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)

The aim of the present study was to determine whether the association between Helicobacter pylori infection and increased concentrations of gastrin in serum is independent of chronic duodenal ulcer disease and whether the mechanism of this association involves a disturbance of feedback inhibition of gastrin release by intragastric acid. Of 48 subjects evaluated, 26 (54%) were seropositive for H. pylori by ELISA. Fasting and peptone meal-stimulated gastrin release at pH 2.5 and pH 5.5 as well as integrated 24-hour plasma gastrin concentrations were significantly higher in the seropositive group, even when subjects with a history of duodenal ulcer were excluded. The inhibitory effect of low pH on the release of gastrin was not attenuated in subjects with positive results in the ELISA. These data indicate that the association between seropositivity for H. pylori and enhanced release of gastrin is independent of a history of duodenal ulcer and is not caused by a disturbance of the normal feedback inhibition of gastrin release by intragastric acid.
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PMID:Elevation of meal-stimulated gastrin release in subjects with Helicobacter pylori infection: reversal by low intragastric pH. 192 7

Acid secretion is regulated by hormonal factors acting peripherally and centrally, as well as neural factors. Gastrin and histamine are the two most important peripheral hormonal stimulants, while the vagus is the predominant nerve affecting acid secretion. Meal related acid secretion occurs in three phases: cephalic, gastric and intestinal. Acid secretion is stimulated in the first two phases while it is inhibited in the intestinal phase. Proteins are potent acid stimulants but carbohydrates and fats are inhibitors. Tea, coffee, milk and alcohol are acid stimulants; on the other hand the damaging influence of spices on the stomach may not be related to increased acid secretion. Psychological stress has a variable effect. The effect of Helicobacter pylori infection on acid secretion is being elucidated. Many drugs modifying acid secretion are available and are useful in the treatment of acid peptic disease.
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PMID:Determinants of acid secretion. 198 28

It has been proposed that the hypergastrinaemia in subjects with Helicobacter pylori infection is caused by the action of the ammonia produced by the organism's urease activity on the antral G cells. To investigate this hypothesis we examined the effect on plasma gastrin of increasing the bacterium's ammonia production by infusing urea intragastrically to eight H pylori positive duodenal ulcer patients. After a 60 minute control intragastric infusion of dextrose solution at 2 ml/minute, a similar infusion containing urea (50 mmol/l) was continued for four hours. During the urea infusion, the median gastric juice urea concentration rose from 1.1 mmol/l (range 0.3-1.6) to 15.5 mmol/l (range 7.9-21.3) and this resulted in an increase in the ammonium concentration from 2.3 mmol/l (range 1.3-5.9) to 6.1 mmol/l (range 4.2-11.9) (p less than 0.01). This appreciable rise in ammonia production did not result in any change in the plasma gastrin concentration. The experiment was repeated one month after eradication of H pylori, at which time the median basal gastrin was 20 ng/l (range 15-25), significantly less than the value before eradication (30 ng/l range 15-60) (p less than 0.05). On this occasion, the gastric juice ammonium concentration was considerably reduced at 0.4 mmol/l (range 0.1-0.9) and the urea infusion did not raise the ammonium concentration or change the plasma gastrin concentration. In conclusion, augmenting H pylori ammonia production does not cause any early change in plasma gastrin.
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PMID:Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations. 199 33

Recent studies have shown that the exaggerated meal-stimulated gastrin release in patients with duodenal ulcer abates after eradication of Helicobacter pylori infection. Bombesin-stimulated gastrin release was compared in 11 H. pylori-infected patients with chronic duodenal ulcer and 8 uninfected healthy volunteers both before and after therapy to eradicate H. pylori. Bombesin infusion significantly increased the gastrin release both in control subjects and in patients with duodenal ulcer. Antimicrobial therapy (bismuth, tetracycline, and metronidazole) to eradicate the H. pylori infection was associated with a significant reduction in bombesin-stimulated gastrin release in patients with duodenal ulcer (from 116.9 +/- 19 pg/mL to 69.5 +/- 7 pg/mL following 50 pmol.kg-1.h-1 bombesin; and from 158 +/- 29 to 83.4 +/- 10 following 200 pmol.kg-1.h-1 bombesin: P = 0.01 for each). Antimicrobial therapy had no effect on gastrin release in uninfected volunteers, thus excluding a nonspecific effect of antimicrobial therapy on antral G-cell function. Serum gastrin was also not increased by feeding 500 mg of urea to 5 H. pylori-infected volunteers. This suggests that access of hydrogen ion to the pH-sensitive sites governing gastrin release by mucosal ammonia produced by H. pylori urease is not a critical factor. These data suggest that exaggerated gastrin release present in patients with duodenal ulcer disease is secondary to H. pylori infection.
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PMID:Helicobacter pylori-associated exaggerated gastrin release in duodenal ulcer patients. The effect of bombesin infusion and urea ingestion. 201 63

