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 prevalence of high total IgE serum levels was evaluated in 232 consecutive patients suffering from peptic ulcer. Twenty-one percent of the patients presented total IgE serum levels above 200 KU/L compared with the 5% found in a healthy control population (p < 0.004). Similar prevalence was found in gastric and/or duodenal ulcers. No significant differences in the duration of the disease, smoking habits, familiarity for peptic ulcer, symptomatology and frequency of complications were observed between patients with high and with normal total IgE serum levels. Gastric function studies (gastric acid secretion, serum pepsinogen and gastrin levels) did not show any significant differences between the two groups. The incidence of Helicobacter pylori infection was 65% in patients with normal IgE levels and 75% in those with high IgE levels (p: n.s.). The response to treatment with full dose of H2-receptor antagonists was comparable in both groups (91.25% and 90.7% of ulcer healing after 6-8 weeks of treatment). A relapse of the ulcer after 6 months of maintenance therapy (half dose of H2-receptor antagonists) was observed in 39.5% of the patients with ulcer and high total IgE serum as against the 11.9% observed in patients with normal IgE (p < 0.001). These data lend further support to the hypothesis of an underlying immuno-allergic reaction in some forms of gastric or duodenal ulcer.
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PMID:High IgE serum levels and "peptic" ulcers: clinical and functional approach. 791 69

Helicobacter pylori infection causes inflammation of the gastric and duodenal mucosa, which results in a disturbance of the regulation of gastrin, gastric acid, and pepsin secretion. Acid secretion may be diminished, normal, or increased, depending on the stage of H. pylori infection, although the meal-stimulated gastrin response is invariably elevated. The exact mechanisms involved are not known, but probably involve the release of cytokines in response to bacterial products initiating mucosal inflammation. Helicobacter pylori is suppressed, although not eradicated, by proton pump inhibitors. In various dose combinations with amoxycillin, omeprazole in a twice daily dose of up to 40 mg b.i.d. eradicates the organism in up to 82% of patients. This synergistic effect may be due to the direct effects of omeprazole, the protection of amoxycillin from acid degradation, or the enhancement of host defense mechanisms accompanying acid suppression.
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PMID:Hp and pH--the relevance of gastric acid to the treatment of Helicobacter pylori infection. 792 Nov 45

The role of laboratory medicine in ulcer disease is poorly defined. However there is increasing evidence of the clinical usefulness of some laboratory tests that investigate secretory functions and defensive properties of the stomach, gastrointestinal hormones and Helicobacter pylori infection. These tests may modify the clinical management of patients with peptic ulcer by identifying H. pylori positive subjects, patients with high acid output, patients who do not respond to antisecretory therapy, and patients with high gastrin levels in whom Zollinger-Ellison syndrome may be suspected. Here we review the clinical value of laboratory tests in ulcer disease, particularly as concerns the cost/benefit ratio. The relative merits of these tests are described giving an indication of their possible role in the diagnostic algorithm.
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PMID:Laboratory medicine in ulcer disease. 792 53

The present strategies for the management of peptic ulceration are well tolerated and clinically effective. Histamine H2-receptor antagonists can be used for mild to moderate disease, and proton pump inhibitors are of particular benefit for patients with severe peptic ulceration and the Zollinger-Ellison syndrome. However, none of these treatments provides protection against recurrent ulceration, except when taken as long-term continuous treatment. Long-term exposure to pharmacological agents raises problems of safety, particularly relating to a lack of intragastric acidity. In addition, the accelerated development of atrophic gastritis in patients receiving omeprazole requires investigation and assessment. It is unlikely that there will be any major development in the area of control of gastric acid secretion, except perhaps the introduction of specific immunization against gastrin. However, the clinical benefit of this strategy awaits assessment. The main area for development must be the introduction of convenient and effective regimens for the eradication of Helicobacter pylori infection. Existing regimens are either simpler and relatively ineffective, or too complicated for widespread application. Bearing in mind the long gestation period of any new drug, it seems likely that the only innovative drug that will be introduced for the management of peptic ulceration before the millennium will be ranitidine bismuth citrate, an antisecretory anti-H. pylori drug that will usually be used in combination with an antibiotic.
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PMID:Treatment of peptic ulcers from now to the millennium. 794 62

