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  • 1
    Electronic Resource
    Electronic Resource
    Large hiatal hernia in patients with iron deficiency anaemia: a prospective study on prevalence and treatment (2004)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 19 (2004), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Although large hiatal hernia may cause bleeding from Cameron erosions, its role in iron deficiency anaemia has been debated, and no data are available on the treatment of these patients with proton pump inhibitors.Aims : To determine the prevalence of large hiatal hernia in out-patients with iron deficiency anaemia and the role of proton pump inhibitors in the prevention of recurrence of anaemia.Methods : Two hundred and twenty-eight out-patients underwent upper/lower endoscopy. Those with large hiatal hernia were given an oesophagogram, discontinued iron supplementation and received proton pump inhibitor treatment with (group 1) or without (group 2) surgery. Anaemia was re-assessed during 1 year of follow-up.Results : Large hiatal hernia was the likely cause of anaemia in 21 patients (9.2%). The median haemoglobin and ferritin values at the diagnosis of anaemia were 7.9 g/dL and 6 µg/L, respectively. Cameron erosions were found in 33% of patients. Ten and eleven patients were included in groups 1 and 2, respectively. Haemoglobin values were 13.8 g/dL and 13.4 g/dL at 3 months of follow-up, and 13.4 g/dL and 13.8 g/dL at 1 year of follow-up, in groups 1 and 2, respectively.Conclusions : Large hiatal hernia may cause iron deficiency anaemia, even without Cameron erosions. Surgery in combination with proton pump inhibitor therapy is no better than proton pump inhibitor therapy alone in preventing the recurrence of anaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2004.01894.x
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  • 2
    Electronic Resource
    Electronic Resource
    Role of Helicobacter pylori serology in atrophic body gastritis after eradication treatment (2002)
    Oxford UK : Blackwell Science Ltd.
    Alimentary pharmacology & therapeutics 16 (2002), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It has been reported that 50% of patients with atrophic body gastritis have positive Helicobacter pylori antibody titres only. In atrophic body gastritis, a decrease in H. pylori antibodies after eradication treatment has been reported, suggesting that serology may indicate an active H. pylori infection.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To investigate the time course of H. pylori antibodies and gastric inflammation after eradication treatment in patients with atrophic body gastritis, and to determine whether serology alone can be considered as a valid tool to assess the efficacy of eradication treatment in patients with atrophic body gastritis.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Twenty-seven patients with atrophic body gastritis (12 serologically H. pylori-positive only, ABG-S+; 15 H. pylori-positive at histology and serology, ABG-H+) were included in the treatment group, and 17 patients (all ABG-S+) in the no treatment group. All patients had gastroscopy plus biopsies evaluated according to the updated Sydney system and H. pylori immunoglobulin G determination: in the treatment group, at baseline and 6 and 24 months after eradication (bismuth-based triple regimens); in the no treatment group, at baseline and after 3 years.〈section xml:id="abs1-4"〉〈title type="main"〉Results:In the treatment group, in ABG-S+ patients, H. pylori antibodies decreased significantly 6 months after treatment [37.5 U/mL (16–100 U/mL) vs. 15 U/mL (0–100 U/mL), P 〈 0.01], but 2 years after treatment no further decrease occurred. In addition, in ABG-H+ patients, a significant decrease in H. pylori antibodies occurred 6 months after treatment [45 U/mL (12.5–100 U/mL) vs. 31 U/mL (0–65 U/mL), P 〈 0.01], but a further decrease was also observed 2 years after treatment [20 U/mL (0–56 U/mL), P 〈 0.01]. In ABG-S+ patients, no correlation was observed between the H. pylori antibodies and gastric inflammation score, whereas, in the ABG-H+ group, this correlation was extremely significant (r=0.5991, P 〈 0.0001). In the no treatment group, at follow-up, a significant decrease in H. pylori antibodies was observed [26 U/mL (15–100 U/mL) vs. 22 U/mL (0–53 U/mL), P 〈 0.05], but the gastric body inflammation remained unchanged.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:This study shows that, in ABG-S+ patients after eradication treatment, serology does not keep in step with gastric inflammation. This suggests that, in patients with atrophic body gastritis, serology alone may not be valid for the assessment of the efficacy of eradication treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2002.01213.x
