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 heterogeneity of muscarinic receptors has been well supported by differential characteristics between pirenzepine and atropine both in receptor binding and in whole tissue pharmacology studies. Under these conditions pirenzepine has been classified as a selective receptor antagonist with high affinity for M1 receptors. The antisecretory properties of pirenzepine on gastric acid and pepsin secretion may be attributed to the antagonistic activity of the drug on muscarinic M1 receptors of gastric intramural plexuses, whereas the effect on parietal muscarinic M2 receptors seems of less importance. Additional inhibitory mechanisms on gastric secretion may be represented by pirenzepine-induced increase in somatostatin release from gastrointestinal system. Significant cytoprotective properties of pirenzepine have been observed on a variety of experimentally induced peptic ulcerations. This protective activity may be due to pirenzepine-induced increase in gastric mucosal blood flow as well as to the increase in gastric transmural electric potential difference. In accordance with this pharmacodynamic profile of pirenzepine, numerous clinical studies have revealed its efficacy in the treatment of both duodenal and gastric ulcerations. In addition to this, the clinical usefulness of the drug has been demonstrated in Zollinger-Ellison syndrome, in stress ulceration, in acute gastrointestinal bleeding as well as in gastritis, duodenitis and non-ulcer dyspepsia. In most of the studies pirenzepine has been found to be well tolerated with a low incidence of antimuscarinic effects which may occur at salivary, ocular, cardiac and urinary sites. The clinical use of pirenzepine alone or in association with H2 blockers is recommended in the treatment of peptic ulcer patients, in the case of acute gastrointestinal haemorrhage and in patients non responders to H2 antagonists.
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PMID:[A selective antimuscarinic agent: pirenzepine. Review of its pharmacologic and clinical properties]. 257 37

A patient with a somatostatin (SRIH)-secreting islet cell tumor, whose only symptoms were dyspepsia and anemia, is described. The diagnosis of somatostatinoma was based on high plasma SRIH concentrations and immunocytochemical findings. The pancreatic exocrine response to secretin was decreased, whereas the insulin and/or glucagon responses to glucose and arginine were normal. Although the basal plasma GH concentration was normal, the plasma GH response to GHRH was subnormal. Gel permeation chromatography studies indicated that SRIH-14 was the predominant form of SRIH in plasma as well as in tumor tissue.
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PMID:Somatostatin-secreting islet cell tumor (somatostatinoma): suppression of growth hormone (GH) release induced by GH-releasing hormone. 289 73

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 patients who present with chronic unexplained upper abdominal pain or discomfort (functional dyspepsia), therapy should ideally be targeted on correcting the individual's disturbed pathophysiology. Here, putative mechanisms implicated in functional dyspepsia and potential approaches to therapy are critically reviewed in order to determine if targeting treatment is of value. Pharmacological therapies reviewed include those that aim to correct disordered gastric emptying (e.g. cisapride, dopaminergic receptor antagonists, macrolides), reduce visceral hypersensitivity (e.g. somatostatin analogues, cholecystokinin antagonists, opioid agonists, serotonin type 3 receptor antagonists), reduce gastric acid secretion (e.g. H2-blockers, acid pump inhibitors), cure Helicobacter pylori infection, enhance muscosal defence (e.g. sucralfate, bismuth) or modify central nervous system processes. It is concluded that the imperfectly understood pathophysiology of functional dyspepsia contributes to the paucity of established efficacious therapies.
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PMID:Review article: functional dyspepsia--should treatment be targeted on disturbed physiology? 760 50

Changes in immunoreactive (ir)-somatostatin, substance P, and calcitonin gene-related peptide concentrations of the human gastric mucosa were examined in subjects with nonulcer dyspepsia (NUD) and peptic ulcer to clarify the relationship between these peptides and dyspeptic symptoms. Fifty-six patients with NUD were divided into two subject subgroups as follows: 22 patients with upper abdominal discomfort, nausea, and/or vomiting (motility disorder group) and 34 patients complaining of upper abdominal pain [ulcer-like disorder (UD) group]. These patients were compared with either an age- and sex-matched group of asymptomatic outpatients without any organic disease (control group: n = 51), or to a group with peptic ulcer (PU group: n = 30). Ir-somatostatin concentrations of the gastric mucosa were significantly higher in UD group than in PU, motility disorder, or control group, and ir-substance P concentrations in the UD group were higher than in the PU group. No difference in ir-calcitonin gene-related peptide concentrations was observed among the four groups. These results indicate that there may be two distinct subgroups in NUD, and that NUD is not just a stage within the spectrum of peptic ulcer disease from the viewpoint of several gastrointestinal-hormone concentrations of the human gastric mucosa.
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PMID:Immunoreactive-somatostatin, substance P, and calcitonin gene-related peptide concentrations of the human gastric mucosa in patients with nonulcer dyspepsia and peptic ulcer disease. 768 83

