Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors review recent progresses made in the understanding of the disturbed gastrin homeostasis in Helicobacter pylori infection and in pernicious anaemia. Regulation of gastrin release in a complex mechanism involving inhibition by a low gastric pH and several peptides including somatostatin, and stimulation by different factors, mainly alimentary peptides and amino-acids. The hypergastrinaemia observed in patients with Helicobacter pylori infection occurs despite a normal intraluminal pH. This may be through alkalinisation of the gastric mucus layer due to the production of ammonia by the bacterial urease or through local release of inflammatory mediators. In pernicious anaemia a factor present in the antacid gastric juice could explain the important hypergastrinaemia observed. The gastrin releasing activity of the gastric juice itself was demonstrated by a decrease of the patients' plasma gastrin concentration during a neutral gastric lavage and by a rise of the gastrin levels in rats whose stomachs were perfused with gastric juice from pernicious anaemia patients. A better understanding of the relation between gastric pH and gastrin release is important not only for these pathological states but also for treatments which suppress acid secretion.
 ...
PMID:[Mechanisms in hypergastrinemia in autoimmune atrophic gastritis and Helicobacter pylori infection]. 826 64

Helicobacter pylori infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylori. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that > 90% of the circulating gastrin consisted of gastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmol/l (8-39) (p < 0.05), entirely because of a fall in G17 from 6 pmol/l (< 2.4-25) to < 2.4 pmol/l (< 2.4-23) (p < 0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmol/l (38-114) to 33 pmol/l (19-88) (p < 0.005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmol/l (< 2.4-52) (p < 0.001). The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmol/l, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylori infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylori predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration of gastrin in H pylori infection is the result of an increase in one of the main biologically active forms of the hormone.
 ...
PMID:Helicobacter pylori related hypergastrinaemia is the result of a selective increase in gastrin 17. 831 7

Helicobacter pylori infection causes inflammation of the gastric and duodenal mucosae, which results in a disturbance of the regulatory mechanisms for gastrin, gastric acid and pepsin secretion. Acid secretion may be decreased, normal or increased, depending on the stage of infection, although the meal-stimulated gastrin response is invariably elevated. The exact mechanisms involved are not known but may be due to the release of cytokines in response to bacterial toxins. H. pylori colonization is reduced by effective acid suppression with proton pump inhibitors, although it is not eradicated. In combination with amoxycillin, omeprazole, up to 40 mg twice daily, eradicated the organism in up to 82% of cases. This synergistic effect may be due to a direct effect of omeprazole on the organism, the protection of amoxycillin from acid degradation, or enhancement of host defence mechanisms accompanying acid suppression.
 ...
PMID:Hp and pH: implications for the eradication of Helicobacter pylori. 834 86

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.
 ...
PMID:Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion. 842 Jul 45

A 60-yr-old man with longstanding duodenal ulcer was found to have hyperchlorhydria, moderate fasting hypergastrinemia, and markedly exaggerated meal-stimulated gastrin release. Antral tissue specimens showed the proliferation of gastrin cells and increased gastrin content, and he was found to have Helicobacter pylori infection in the antral mucosa. His illness was diagnosed as primary gastrin cell hyperplasia with H. pylori infection. Eradication of H. pylori normalized not only gastrin hypersecretion but also gastrin cell hyperplasia. These results indicate that H. pylori infection could be one of the causes of this syndrome.
 ...
PMID:Eradication of Helicobacter pylori normalizes serum gastrin concentration and antral gastrin cell number in a patient with primary gastrin cell hyperplasia. 843 56

In both rodents and humans the development of gastrin-promoted gastric argyrophil enterochromaffin-like cell carcinoids requires the involvement of a genetic factor inherent to multiple endocrine neoplasia syndrome or of type A autoimmune chronic atrophic gastritis. Prolonged severe hypergastrinaemia acting on non-gastritic mucosa, as in Zollinger-Ellison syndrome patients, results in diffuse argyrophil enterochromaffin-like cell hyperplasia but, as a rule, does not produce tumours. Combination of chronic atrophic gastritis (mostly related to Helicobacter pylori infection) with hypergastrinaemia frequently causes linear and micronodular hyperplasia of argyrophil cells, whereas carcinoids are exceptional. No tumours or pre-neoplastic lesions have been observed in patients treated long-term with proton pump inhibitors, apart from rare cases in patients with combined Zollinger-Ellison and multiple endocrine neoplasia syndromes. A moderate increase in the incidence of argyrophil cell clustering, with or without hyperplasia, probably results from the parallel evolution of ulcer-associated Helicobacter gastritis into chronic atrophic gastritis. Eradication of H. pylori with a combination of proton pump inhibitors and antibiotics suppresses gastritis and prevents ulcer recurrence.
 ...
PMID:Proton pump inhibitors, enterochromaffin-like cell growth and Helicobacter pylori gastritis. 849 76