Our experience shows that neither basal nor pentagastrin-stimulated acid, pepsin, pepsinogen group A and gastrin secretion significantly change across the age spectrum in subjects with peptic ulcer, even though the typical secretory patterns of patients with GU remain well-defined compared to those with duodenal ulcer (DU), even in the later decades of life. Very little is currently known about age-related changes in the various components of the gastric mucosal barrier; however, a significant reduction of the prostaglandin levels in the gastric mucosa of elderly subjects was recently reported. In elderly GU patients, the concentration of neutral glycoproteins and N-acetylneuraminic acid (NANA) was significantly higher than in young adult GU patients perhaps resulting from the migration of the border between the mucosa of the corpus and the antrum that occurs in the aged stomach. Other factors of pathogenetic importance in GU, such as Helicobacter pylori infection, gastroduodenal motility, gastrointestinal hormones, immune disorders and psychological and social characteristics of the elderly should certainly be further investigated. To date, the published data on the treatment of acute GU in the elderly patients concern studies with H2 blockers: famotidine, ranitidine and nizatidine with healing rates ranging from 67.6% to 90.9% after 6 weeks and 83.8% to 96.0% after 12 weeks of treatment. t present the data available on long-term maintenance treatment of GU disease in the elderly are few: a recent randomized, double-blind study conducted on 61 elderly GU patients with nizatidine vs ranitidine both at the dosage of 150 mg/day showed a relapse rate of 8.29% after 6 months and 34.4% after 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gastric ulcer in the elderly. 801 78

The influence of Helicobacter pylori infection on serum levels of pepsinogen I and gastrin in gastric carcinoma was investigated by simultaneous determination of serum pepsinogen I, gastrin, and IgG antibodies against Helicobacter pylori in 100 patients with gastric carcinoma, and in another 100 age- and sex-matched healthy controls. Serum pepsinogen I level was significantly lower in gastric carcinoma than in controls (55.5 +/- 28.1 vs. 76.9 +/- 25.1 ng/ml, p < 0.005), but there was no difference in serum gastrin between them (63.2 +/- 30.2 vs. 57.4 +/- 28.5 pg/ml, p = 0.16). Helicobacter pylori infection caused a significant increase in serum PGI level in advanced, intestinal type, and non-cardia gastric carcinoma. The serum gastrin level was affected by neither Helicobacter pylori infection nor any of the tumor characteristics. It is concluded that pepsinogen I, rather than gastrin, in the serum is greatly influenced by Helicobacter pylori infection and tumor characteristics in gastric carcinoma.
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PMID:Serum levels of pepsinogen I and gastrin in gastric carcinoma: the influence of Helicobacter pylori infection and tumor characteristics. 811 48

Gastric acid secretion has been considered to decline with increasing age but this view is being re-evaluated as the importance of Helicobacter pylori infection emerges. This study aimed to determine the effect of age, H pylori, and gastritis with atrophy on the serum gastrin concentration, gastric secretory volumes, and acid output in healthy, asymptomatic men. Young men (mean (SD) age 22.9 (0.6) years; n = 22) were compared with old men (72.9 (1.2) years; n = 28) in respect of basal serum gastrin and basal, sham fed, pentagastrin stimulated maximal and peak acid secretion. Antral, corpus, and fundal biopsy specimens were taken for histology and H pylori status (histology, culture, and rapid urease test). H pylori associated gastritis was present in three of 22 young (13.6%) and 16 of 28 old (57.1%) men. Gastritis with atrophy was present in 11 old subjects, 10 of whom were H pylori positive. These subjects had higher mean (SD) serum gastrin concentrations than old subjects without atrophy and young subjects (61.8 (9.2); 40.0 (2.9); 36.8 (2.3) pmol/l respectively; p < 0.001). H pylori infected subjects had higher gastrin values than uninfected subjects, overall (55.3 (5.9); 36.0 (1.8) pmol/l; p < 0.001) and in subjects without atrophy (45.3 (4.2); 36.0 (1.8) pmol/l; p < 0.03). In subjects without H pylori infection, gastrin values did not differ with age (old 37.1 (1.7); young 35.4 (2.1) pmol/l). The maximal gastric secretory volume was lower in old subjects with atrophy. Acid output (mmol/h) in subjects with atrophy was lower than in subjects with no atrophy (basal: 3.0(1.1); 5.1(0.7); p=NS; sham led: 5.4 (1.4); 9.3 (0.8); p<0.02; maximal: 18.9 (4.0); 31.4(1.8); p<0.002; peak: 25.1(5.3); 43.4(2.7); p<0.003). However, acid secretion in old subjects without atrophy was not different to that in young subjects, irrespective of H pylori status. These results did not differ when acid output was expressed as mmol/h/kg lean body mass or mmol/h/kg fat free body weight. Using multiple linear regression analysis, gastritis with atrophy was the only factor that had an independent negative effect on acid secretion. In healthy men without atrophy, gastric acid secretion is preserved with ageing and is independent of H pylori status. Atrophy, which is closely related to H pylori infection, is associated with a decline in acid secretion. Increased basal serum gastrin is related to both atrophy and H pylori infection but not to ageing per se.
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PMID:Effect of age, Helicobacter pylori infection, and gastritis with atrophy on serum gastrin and gastric acid secretion in healthy men. 817 48

