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

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.
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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.
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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.
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PMID:Basal and food-stimulated levels of gastrin and pancreatic polypeptide in non-ulcer dyspepsia and duodenal ulcer. 372 53

Simultaneous measurement of food-stimulated serum pancreatic polypeptide and serum gastrin was carried out in 18 patients with functional dyspepsia and correlated to the shape of the duodenal loop. Significantly higher serum concentrations of pancreatic polypeptide and gastrin were encountered in patients with an abnormal shape of the duodenal loop compared to patients with a normal shape. Although no cause could be given to the phenomenon it may be taken into account when evaluating hormone profiles in patients with functional dyspepsia.
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PMID:Increased serum pancreatic polypeptide and serum gastrin secretion in patients with functional dyspepsia: correlation to the shape of the duodenal loop. 408 30

Somatostatinoma is one of the rarest tumours of the endocrine pancreas. Cardinal manifestations of a somatostatinoma include gallstones, mild diabetes mellitus, steatorrhoea, diarrhoea and dyspepsia. Like any other pancreatic islet cell carcinoma, a somatostatinoma may also produce several different hormones such as adrenocorticotropic hormone, calcitonin, vasoactive intestinal polypeptide, pancreatic polypeptide, gastrin, insulin, and glucagon. In many cases, the clinical picture is dominated by the effect of these other hormones. We present a patient with somatostatinoma in which an immunocytochemical study of the specimens from pancreas and liver showed a weak positive reaction for gastrin besides a strong positive reaction for somatostatin. Interestingly, this patient also showed the signs of carcinoid syndrome which was successfully treated with octreotide.
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PMID:Carcinoid syndrome due to a malignant somatostatinoma. 749 79

In clinical practice, exogenous pancreatic enzymes are administered for the treatment of pancreatogenic steatorrhea or with the intention to relieve pain due to chronic pancreatitis. Moreover, a large number of patients take pancreatin (i.e., exogenous pancreatic enzymes) for functional dyspepsia. The effect of exogenous pancreatic enzymes on the enteropancreatic axis is a complex issue. Intraduodenal but not intrajejunal protease activity appears to exert a dose-dependent negative feedback on exocrine pancreatic secretion. Only enzymes with a proteolytic activity but not amylase and lipase exert a control on pancreatic secretion. The mechanism responsible for this feedback regulation is debated, but the cholinergic system seems to play a major role. Intraduodenal pancreatic enzymes (pancreatin) lead to an increased release of pancreatic polypeptide but do not affect the release of insulin and glucagon. In addition, pancreatic enzymes have an influence on the release of some gastrointestinal hormones (i.e., cholecystokinin, motilin, gastric inhibitory polypeptide). Neither exogenous nor endogenous pancreatic enzymes seem to play a major role in the regulation of interdigestive gastrointestinal motility. However, an adequate rate of postprandial pancreatic output is required to control gastric emptying. Current knowledge on the effect of exogenous pancreatic enzymes on the enteropancreatic axis, gut peptide release and gastrointestinal motility are updated in the present article.
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PMID:Effect of exogenous pancreatic enzymes on gastrointestinal and pancreatic hormone release and gastrointestinal motility. 822 68

This paper describes a 6-year-old Simmental bull with diabetes mellitus. The animal was referred to our clinic because of severe weight loss and chronic indigestion. Clinical examination revealed markedly disturbed general condition, impaired forestomach function and polyuria. There was aciduria, glucosuria and ketonuria. The most important biochemical findings were severe hyperglycemia, markedly increased activities of hepatic enzymes and severe metabolic acidosis. Plasma concentrations of insulin, insulin-like growth factor-I, thyroxine and 3,5,3'-triiodothyronine were lower than normal, whereas those of glucagon were higher than normal. Based on these findings, a diagnosis (secondary) diabetes mellitus was made. The bull was slaughtered and histological examination revealed mixed cell pancreatitis with severe degeneration of islet cells. Immunohistochemical examination of the pancreas showed that very few insulin-, glucagon-, somatostatin- and pancreatic polypeptide, insulin-like growth factor-I and adrenomedullin-producing islet cells were present.
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PMID:[Diabetes mellitus caused by pancreatitis in a bull]. 1123 31

