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

Helicobacter pylori infection in humans has been shown to be associated with changes in gastric physiology, including exaggerated basal and meal-stimulated gastrin levels. This has been suggested to be due to the direct effects of the bacterium through inflammation and its urease enzyme. The gastric bacteria Helicobacter felis and Helicobacter heilmannii colonize the antrum of rats in large numbers and induce no significant inflammatory response. Thus, the direct effect of Helicobacter infection on gastric physiology, independent of gastritis, could be studied. Basal, freely fed and stimulated acid and gastrin levels were recorded from animals infected with H. felis, H. heilmannii or uninfected controls over a 30 week period. No significant difference was found between freely fed gastrin over 7 weeks or fasting gastrin over 24 weeks or basal and stimulated acid over 30 weeks between all three groups. Triple therapy did not alter gastrin or acid output. The antrum of all Helicobacter-infected rats was well colonized; triple therapy cleared H. felis but not H. heilmannii. Very little inflammation was seen in control or Helicobacter-infected animals. In conclusion, Helicobacter-induced effects on gastric physiology are unlikely to be due to direct bacterial effects, but are best explained by other factors (i.e. inflammatory damage).
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PMID:Gastrin release and gastric acid secretion in the rat infected with either Helicobacter felis or Helicobacter heilmannii. 973 79

There are three main types of blood test available for the management of Helicobacter pylori infection: those that detect an antibody response; tests of the pathophysiological state of the stomach; and those that indicate an active infection. Enzyme linked immunosorbent assay (ELISA) based kits are the most numerous of the commercially available tests. Originally the kits used crude antigen preparations but many of the newer kits use a more purified antigen preparation giving increased specificity but a lower sensitivity. The sensitivity, specificity, and predictive values of the tests can also be affected by the population under test and coexistent disease in the patients. Near patient test kits are based on either latex agglutination or immunochromatography. Generally, they have low sensitivities compared with laboratory tests. Commercial western blotting kits have also been developed and are used to detect the presence of specific virulence markers. The exact role of serology in the management of Helicobacter infection has still to be defined, although there is evidence that, used as a screening procedure, it can reduce endoscopy cost and workload. Gastrin and pepsinogen blood concentrations may provide valuable information on the pathophysiological state of the stomach--for example, the presence of inflammation or gastric atrophy. A combination of serology and serum concentrations of gastrin and pepsinogen may be used effectively to detect serious gastroduodenal disease in patients.
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PMID:Blood tests in the management of Helicobacter pylori infection. Italian Helicobacter pylori Study Group. 976 39

Tham et al. show that Helicobacter pylori infection lowers the density of immunoreactive somatostatin cells (D-cells) in the antral mucosa and elevates plasma gastrin concentrations. According to current hypothesis, the lack of inhibition by somatostatin allows excessive release of gastrin, which stimulates acid secretion and thus causes duodenal ulcers. The cytokine tumour necrosis factor-alpha which is released in H. pylori gastritis inhibits D-cells in culture and may be responsible. Why do not all infected persons get duodenal ulcers? Recent work shows that more aggressive strains of H. pylori have greater effects on somatostatin/gastrin physiology. Another variable is whether the infection causes corpusitis or not. Inflammation of the gastric corpus diminishes acid secretion, which greatly decreases the likelihood of duodenal ulcers but increases the risk of gastric cancer. Factors which promote corpusitis include diets with high salt content or lacking in antioxidant vitamins. Work in this area is elucidating how H. pylori causes different diseases. Hopefully this will allow us to predict and prevent its serious sequelae.
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PMID:Helicobacter pylori and somatostatin cells. 985 43

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.
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PMID:Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection. 1058 48