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  • 3
    Electronic Resource
    Electronic Resource
    Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection (2001)
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 15 (2001), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Helicobacter pylori infection, gastric acid hypersecretion and NSAID consumption may cause peptic ulcer.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To investigate the respective roles of H. pylori and acid secretion in bleeding duodenal ulcer.〈section xml:id="abs1-3"〉〈title type="main"〉Patients and methods:A total of 99 duodenal ulcer patients were referred for evaluation of acid secretion: seven with Zollinger–Ellison Syndrome; 14 with hypersecretory duodenal ulcer, defined by the coexistence of elevated basal acid output and pentagastrin acid output; and 78 duodenal ulcer patients with normal acid output. All non-Zollinger–Ellison Syndrome patients were H. pylori-positive and cured of infection. All patients were followed-up for a 36-month period, to assess the occurrence of bleeding episodes.〈section xml:id="abs1-4"〉〈title type="main"〉Results:Twenty-nine patients had at least one bleeding episode in the 4 years before the study. Bleeding was more frequent in males and in patients on NSAIDs. The mean basal acid output was not higher among bleeders. In the 21 patients (14 hypersecretory duodenal ulcer, seven Zollinger–Ellison Syndrome) with basal acid output 〉 10 meg/h and pentagastrin acid output 〉 44.5 meg/h, the risk of bleeding was higher (OR 6.5; 95% CI: 2–21). In the follow-up period, three out of 83 (3.3%) non-Zollinger–Ellison Syndrome patients had a H. pylori-negative duodenal ulcer with bleeding. The risk of bleeding after H. pylori cure was not higher in hypersecretory duodenal ulcer patients (P 〉 0.3), nor among patients with previous bleeding episodes (P 〉 0.2).〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:In H. pylori-positive duodenal ulcer patients, the coexistence of elevated basal acid output and pentagastrin acid output leads to a sixfold increase in the risk of bleeding. After H. pylori cure, gastric acid hypersecretion is not a risk factor for bleeding. However, duodenal ulcer recurrence with bleeding may occasionally occur in patients cured of H. pylori, even if acid output is normal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.00992.x
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  • 4
    Electronic Resource
    Electronic Resource
    Involvement of the corporal mucosa and related changes in gastric acid secretion characterize patients with iron deficiency anaemia associated with Helicobacter pylori infection (2001)
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 15 (2001), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Recent studies have reported an association between iron deficiency anaemia and Helicobacter pylori. Helicobacter pylori could cause iron deficiency anaemia by altering iron absorption. We observed that most patients with Helicobacter pylori infection and iron deficiency anaemia present a chronic superficial pangastritis.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To investigate whether Helicobacter pylori-positive patients with iron deficiency anaemia have peculiar histological and functional features when compared with non-anaemic Helicobacter pylori-positive subjects.〈section xml:id="abs1-3"〉〈title type="main"〉Patients:Fifty-one patients with iron deficiency anaemia, in whom chronic superficial Helicobacter pylori gastritis was the only gastrointestinal finding, and 103 non-anaemic Helicobacter pylori-positive controls were included in the study. Thirty-seven patients were randomly matched with 37 controls of the same sex and age.〈section xml:id="abs1-4"〉〈title type="main"〉Methods:Gastroscopy, with antral (n=3) and body (n=3) biopsies, was performed. Gastrin and pepsinogen I levels and antiparietal cell antibodies were evaluated. Intragastric pH was also measured.〈section xml:id="abs1-5"〉〈title type="main"〉Results:Gastritis involved the corporal mucosa in 90% of patients compared to 42.7% of controls (P 〈 0.0001). The mean inflammatory score in the gastric body was significantly higher among patients than in controls (2.2 vs. 0.6; P=0.012). Gastrin was significantly higher in patients than in controls (mean 60.2 vs. 29 pg/mL; P=0.0069). Intragastric pH was higher in patients than in controls (median 5.7 vs. 2; P=0.0026).〈section xml:id="abs1-6"〉〈title type="main"〉Conclusions:These data suggest that patients with iron deficiency anaemia and Helicobacter pylori infection have a peculiar pattern of gastritis with corporal involvement and related changes in intragastric pH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.01101.x