Helicobacter pylori infection may be associated with duodenal ulcer (DU) and accompanied by enhanced gastrin release but the mechanism of this H pylori related hypergastrinaemia in DU patients is unclear. Cholecystokinin (CCK) has been implicated in the feedback control of gastrin release and gastric acid secretion in healthy subjects. This study therefore investigated if CCK participates in the impairment of postprandial gastrin release and gastric secretion in six DU patients. Tests were undertaken with and without elimination of endogenous CCK by loxiglumide, a selective CCK-A receptors antagonist, before and after eradication of H pylori with triple therapy (omeprazole, amoxicyllin, bismuth). In H pylori positive DU patients, the post-prandial decline in pH (with median pH 3.5) was accompanied by a pronounced increment in plasma gastrin but the administration of loxiglumide did not affect significantly this postprandial rise in plasma gastrin and gastric pH profile. After eradication of H pylori, the plasma gastrin concentration was reduced while the median postprandial pH was significantly increased (median pH 4.3). The administration of loxiglumide resulted in significantly greater increase in postprandial plasma gastrin and greater decrease in pH (median pH 3.1) in these patients. This study shows that (a) infection with H pylori is accompanied by an enhanced gastrin release and gastric acidity in DU patients, (b) the failure of loxiglumide to affect plasma gastrin or gastric acid secretion in H pylori infected DU patients could be attributed, at least in part, to the failure of endogenous CCK to control gastrin release and gastric secretion by releasing somatostatin, and (c) the test with loxiglumide may be useful in the identification of patients with impaired feedback control of gastrin release and gastric secretion resulting from infection with H pylori.
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PMID:Eradication of Helicobacter pylori restores the inhibitory effect of cholecystokinin on postprandial gastrin release in duodenal ulcer patients. 748 32

This review covers major advances in peptic ulcer disease over the last 25 years. Flexible endoscopy enables accurate diagnosis of peptic ulcer to be made and its introduction made possible the large number of controlled clinical trials on the use of various agents in peptic ulcer treatment. The histamine H-2 receptor antagonists, which reduce gastric acid output, were the first major group of potent ulcer healing drugs introduced. Subsequently, other ulcer healing agents with different modes of action, e.g. colloidal bismuth, sucralfate, prostaglandin analogues, omeprazole were also shown to be effective. The identification of Helicobacter pylori ten years ago was another major advance in peptic ulcer disease. This bacterium is now thought to be the most important cause of peptic ulcer disease and its eradication cures the disease. There are still unanswered questions regarding varying sequelae of Helicobacter pylori infection, the effect of the infection on gastric acid and gastrin secretion while a convenient and effective treatment regime remains to be developed. Non-steroidal anti-inflammatory drugs are now thought to be the second most important cause of peptic ulcer disease and a major risk factor for ulcer complications and mortality. While misoprostol and histamine H-2 antagonists can prevent peptic ulcer associated with these substances, indications for prophylaxis have not yet been defined. If Helicobacter pylori infection could be controlled through improved socio-economic standards and possible development of a vaccine, and if anti-inflammatory drugs devoid of gastric side effects can be developed, peptic ulcer may become a less important health problem in the future.
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PMID:Peptic ulcer--a new look. 765 63

We evaluated in children with abdominal complaints the prevalence of Helicobacter pylori gastric and duodenal colonization and the histological features of gastric and duodenal mucosae. Fifty patients, aged 1-17 years, underwent upper endoscopy for recurrent abdominal pain, vomiting and/or gastrointestinal bleeding. With serological, bacteriological and/or histological methods twenty-eight children were demonstrated to be Helicobacter pylori-positive. No statistically significant differences were observed with regard to age, sex and indication to perform endoscopy. Eighty-two percent of Helicobacter pylori-positive patients had gastritis and/or duodenitis. The Helicobacter pylori-positive children had higher Helicobacter pylori specific IgG levels than the Helicobacter pylori-negative ones (p < 0.001). No statistically significant differences were found between Helicobacter pylori-positive and Helicobacter pylori-negative subjects, for gastrin and pepsinogen I. Since the frequency of Helicobacter pylori infection in children with gastrointestinal complaints is high, in patients undergoing upper endoscopy, the sistematical examination of bioptic samples for bacteriological and histologic procedures is of great importance.
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PMID:[High incidence of Helicobacter pylori infections in an endoscopic pediatric patient series]. 780 63