Gastrin releasing peptide (GRP) has proved to be a particularly valuable tool in detecting disturbances of gastric secretory function associated with duodenal ulcer disease and Helicobacter pylori infection, and it has furthered understanding of the pathophysiology of these conditions. Its attractiveness lies in the fact that it simultaneously activates many physiological control processes, both stimulatory and inhibitory. This facilitates the detection of a defect in any of the many controls involved in regulating biological function. Other gastrointestinal functions such as gall-bladder contraction, pancreatic secretion and gastrooesophageal motility are also subject to complex regulatory controls, and GRP may also be of value in investigating disturbances of these processes.
 ...
PMID:Review article: gastrin releasing peptide and its value in assessing gastric secretory function. 852 10

The aim of this study was to investigate the consequence of Helicobacter pylori eradication on gastric mucosa and antral G and D-cells. Forty children, aged 5-17 years with Helicobacter pylori infection were assessed. Helicobacter pylori was detected by a urease test and identified by serological and microbiological methods. Twenty children were again assessed after the therapy (the combination of colloid bismuth subcitrate, amoxycillin and metronidazole). Gastroscopic examination was performed and at least six bioptic specimens were taken from the antrum, body and fundus. Tissue samples, processed with the paraffin method and stained with hematoxyllin and eosin, were assessed. Monoclonal antiserum Gastrin PAP kit 516 and somatostatin PAP kit 512 (DAKO) in the peroxidase-antiperoxidase technique (PAP) have been used to detect G and D-cells. Helicobacter pylori in the gastric mucosa was demonstrated with the Giemsa method. The results show the coincidence of Helicobacter pylori infection and the count of antral G and D-cells and active chronic gastritis in children. After the treatment Helicobacter pylori was eradicated in 70% of children. In 34% of these cases the eradication was followed by a diminution of activity of gastric antral mucosa inflammation and in 20% of these children the resolution of the inflammatory infiltration in the gastric mucosa was seen. A decrease of the antral G and D-cells count and also a diminution of G/D index in these cases were observed.
 ...
PMID:Morphological and immunohistochemical examinations of the dynamic changes of gastric mucosa associated with the treatment of helicobacter pylori infection in children. 877 26

The aim of this study was the effect of antacids containing inorganic bismuth compounds on the morphology of the gastric mucosa and healing of the duodenal ulcer (DU) in patients with exacerbation of the ulcer disease. 169 patients were treated for four weeks with low-dose antacids (two drugs containing bismuth subnitrate--Gastrin and Wikalina, with buffering capacity below 200 mmol HCl per day) and for comparison with ranitidine, colloidal bismuth subcitrate and placebo. We evaluated the effect of these drugs on the morphology of gastric mucosa using endoscopic, histologic and morphometric methods, as well as healing of DU, ulcer symptoms and drug tolerance. Antacids and colloidal bismuth subcitrate decreased both the chronic active gastritis of praepyloric region and frequency of Helicobacter infection, however without the full eradication. Antacids, ranitidine and colloidal bismuth subcitrate did not affect the height of surface epithelium, thickness of foveolar and glandular mucosa as well as the number and size of parietal cells, thus they were without any trophic effects on the gastric mucosa. All mentioned drugs healed DU in 68-73% of patients and significantly better than placebo (46%). These drugs were well tolerated by patients, however antacids caused slight increase in pH of urine and transient hipermagnesemia. Because the etiopathogenese of ulcer disease is still unclear, its therapy is unsuccessful in many cases. We should stress that the treatment with antacids in some cases can be a good and safe alternative therapy in spite of many other currently used medications.
 ...
PMID:[Morphology of the gastric mucosa in patients with duodenal ulcer treated with bismuth-containing drugs]. 883 68

A relationship between allergic diseases and Helicobacter pylori infection has recently been noted. We report a case of atopic dermatitis and H. pylori infection in a 14-year-old girl. She had had widespread diffuse skin erythema with erosions and pigmentation since the age of 3 years. Endoscopically, there was chronic antral gastritis with H. pylori infection and histological eosinophilic infiltration. A high titer of H. pylori-specific IgG was present in serum. She was treated with a proton pump inhibitor (lansoprazole 60 mg), an antibiotic (clarithromycin 800 mg), and plaunotol (a mucosal protective agent, 480 mg) for 2 weeks to eliminate the infection. After 10 days of treatment, erythema and itching were more widespread and vesicle formation was seen on the foot. Generalized skin lesions abated a few days later. After eradication of the bacterium by the treatment, eosinophils decreased from 38.8% to 19.0%, and the clinical signs of atopic dermatitis almost disappeared. Serum gastrin level and the pepsinogen I/II ratio were normalized and histological findings of gastric mucosa showed improvement. H. pylori-specific IgE antibody, analyzed by the Western blot method, gradually decreased with the eradication treatment.
 ...
PMID:Atopic dermatitis successfully treated by eradication of Helicobacter pylori. 895 27


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>