The adverse effect profile of proton-pump inhibitors is presented. The proton-pump inhibitors are a well-tolerated class of drugs. The most common adverse events of headache, diarrhea, and nausea have been reported in fewer than 5% of patients treated with lansoprazole or omeprazole. The frequency of these adverse events with the two proton-pump inhibitors is comparable to that of placebo and histamine H2-receptor antagonists. Few clinically important interactions have been observed between proton-pump inhibitors and other drugs metabolized by the cytochrome P-450 system. The interaction potential should be considered when drugs with a narrow therapeutic window, such as phenytoin, warfarin, and theophylline, are used concomitantly with proton-pump inhibitors. Theoretical concerns about the consequences of chronic administration of proton-pump inhibitors, such as the impact of sustained hypergastrinemia on gastric morphology and the development of atrophic gastritis, have been dismissed. While increased gastrin levels are observed among patients taking proton-pump inhibitors, for the majority they remain within the normal range. After long-term use of the drugs, patients do not appear to be at increased risk of atrophic gastritis or gastric cancer. Helicobacter pylori infection, rather than acid suppression, may be the more important factor for the development of atrophic gastritis. Bacterial overgrowth and altered nutrient absorption resulting from sustained hypochlorhydria induced by chronic administration of proton-pump inhibitors have not been realized as clinical concerns. Not only are proton-pump inhibitors well tolerated during short-term administration, but there also do not appear to be clinically important adverse sequelae associated with their long-term use.
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PMID:Safety profile of the proton-pump inhibitors. 1059 19

Gastrin levels have been reported to be often increased in patients with primary hyperparathyroidism (PHPT) considered to be caused by hypercalcemia. To determine the prevalence of increased basal gastrin and to investigate its causes, 52 consecutive patients with PHPT were studied prospectively, undergoing a clinical, biochemical, and gastric morphofunctional assessment before any parathyroid surgical procedure. This included evaluation of basal and secretin-stimulated gastrin, basal and pentagastrin-stimulated gastric acid secretion, upper gastrointestinal endoscopy, with histological evaluation for gastritis and Helicobacter pylori infection. Twenty of the 52 PHPT patients (38.5%) had increased fasting gastrin. Further investigation allowed us to clearly demonstrate the causes of hypergastrinemia in 16 of these 20 patients. In 7 of 20 (35%), hypergastrinemia was caused by gastric fundus atrophy; in 3 patients (15%), Zollinger-Ellison syndrome with Multiple Endocrine Neoplasia type I was diagnosed; whereas in another 20% of patients, mild hypergastrinemia was ascribed to Helicobacter pylori gastritis. Finally, in 2 patients, additional clinical history revealed an occasional use of the gastric antisecretory drug omeprazole a few days before the serum gastrin determination. This study shows that the hypercalcemic status per se is not sufficient to produce an increase in fasting gastrin levels. Furthermore, gastric fundus atrophy, and not gastrinoma, is the major cause of relevant (>160 pg/mL) hypergastrinemia.
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PMID:Prevalence and causes of hypergastrinemia in primary hyperparathyroidism: a prospective study. 1059 18

The effects of Helicobacter pylori infection on gastric acid secretion has not been clarified. The aim of this study was to elucidate the effects of H. pylori infection on gastric juice pH in relation to gene expression of interleukin-1beta (IL-1beta), which is reported to inhibit gastric acid secretion. Gastric juice pH and serum gastrin levels were measured in patients with peptic ulcer disease. The amount of IL-1beta mRNA in gastric fundic gland mucosa was also measured by a competitive reverse transcription-polymerase chain reaction method. These parameters were determined before and after treatment with lansoprazole and amoxicillin. Before treatment a significant positive relation was observed between the amount of IL-1beta mRNA in gastric fundic gland mucosa and gastric juice pH. After treatment significant decreases in the amount of IL-1beta mRNA, gastric juice pH, and serum gastrin levels were observed in patients with eradication of H. pylori, whereas no significant changes were observed in patients without eradication. These results suggest that H. pylori infection induces IL-1beta and suppresses acid secretion, resulting in increases in gastric juice pH and serum gastrin levels. Eradication of H. pylori decreases IL-1beta induction, resulting in an increase in gastric juice acidity and normalization of serum gastrin levels.
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PMID:Relation between interleukin-1beta messenger RNA in gastric fundic mucosa and gastric juice pH in patients infected with Helicobacter pylori. 1061 59