Helicobacter pylori infection is the most common cause of duodenal ulcer disease, yet duodenal ulcer is an uncommon outcome of H. pylori infection. We reviewed the possible explanations such as differences in the host or in the strain of H. pylori. Host factors reviewed included genetic susceptibility to H. pylori infection and excess gastric acid secretion. The role of potential H. pylori virulence factors not present in all strains such as the cagA gene and the results of other molecular methods to identify disease-specific differences among isolates was also reviewed. Although cure of H. pylori infection resolves gastrin releasing peptide stimulated acid secretion there was no change in parietal cell mass. Twin studies have shown genetic differences in H. pylori susceptibility. There was no difference in the prevalence of the cagA gene between H. pylori infected asymptomatic volunteers and duodenal ulcer patients (P = 1.0). DNA-DNA hybridization of whole genomic DNA in solution and cluster analysis of rep-PCR genomic DNA fingerprints suggest that isolates from patients with duodenal ulcer disease are different from those obtained from individuals with asymptomatic gastritis. Cluster analysis of the rep-PCR DNA fingerprints revealed two major groups of the strains; one set consisted of strains from patients with duodenal ulcer disease and the second cluster consisted largely of strains from individuals with asymptomatic gastritis. Recent molecular studies suggest that disease-specific cell lineages or strains may exist among H. pylori isolates leading to the various outcomes observed in patients with H. pylori infection.
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PMID:How does Helicobacter pylori cause duodenal ulcer disease: the bug, the host, or both? 788 Oct 25

Helicobacter pylori infection is associated with abnormalities in serum gastrin concentration, antral gastrin and somatostatin content, and D-cell density in adults. We have studied the effects of H pylori infection in children. We studied 13 children positive for H pylori and 7 negative children. The median antral somatostatin content was significantly lower in the positive than in the negative group (0.69 [range 0.35-0.91] vs 1.31 [0.73-1.67] ng/mg, p = 0.007). Both antral and serum gastrin concentrations were significantly higher in the positive group (30.1 [15.3-83.6] vs 14.8 [13.8-28.8] ng/mg, p = 0.008; and 89.9 [59.4-313.2] vs 29.5 [13.9-71.1] pg/mL, p = 0.006). Treatment to eradicate H pylori was successful in 11 of the 13 positive patients. With eradication antral somatostatin increased to within the normal range (by a median of 0.41 [0.21-0.86] ng/mg to 1.10 [0.81-1.55] ng/mg, p = 0.016). Serum and antral gastrin decreased (by 37.1 [5.5-265.2] pg/mL to 52.8 [21.4-267.5] ng/mg, p = 0.001; and by 8.0 [2.0-47.2] ng/mg to 22.1 [10.9-37.5] ng/mg, p = 0.001). Eradication of H pylori also significantly increased antral D-cell density (8 [5-22] to 15 [9-22] cells per mm, p = 0.031) and decreased G-cell density (138 [89-161] to 88 [33-121] cells per mm, p = 0.016). The hypergastrinaemia in children positive for H pylori may be due to a deficiency of antral somatostatin, which inhibits gastrin synthesis and release.
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PMID:Effect of Helicobacter pylori eradication on G-cell and D-cell density in children. 790 69

Helicobacter pylori infection is associated with increased meal stimulated gastrin secretion, but the reason for this is unknown. Sequence specific radioimmunoassays were used to measure the concentration of alpha-amidated gastrin, the total progastrin product, and somatostatin in biopsy specimens of human antral mucosa. The antral concentrations of alpha-amidated gastrin and of total progastrin products were significantly higher in H pylori infected patients than in those not infected by this organism. In contrast, the antral somatostatin concentration was significantly decreased in infected patients. Progastrin processing, determined by gel chromatography, seemed unaffected by H pylori infection. The results suggest that the finding of increased gastrin secretion from the antral G cells in H pylori infected patients may be a result of reduced inhibition of G-cell secretion by somatostatin.
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PMID:Gastrin and somatostatin in Helicobacter pylori infected antral mucosa. 791 Nov 15


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