There is no general agreement as regards the effect of Helicobacter pylori infection on gastric emptying in patients with functional dyspepsia. Food releases several gastrointestinal hormones, and some of these are known to contribute to the regulation of gastric emptying. The aim of this study was to investigate the influence of H. pylori on gastric emptying in dyspeptic and healthy subjects and to verify whether different hormone secretion patterns are affected by the presence of the bacterium. Twenty-seven patients affected by functional dyspepsia and 30 asymptomatic healthy subjects entered the study. H. pylori presence was assessed in controls by IgG antibodies to H. pylori and [13C] urea breath test, and that in patients by Warthin-Starry stain on gastric biopsies. After ingesting a standard solid-liquid meal, an ultrasound examination of gastric emptying was performed. Plasma concentrations of gastrin, cholecystokinin, and pancreatic polypeptide were measured in the fasting and postprandial period for 4 hours. The incidence of H. pylori infection was not higher in functional dyspepsia patients than in controls. As regards gastric emptying, no difference was detected between patients and controls with and without H. pylori infection. On the contrary, the presence of H. pylori infection determined alterations in gastrin levels, which were higher in controls than in patients. Basal CCK levels were higher in the H. pylori-negative patients than H. pylori-positive patients and controls. In conclusion, H. pylori infection seems not to cause alterations in gastric emptying, but rather alterations in gastrin levels. In contrast, the altered levels of CCK account for its involvement in the pathophysiology of H. pylori-negative dyspepsia.
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PMID:Effect of Helicobacter pylori infection on gastric emptying and gastrointestinal hormones in dyspeptic and healthy subjects. 1127 Jul 93

The distribution and density of gastric endocrine cells in Balb/c mice bearing CT-26 carcinoma cells were studied immunohistochemically employing specific antisera against serotonin, somatostatin, glucagon, gastrin, cholecystokinin (CCK)-8 and human pancreatic polypeptide (hPP). The animals were divided into two groups, a non-implanted sham group and a CT-26 carcinoma cell-implanted group. Samples were collected from two regions of the stomach (fundus and pylorus) at 28 days after implantation of the medium or the CT-26 cells (1x10(5) cells/mouse). Five of the 6 types of immunoreactive (IR) cells were identified, with only the hPP IR cells not being detected. The regional distribution of the gastric endocrine cells in the CT-26 implanted group was similar to that of the non-implanted sham group. However, the endocrine cells were significantly decreased in the CT-26-implanted group as compared to those of the non-implanted sham group. Serotonin- and somatostatin-IR cells in the fundus and pylorus , and gastrin- and CCK-8-IR cells in the pylorus of the CT-26 implanted groups were significantly decreased compared to those of the sham group. In addition, glucagon-IR cells were restricted only to the fundus of the sham animals. hPP-IR cells were not detected in either the T-26 implanted- or the non-implanted group. Since endocrine cells are the anatomical units responsible for the production of gut hormones, a change in their density may reflect a change in their capacity to produce such hormones. Implantation of the tumor cell mass induced severe quantitative changes in gastric endocrine cell density, an abnormality which may contribute to the development of gastrointestinal symptoms, such as anorexia and indigestion, frequently encountered in cancer patients.
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PMID:Changes in gastric endocrine cells in Balb/c mice bearing CT-26 carcinoma cells: an immunohistochemical study. 1721 38

Brainstem vago-vagal neurocircuits modulate upper gastrointestinal functions. Derangement of these sensory-motor circuits is implicated in several pathophysiological states, such as gastroesophageal reflux disease (GERD), functional dyspepsia and, possibly, pancreatitis. While vagal circuits controlling the stomach have received more attention, the organization of brainstem pancreatic neurocircuits is still largely unknown. We aimed to investigate the in vitro and in vivo modulation of brainstem vagal circuits controlling pancreatic secretion. Using patch clamp techniques on identified vagal pancreas-projecting neurones, we studied the effects of metabotropic glutamate receptor (mGluR) agents in relation to the effects of exendin-4, a glucagon-like peptide 1 analogue, cholecystokinin (CCK) and pancreatic polypeptide (PP). An in vivo anaesthetized rat preparation was used to measure pancreatic exocrine secretion (PES) and plasma insulin following microinjection of metabotropic glutamate receptor (mGluR) agonists and exendin-4 in the brainstem. Group II and III mGluR agonists (2R,4R-4-aminopyrrolidine-2,4-dicarboxylate (APDC) and L(+)-2-amino-4-phosphonobutyric acid (L-AP4), respectively) decreased the frequency of miniature inhibitory and excitatory postsynaptic currents (mIPSCs and mEPSCs, respectively) in the majority of the neurones tested. All neurones responsive to L-AP4 were also responsive to APDC, but not vice versa. Further, in neurones where L-AP4 decreased mIPSC frequency, exendin-4 increased, while PP had no effect upon, mIPSC frequency. Brainstem microinjection of APDC or L-AP4 decreased plasma insulin secretion, whereas only APDC microinjections increased PES. Exendin-4 microinjections increased plasma insulin. Our results indicate a discrete organization of vagal circuits, which opens up promising avenues of research aimed at investigating the physiology of homeostatic autonomic neurocircuits.
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PMID:Pancreatic insulin and exocrine secretion are under the modulatory control of distinct subpopulations of vagal motoneurones in the rat. 2271 59


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