the stomach and the duodenum causes dyspeptic symptoms; whether and to what extent there is a symptom cluster characteristic for H. pylori-related gastroduodenitis; whether and to what extent H. pylori infection is demonstrable in the chronic dyspeptic population; and whether and to what extent H. pylori infection interferes with gastrin homoeostasis and acid secretion or induces motor disturbances. Well-designed prospective H. pylori-eradication studies may further contribute in unravelling its role in chronic dyspepsia, especially in patients with active polymorphonuclear gastroduodenitis and hyperacidity.
 ...
PMID:Is gastroduodenitis a cause of chronic dyspepsia? 189 28

Prior to the 17th century, there was considerable confusion regarding the process of digestion. Although some physicians were certain that it was initiated by acid in the stomach, both the source and the nature of the acid were unclear. In the early 19th century, Prout confirmed the active secretion of hydrochloric acid by the stomach and related it to the symptoms of dyspepsia. Jacob Helm and, subsequently, Beaumont studied digestion in humans with gastric fistulas and each commented extensively on the physiologic manifestation of digestion. The role of the vagus nerves in the control of gastric acid secretion was identified in the early and mid-19th century by Brodie, and subsequently elaborated upon by Pavlov. By the early 20th century, Latarjet and Jaboulay in France, performing operations for abdominal pain and tabes, reported the effects of vagotomy on acid secretion and gastric motility. In 1943, Dragstedt, in the United States, reported the cure of duodenal peptic ulcer disease by supradiaphragmatic vagotomy. He later observed the substantial delays in emptying of the stomach, which necessitated the introduction of concomitant gastric drainage procedures, such as gastrojejunostomy and pyloroplasty. In 1902, Bayliss and Starling had described the existence of a chemical regulator of function--secretin--which they termed a hormone. Shortly thereafter, Edkins reported results of studies that supported the presence of an acid regulatory hormone, gastrin, in the antrum of the stomach. Unfortunately, controversy marred this observation, and the action of gastrin was for more than 30 years ascribed to histamine. Komarov, in 1938, confirmed the existence of gastrin and its stimulatory effects on acid secretion. Physiologic recognition of the roles of vagal stimulation and antral gastrin in the secretion of acid from the stomach resulted in the development of the operation of vagotomy and antrectomy for peptic ulcer disease. Studies of the pylorus and the motility of the stomach resulted in an appreciation of the genesis of the postgastrectomy syndromes. By the middle of the 20th century, a clear appreciation of the morphologic characteristics of the parietal cell and its ability to secrete hydrochloric acid was under way. The complex metabolic process of the cell was correlated with the major morphologic transformation necessary to generate secretion of hydrochloric acid. The development of sophisticated research technology allowed the appreciation of the complex intracellular processes necessary to allow the generation of a 2.5 million-fold gradient of hydrogen ion secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:From Prout to the proton pump--a history of the science of gastric acid secretion and the surgery of peptic ulcer. 215 87

Gastric mucosal histology and function were evaluated in 57 Italian subjects with dermatitis herpetiformis (DH), by means of multiple endoscopic biopsies, gastrin and pepsinogen I (Pg I) serum levels, and parietal cell antibodies (PCA). One hundred and forty-nine patients with nonulcer dyspepsia served as reference population for the prevalence of atrophic gastritis of the body. Seventeen DH patients (30%) and 23 controls (15.4%) showed atrophic gastritis of the body mucosa (p less than 0.05). Nine of the DH patients with atrophic gastritis of the body also had atrophic changes in the antrum. Six patients, all with severe atrophic gastritis, had high gastrin levels and PCA; five of these six also had low Pg I levels. We found an increased prevalence of abnormal indirect function tests among patients with atrophic gastritis is due to the younger age of the patients in our series. Thus, atrophic gastritis can be detected early on a histologic basis, but functional impairment occurs later, as the mucosal damage increases in severity.
 ...
PMID:Gastric histology and function tests in Italian patients with dermatitis herpetiformis. 233 46

The etiology of peptic ulcer disease is completely unknown. However, gastric acid secretion plays an important role in the pathogenesis of the disease. Acetylcholine, gastrin and histamine are recognized as the main stimulators of the acid secretion. Extensive studies on blood gastrin have not incriminated this hormone in the pathogenesis of the disease. The present study was done to evaluate the role of circulating histamine in peptic ulcer disease using a sensitive and specific radioimmunoassay method. Since gastrin at least in some species seems to exert its stimulatory effect by releasing histamine, serum gastrin was also determined. There was no significant difference in plasma histamine between patients with duodenal or gastric ulcer, nonulcer dyspepsia or ulcer patients after proximal gastric vagotomy. However, patients taking a histamine-2 blocker (cimetidine or ranitidine) had significantly higher plasma histamine than those not taking these drugs. This effect was not due to interference in the histamine assay. There was no correlation between plasma histamine and plasma gastrin. Plasma gastrin was significantly increased in patients having been operated on with a proximal gastric vagotomy. In conclusion, plasma histamine is similar in patients with different upper gastrointestinal disorders. However, histamine-2 blockers may increase plasma histamine.
 ...
PMID:Histamine and gastrin in plasma of patients with upper gastrointestinal diseases. 276 43

