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)

Pentagastrin-stimulated maximal acid output and postprandial integrated gastrin response (sigma gastrin) were measured in 170 consecutive patients with duodenal ulcers. Within both acid normosecretor and hypersecretor groups, patients with positive family history of ulcer dyspepsia had significantly higher mean maximal acid output than did those without such history. In early-onset (symptoms before age 30) but not late-onset (symptoms after age 30) patients, mean sigma gastrin was significantly greater in those with positive than in those with negative family histories, and in normosecretors than in hypersecretors. Among early-onset patients, family-history-positive normosecretors had a significantly positive correlation between maximal acid output and sigma gastrin, whereas family-history-positive hypersecretors had a significantly negative correlation between these variables. Thus, two subgroups of familial ulcers were identified among early-onset patients. A drive mainly on the G cells may be present in the former group, whereas a drive mainly on the parietal cells may be present in the latter.
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PMID:Identification of two subgroups of familial early-onset duodenal ulcers. 743 86

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

Acid secretion in response to gastrin releasing peptide (GRP) is increased six-fold in Helicobacter pylori positive duodenal ulcer (DU) patients and threefold in H pylori positive healthy volunteers, and this fully resolves after eradication of the infection. This study was undertaken to determine whether a proportion of H pylori positive patients with non-ulcer dyspepsia (NUD) have an acid secretion disturbance similar to DU patients. Basal and GRP stimulated gastrin concentrations and acid output were examined in 25 H pylori positive NUD patients and the results compared with those of 25 H pylori positive healthy volunteers, 25 H pylori negative healthy volunteers, and 25 H pylori positive DU patients. Compared with the H pylori negative healthy volunteers, GRP stimulated gastrin was increased approximately three fold in each of the three infected groups. GRP stimulated acid secretion (median, range) was higher in the H pylori positive NUD patients (29.6 mmol/h (5.2-46.5)) (p < 0.005) than in the H pylori positive healthy volunteers (19.0 (1.0-38.3)) (p < 0.001) or H pylori negative healthy volunteers (6.3 (2.8-20.9)) (p < 0.0001). The H pylori positive NUD patients, however, had lower acid output than the DU patients (39.1 (17.9-64)) (p < 0.005). These findings are consistent with approximately 50% of the NUD patients having a similar disturbance of GRP stimulated acid secretion to DU patients.
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PMID:A substantial proportion of non-ulcer dyspepsia patients have the same abnormality of acid secretion as duodenal ulcer patients. 773 59

Endocrine cells of the gastric oxyntic mucosa, and especially the enterochromaffin-like (ECL) cells, are the progenitors of gastrin-promoted proliferative lesions whose tumorigenic potential largely depends on the background condition in which they arise. Hypertrophic gastropathy due to the familial multiple endocrine neoplasia (MEN-1)-associated or sporadic Zollinger-Ellison syndrome (ZES), diffuse chronic atrophic gastritis restricted to the corpus-fundus (type A CAG), with or without associated pernicious anemia, and Helicobacter pylori-related multifocal chronic atrophic gastritis are the usual background for such growths. The endocrine cell lesions have been classified as pseudohyperplasia (cell clustering unassociated with cell proliferation), hyperplasia (diffuse, linear, micronodular, adenomatoid), dysplasia (enlarged, adenomatous or fused micronodules, microinfiltration, nodular growth), and neoplasia (intramucosal or invasive carcinoids). The entire spectrum of endocrine cell proliferation, from hyperplasia to dysplasia and neoplasia, has been observed in MEN-ZES and diffuse type A CAG. Both hyperplastic and pseudohyperplastic changes occur with some frequency in the H. pylori-related chronic gastritis associated with ulcer disease or dyspepsia. However, because no progression to dysplastic or neoplastic lesions has thus far been documented in these latter conditions, their role in gastric endocrine cell tumorigenesis appears negligible.
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PMID:Hyperplastic, dysplastic, and neoplastic enterochromaffin-like-cell proliferations of the gastric mucosa. Classification and histogenesis. 776 35

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

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.
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PMID:Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion. 842 Jul 45

One hundred and fourty four patients with non-ulcer dyspepsia (NUD), as defined by the working party of AGA in 1987, (67 men and 77 women, 16-76 years, mean age 42.9 +/- 1.2 years) and 34 asymptomatic controls (25 men and 9 women, 17-75 years, mean age 50.6 +/- 2.4 years) parameters of gastrophysiological function (gastric acid secretion, postprandial gastric emptying-acetaminophen method, serum gastrin levels and cutaneous electrogastrography (EGG)) and the prevalence of Helicobacter pylori (Hp) (histological and urease test of biopsy specimens) were investigated. Based on symptom patterns, there were 68 patients with dysmotility-like dyspepsia, 27 with ulcer-like dyspepsia, 17 with reflux-like dyspepsia, 6 with aerophagia and the 26 with nonspecific or idiopathic dyspepsia. The age distribution of NUD was predominant in the fourth decade, and the sex distribution was not significantly different. In general, hypersecretion of gastric acid and hypergastrinemia were rare in NUD patients. There was no significant difference in gastric acid secretion, basal and food stimulated serum gastrin levels and prevalence of Hp between the two groups. But 51 of 144 NUD patients (41.1%) had delayed gastric emptying (p < 0.05) compared to controls. Indeed gastric emptying was markedly prolonged in patients with dysmotility-like (58.1%) and reflux-like (42.9%) dyspepsia. On EGG, about a half of NUD patients showed evidence of bradygastria or tachygastria, in particular in the postprandial state, which was related to delayed gastric emptying. By chronic administration of cisapride, score of symptoms was significantly decreased and postprandial gastric emptying was significantly accelerated in delayed gastric emptying cases. We conclude that in NUD patients, in particular those with dysmotility-like dyspepsia, tests of postprandial gastric emptying and/or EGG are useful for investigation of gastric motor disorder and therapeutic effects of several prokinetic drugs clinically.
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PMID:[Investigation of gastric function and prevalence of Helicobacter pylori in non-ulcer dyspepsia]. 849 67

Liver affects the release and clearance of many hormones, but the interactions between gastrointestinal peptides and liver function are obscure. Aim of this study was to evaluate plasma concentrations of gastrointestinal peptides during acute hepatic cytonecrosis and during liver regeneration in man. The study was performed in ten patients with viral hepatitis (8 virus A, 2 virus B) in the acute phase (alanine transaminase = 3073 +/- 739 U/L; mean +/- SEM), and at days 7, 45 and 52 after the initial evaluation, during clinical and biochemical recovery (52nd day, alanine transaminase = 77 +/- 26). Plasma concentrations of the following hormones were evaluated by radioimmunoassay: glucagon, insulin, gastrin, vasoactive intestinal peptide, bombesin, neurotensin, cholecystokinin, secretin and motilin. Only serum bombesin and cholecystokinin were significantly (p < 0.01) increased in the acute phase of hepatitis (bombesin: 138 +/- 21 pg/ml; cholecystokinin: 57 +/- 7 pg/ml); they returned to normal values during convalescence (bombesin: 60 +/- 8; cholecystokinin: 31 +/- 4). During hepatocellular necrosis, plasma concentrations of cholecystokinin and bombesin, which are both cellular growth factors and regulatory signals of food introduction and satiety state, were increased by 83% and 130%, respectively. Increase of these hormones may cause the dyspepsia and lack of appetite that characterizes the initial phase of acute viral hepatitis.
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PMID:Gastrointestinal peptide hormones in acute viral hepatitis. 878

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


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