Etiologic role for HP appears to be best established in histologically proven gastritis. The major factors mediating gastritis induced by the colonization of the "gastric type" mucosa with HP are probably cytotoxins, cytokines and free radicals activated by this organisms. The deficiency of negative feedback in somatostatin-gastrin link in antral gastritis may result in an excessive gastrin release and increased gastric acid secretion with increased duodenal acid load under basal state and after meal. Recent NIH consensus 1994 proposes that: (1) ulcer patients with HP require treatment with antimicrobial agents whether on first presentation or on recurrence; (2) the value of treatment of HP infection in non-ulcer dyspepsia remains to be determined and (3) the asymptomatic subjects with HP infection do not require treatment with antimicrobial agents.
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PMID:Role of Helicobacter pylori infection in gastro-duodenal secretion and in pathogenesis of peptic ulcer and gastritis. 784 47

Immunoreactive-somatostatin (ir-SS) concentrations of the gastric mucosa and mood state in patients with functional dyspepsia were examined. The subjects were 12 patients with upper abdominal discomfort, nausea and/or vomiting (motility disorder group) and 14 patients complaining of upper abdominal pain (ulcer-like disorder group) for more than a month without any organic upper-gastrointestinal tract disease proven by endoscopy. These patients were compared with either an age- and sex-matched group of asymptomatic outpatients without any organic disease (control group: n = 26) or to a group of patients with peptic ulcer (n = 19). Somatostatin concentrations of the stomach were measured by radio-immunoassay, and the mood state of each subject was assessed by Manifest Anxiety Scale (MAS) and Self-rating Depression Scale test. Immunoreactive-somatostatin concentrations of the gastric mucosa were significantly higher in the ulcer-like disorder group than in the peptic ulcer, motility disorder or control group, and gastric juice levels were higher in the ulcer-like disorder group. The psychometric tests showed that the motility disorder group was more depressive than the ulcer-like disorder group, but there were no differences between the motility disorder, ulcer-like disorder and peptic ulcer group in MAS scores or environmental factors. These results indicate that there may be two different subgroups in functional dyspepsia influenced by both ir-SS concentration of the stomach and/or mood state.
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PMID:Immunoreactive-somatostatin concentrations of the human stomach and mood state in patients with functional dyspepsia: a preliminary case-control study. 810 48

Gastric and duodenal biopsies from 90 patients with various acid peptic disorders-reflux esophagitis (n = 24), gastric ulcer (n = 13), duodenal ulcer (n = 47) and nonulcer dyspepsia (n = 6)-were examined. Seven patients with minimal dyspeptic symptoms and an endoscopically and histologically normal stomach and duodenum served as controls. Immunoperoxidase staining for gastrin-producing G cells, somatostatin-producing D cells and serotonin-producing EC cells was carried out on fundic, antral and duodenal biopsies, and was quantified using a Zeiss MOP Videoplan using the peroxidase-antiperoxidase technique of Sternberger. In the gastric antrum, a G:D:EC cell ratio of approximately 1.6:1:1-was observed. In the duodenum the corresponding ratio was 1:1:2.4. No significant differences were observed within any of the major diagnostic categories. Patient age, sex, duration of symptoms, smoking habits, alcohol consumption and nonsteroidal anti-inflammatory drug use had no effect on endocrine cell densities. Reduced G cell density in the descending duodenum was observed in the presence of mild duodenitis in four patients. In four patients with evidence of antral intestinal metaplastic changes, a significant increase in duodenal G cell densities was found. These results suggest that a change in the number of G, D or EC cells does not play a primary role in the pathophysiology of acid peptic disorders in the majority of patients.
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PMID:Immunocytochemical and morphometric studies of gastrin-, somatostatin- and serotonin-producing cells in the stomach and duodenum of patients with acid peptic disorders. 919 76

Changes in endocrine and secretory functions and in the morfology of gastric mucosa in the course of quadruple H. pylori eradication regimen in 50 H. pylori positive patients: 25 with duodenal ulcer (DU) and 25 with non ulcer dyspepsia (NUD) were studied and compared to 10 healthy controls. Therapy resulted in ulcer healing in all DU patients and in 92% eradication of H. pylori in both groups of patients-DU and NUD. In DU and NUD patients in the course of eradication significant decrease in plasma gastrin was observed. Somatostatin concentration in gastric juice increased significantly in DU patients after anti-H. pylori therapy. EGF in gastric content of DU and NUD patients has risen statistically significantly in the course of H. pylori eradication. Gastric acid output and volume flow decreased insignificantly in both groups. The elimination of H. pylori from gastric mucosa in both DU and NUD patients led to significant decrease in the density and activity of gastritis.
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PMID:Hormonal, secretory and morphological alterations in gastric mucosa in the course of Helicobacter pylori eradication in patients with duodenal ulcer and non-ulcer dyspepsia. 928 34

Microstructural, endo- and exocrine changes in gastric mucosa of Non-Ulcer Dyspepsia patients with H. pylori infection in the course of eradication has been studied. Before, during and after anti H. pylori therapy plasma gastrin and somatostatin levels, EGF and somatostatin concentration in gastric juice and basal and pentagastrin stimulated gastric acid secretion were measured. Moreover microstructure of gastric mucosa specimens has been studied. Maximal Acid Output initially higher in NUD patients than in healthy volunteers increased slightly in the course of eradication. Plasma gastrin decreased while EGF and somatostatin concentration in gastric juice increased. After treatment the ratio of patients with pronounced features (activity) of gastritis was significantly reduced.
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PMID:[Endocrine and exocrine gastric mucosal secretion in the course of H. pylori eradication in patients with non-ulcer dyspepsia]. 942 1


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