Helicobacter pylori infection of the gastric mucosa is accompanied by an activated histamine metabolism. Histamine plays a central role in the regulation of gastric acid secretion and is involved in the pathogenesis of gastroduodenal ulcerations. Histidine decarboxylase (HDC) is the rate-limiting enzyme for histamine production, and its activity is regulated through transcriptional mechanisms. The present study investigated the effect of H. pylori infection on the transcriptional activity of the human HDC (hHDC) promoter in a gastric epithelial cell line (AGS) and analyzed the underlying molecular mechanisms. Our studies demonstrate that H. pylori infection potently transactivated the hHDC promoter. The H. pylori-responsive element of the hHDC gene was mapped to the sequence +1 to +27 base pairs, which shows no homology to known cis-acting elements and also functions as a gastrin-responsive element. H. pylori regulates the activity of this element via a Raf-1/MEK/ERK pathway, which was activated in a Ras-independent manner. Furthermore, we found that H. pylori-induced transactivation of the hHDC promoter was independent of the cag pathogenicity island and the vacuolating cytotoxin A gene and therefore may be exerted through (a) new virulence factor(s). A better understanding of H. pylori-directed hHDC transcription can provide novel insights into the molecular mechanisms of H. pylori-dependent gene regulation in gastric epithelial cells and may lead to new therapeutic approaches.
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PMID:Helicobacter pylori activates the histidine decarboxylase promoter through a mitogen-activated protein kinase pathway independent of pathogenicity island-encoded virulence factors. 1065 59

Parietal cell protrusion (PCP), swelling and bulging of parietal cells, has been observed in the oxyntic mucosa of patients receiving omeprazole. The frequency of this event and the underlying mechanisms remain to be clarified. As such, it is unknown whether there is a relation with either serum gastrin or Helicobacter pylori infection, and whether PCP predisposes to the development of fundic gland cysts (FGC). We therefore investigated the development of PCP and FGC in gastroesophageal reflux disease (GERD) patients treated with omeprazole and correlated findings to duration of therapy, gastrin, and H pylori infection. In a randomized, double-blinded study, GERD patients were evaluated by endoscopy with biopsy sampling for histology and culture at baseline, and after 3 and 12 months' therapy with omeprazole 40 mg daily. H pylori-positive patients were randomized to additional eradication therapy or placebo antibiotics at baseline. All histological slides were scored blinded for time and outcome of culture for the presence of PCP and FGC. Fasting serum samples from all visits were used for gastrin measurements. The prevalence of PCP increased during omeprazole therapy from 18% at baseline to 79% and 86% at 3 and 12 months (P < .001, baseline v both 3 and 12 months). The prevalence of FGC increased from 8% to 17% and 35% (P < .05, baseline v 12 months). The prevalence of PCP and FGC did not differ among the H pylori-positive and H pylori-negative patients at baseline (PCP 16% v 20% and FGC 7% v 8%, respectively). Whereas H pylori eradication did not significantly affect development of PCP (P = .7), FGC developed significantly more often in the H pylori-eradicated patients when compared with persistent H pylori-positive patients (P < .05). PCP development was related to serum gastrin rise during therapy. In conclusion, PCP occurs in most patients within the first months of omeprazole treatment and is related to increased gastrin levels. FGC develops more gradually and is enhanced by H pylori eradication.
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PMID:Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment. 1115 Mar 84

The association between Helicobacter pylori infection and gastric motility abnormalities is still controversial, partly because of the lack of an appropriate animal model. H. heilmannii type 1 (Hh1), a spiral bacterium that infects the stomach of both man and pigs, easily colonises and induces an inflammatory response in the gastric mucosa of rodents. For these reasons, the present study investigated the relationship between gastric motility in rats experimentally infected with Hh1 and correlated the results with serum gastrin and gastric somatostatin concentrations, as these hormones seem to be involved in gastric motility. Ten rats were inoculated with gastric mucus from an Hh1-positive pig and 10 animals with gastric mucus from an Hh1-negative pig (control group). After 56 days, gastric emptying was studied in vivo by scintigraphy. The animals were then killed, blood samples were collected for serum gastrin measurement, strips of the gastric wall were obtained for an in-vitro motor study and fragments of the gastric antrum were obtained for somatostatin content evaluation, Hh1 diagnosis and histological study. There was a significant increase in gastric emptying in the test group compared with the controls as demonstrated by the in-vivo and in-vitro studies. Serum gastrin levels were significantly higher and somatostatin levels were lower in the test group than in the controls. In addition, infected animals showed evidence of gastritis on histological examination. Gastric motility is altered in rats infected with Hh1, a fact possibly related to concurrent abnormalities of gastrin and somatostatin secretion.
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PMID:Increased gastric emptying induced by Helicobacter heilmannii type 1 infection in rats. 1088 88


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