The survey is based on nine previously published papers and is divided into three main sections dealing with the relationship between the duodenal loop and the radiological, the physiological and the clinical examinations in patients with X-ray negative dyspepsia. In the first section the development of the duodenal loop, the various types of development anomalies and their radiological image are discussed. Furthermore the causes of the extensive variation in the indications of the duodenal anomaly incidence and the duodenal anomalies which have been the basis of the examinations, are discussed. Only severe duodenal anomaly is included in these examinations, namely those demonstrable both in the supine and the erect position, which means developmental anomalies corresponding to the superior and transverse parts of the duodenum. Patients with a normal duodenal shape have been used as controls. Patients with duodenal anomaly had reduced food-stimulated gastro-oesophageal sphincter pressure, more frequently a positive acid-reflux-test and increased food-stimulated serum-gastrin and serum-pancreatic polypeptide secretion. The results of the examinations for duodeno-gastric reflux and gastric emptying varied. Patients with anomalies located at the transverse part of the duodenum had prolonged gastric emptying and an increased tendency to duodeno-gastric reflux, whereas patients with anomalies located at the superior part of the duodenum showed quick gastric emptying and the same frequency of duodeno-gastric reflux as patients with a normal duodenal shape. Furthermore, patients with anomalies located at the transverse part of the duodenum had a significantly higher food-stimulated duodenal contraction frequency compared to patients with anomalies located at the superior part of the duodenum and patients with a normal duodenal shape. On the other hand the three groups had a similar food-stimulated antral contraction frequency. The shape of the duodenal loop was related to dyspeptic symptoms. Food-provocation, symptoms of gastrooesophageal reflux, and irritable bowel were found in patients with duodenal anomalies as well as in patients with a normal duodenal shape. However, the symptoms seemed significantly more frequent in patients with duodenal anomalies. At a 5-year follow-up examination this difference could not be demonstrated except for food-provocation, but unchanged or exacerbated dyspeptic inconveniences seemed significantly more frequent in patients with duodenal anomalies.
 ...
PMID:The shape of the duodenal loop. Radiological, physiological and clinical aspects in patients with X-ray negative dyspepsia. 321 86

Fasting and post-prandial circulating levels of insulin, gastrin, gastric inhibitory polypeptide, pancreatic polypeptide and neurotensin were measured in patients with flatulent dyspepsia, with and without gallbladder disease and post-cholecystectomy. Levels were also measured in non-dyspeptic patients with gallbladder disease and normal controls. There were no consistent significant differences from controls for fasting and post-prandial responses in patients with a history of dyspepsia or those who experienced dyspepsia at the time of the test. In patients with gallbladder disease, with and without dyspepsia, there was a reduced neurotensin response compared to normal controls. It is concluded that circulating levels of these hormones are not related to symptoms of flatulent dyspepsia.
 ...
PMID:Circulating gastrointestinal hormones in patients with flatulent dyspepsia, with and without gallbladder disease. 354 53

Basal and food-stimulated levels of gastrin and pancreatic polypeptide (PP) were studied in 86 patients with non-ulcer dyspepsia (NUD), defined as chronic or recurrent epigastric pain without anatomical antecedents and without concomitant symptoms of irritable bowel. Thirteen patients with endoscopically confirmed duodenal ulcer disease (DU) and 13 healthy subjects constituted the reference groups. The mean basal gastrin concentration was moderately but significantly (p less than 0.05) higher in the NUD group than in the reference groups (24.3 +/- 1.6 (SEM) pmol/l in NUD, compared with 15.0 +/- 1.5 and 13.6 +/- 1.0 pmol/l among DU patients and healthy subjects, respectively). The well-established postprandial hypergastrinemia in duodenal ulcer patients could be confirmed in this study, and their gastrin response to food was significantly (p less than 0.01) greater than the responses observed both in healthy subjects and in NUD patients. The two latter groups did not differ significantly with regard to gastrin increments, but there was a tendency towards greater increases in the NUD group. A significantly (p less than 0.05) enhanced PP response to the test meal was observed among the DU patients, whereas the response pattern in NUD was closely similar to that in healthy subjects.
 ...
PMID:Basal and food-stimulated levels of gastrin and pancreatic polypeptide in non-ulcer dyspepsia and duodenal ulcer. 372 53

Cigarette smoking has been linked with duodenal ulcer disease although the mechanism of this association is unclear. This study assessed basal gastric secretory response to acute smoking of smokers with an active duodenal ulcer; in addition the possible effects of chronic smoking on gastric secretory capacity, as expressed by pentagastrin stimulated gastric acid secretion and fasting serum pepsinogen I (PG I) concentrations, were investigated in patients with active duodenal ulcer, or non-ulcer dyspepsia. In 10 smokers with duodenal ulcer smoking four cigarettes during 40 minutes did not influence basal gastric secretion of acid and pepsin, or serum PG I and gastrin concentrations. In 136 patients with duodenal ulcer and 90 controls with non-ulcer dyspepsia, pentagastrin stimulated acid secretion and fasting serum PG I concentrations were significantly higher among habitual heavy smokers than among non-smokers. These findings suggest that in heavy smokers with duodenal ulcer acid- and pepsin-secreting cell function is not affected by acute cigarette smoking. By contrast, chronic cigarette smoking seems to be associated either with an increase of parietal- and chief-cell mass, or with an enhancement of their secretory capacity.
 ...
PMID:Cigarette smoking, gastric acid secretion, and serum pepsinogen I concentrations in duodenal ulcer patients. 393 54


1 2 3 4 5 6 7 Next >>