The pathogenesis of peptic ulcer is a complex phenomenon and several factors are thought to be involved in this process. Among others, Helicobacter pylori infection, hypergastrinaemia and some proteases seem to play an essential role in inducing peptic ulceration. We investigated whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (a lysosomal hydrolase which seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori infection and mucosal content of gastrin. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer and 11 with duodenitis. Tryptase and cathepsin D were measured in mucosal biopsy specimens (body and antrum of the stomach and duodenum) using IRMA methods. Gastrin was assayed in the antral mucosa by means of a RIA method. Helicobacter pylori infection was histologically evaluated (Giemsa). Tryptase and cathepsin D levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. The mucosal content of cathepsin D, but not that of tryptase, was associated with Helicobacter pylori infection. Tryptase, on the other hand, was related to gastrin content. No correlation was found between the two enzymes. It is concluded that tryptase and cathepsin D probably reflect different pathophysiological modifications in ulcer disease. Cathepsin D seems to be mainly related to the phlogistic reaction of the mucosa to Helicobacter pylori infection; tryptase may reflect and indirect link between the action of gastrin and the function of mast cells.
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PMID:Are tryptase and cathepsin D related to Helicobacter pylori infection and mucosal gastrin in peptic ulcer? 820 35

Helicobacter pylori infection is associated with exaggerated gastrin release. We investigated whether this abnormality was due to the bacteria or the immune response. Fasting and meal-stimulated 'total' and amidated gastrin were measured in 10 H. pylori-infected volunteers before eradication therapy, after 2 and 14 days of therapy, and 4 weeks after completion of therapy. The exaggerated meal-stimulated gastrin concentration remained unchanged after 2 days of therapy, although the polymorphonuclear cell infiltrate and H. pylori bacteria were no longer evident. The expected fall in gastrin concentration after 14 days of therapy was associated with a reduction in the density of mucosal mononuclear cells, suggesting exaggerated gastrin release was related to chronic inflammation or to H. pylori or its products. The effect of H. pylori on normal progastrin processing was also assessed; 2 control groups were included: 10 H. pylori-uninfected volunteers and 13 patients with H. pylori peptic ulcers. There was a significant difference in the proportion of circulating gastrins that were biologically active amidated gastrins between ulcer patients and uninfected controls (56.7 +/- 4% versus 33.8 +/- 4%, p < 0.001). The proportion of amidated to total gastrins did not increase after successful eradication.
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PMID:Helicobacter pylori infection and exaggerated gastrin release. Effects of inflammation and progastrin processing. 821 Sep 84

The effects of oral indomethacin on intragastric pH and serum gastrin were investigated in rheumatoid arthritis patients. Nine patients (1 male, 8 female) without a history of peptic ulcer disease and 6 patients with a history of peptic ulcer disease (5 male, 1 female) were studied. To obviate Helicobacter pylori infection as a confounding factor, only patients with positive H. pylori serology were included. After a 5-day period of placebo treatment and after a 5-day period of indomethacin (50 mg t.d.s.; total dose 750 mg), 24-h intragastric pH and basal and meal-stimulated serum gastrin levels were measured in a double-blind placebo controlled cross-over study. There were no differences in the median 24-h pH values between placebo and indomethacin users irrespective of peptic ulcer disease history. Indomethacin resulted in a higher basal and stimulated gastrin response than placebo in patients with a history of peptic ulcer disease. The basal and incremental responses were lower in patients with a history of peptic ulcer disease than in patients without a history of peptic ulcer disease, both during indomethacin and placebo. The same basal and stimulated incremental serum gastrin responses were found during placebo and indomethacin treatment in patients without a history of peptic ulcer disease. No correlation was established between median 2-h post-prandial intragastric pH and post-prandial incremental serum gastrin concentration. We conclude that indomethacin does not influence the intragastric pH of rheumatoid arthritis patients irrespective of history of peptic ulcer disease.
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PMID:Effects of indomethacin on intragastric pH and meal-stimulated serum gastrin secretion in rheumatoid arthritis patients. 821 53


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