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  • 5
    Electronic Resource
    Electronic Resource
    Antral gastrin cell hyperfunction and Helicobacter pylori infection (1996)
    Oxford BSL : Blackwell Science
    Alimentary pharmacology & therapeutics 10 (1996), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Antral gastrin cell hyperfunction (AGCH), is a rare cause of duodenal ulcer associated with non-tumour hypergastrinaemia and acid hypersecretion. Aim: To investigate the role of Helicobacter pylori in AGCH. Patients: Twelve AGCH patients and eight H. pylori-positive non-hypergastrinaemic duodenal ulcer patients were compared. Methods: Basal and peak acid outputs, gastrin-stimulation (meal and bombesin) tests, and immunohistochemistry for antral G and D cells were performed. One year after H. pylori eradication, six AGCH patients were again investigated with the same tests. Results: Significantly more basal, and stimulated gastrin and acid secretion, were found in AGCH compared to the H. pylori-positive duodenal ulcer patients (P〈0.01). G cell counts were significantly higher in AGCH than in duodenal ulcer patients (118.8, range 58–192.4, vs. 86.1, range 49–184; P〈0.05), and the resulting G/D cell ratio was also higher in AGCH patients (4.2, range 2.6–5.6, vs. 3.3, range 1.9–4.3; P〈0.05). H. pylori was present in the gastric mucosa of all 12 AGCH patients. Cure of infection in six AGCH individuals resulted in marked a decrease of gastrin levels associated with a significant (23.7%; P〈0.05) decrease of G cell count and an increase (12%; P〈0.05) of D cell count. Conclusions: The results indicate that AGCH may result from H. pylori overstimulation of gastrin cell function in patients with some presently undefined, familial predisposition and that an imbalance of the G/D cell ratio may have a role in the genesis of hypergastrinaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.1996.31173000.x
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  • 6
    Electronic Resource
    Electronic Resource
    Occurrence and risk factors for benign epithelial gastric polyps in atrophic body gastritis on diagnosis and follow-up (2005)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 21 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Benign epithelial gastric polyps have been reported to be more common in atrophic body gastritis. The role of Helicobacter pylori infection in the induction of gastric atrophy is well-known. The development of hyperplastic polyps may be in relation to H. pylori infection.Aim : To investigate occurrence of benign epithelial gastric polyps in atrophic body gastritis patients at diagnosis and follow-up, and the role of H. pylori and other risk factors for the development of benign epithelial gastric polyps.Methods : A total of 259 consecutive atrophic body gastritis patients included in a follow-up programme, of whom 202 were followed up for median period of 4 years (range: 2–11). At baseline and follow-up gastroscopies, the presence of benign epithelial gastric polyps was evaluated. Biopsies for histology were obtained from all detected benign epithelial gastric polyps.Results : Frequency of benign epithelial gastric polyps in atrophic body gastritis patients were 4.6% at baseline and 5.9% at follow-up. About 91.7% were hyperplastic polyps. H. pylori infection was detected in 79.2% atrophic body gastritis patients with benign epithelial gastric polyps, and in 70.8% without benign epithelial gastric polyps. Smoking was more frequent among patients with benign epithelial gastric polyps [42% vs. 20%, OR 2.8 (95% CI: 1.2–6.9)].Conclusions : Benign epithelial gastric polyps occur in about 5% of atrophic body gastritis patients, and the vast majority are hyperplastic polyps. Smoking habit, but not H. pylori infection, increases the risk for benign epithelial gastric polyps in atrophic body gastritis patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2005.02399.x
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  • 7
    Electronic Resource
    Electronic Resource
    The long-term effects of cure of Helicobacter pylori infection on patients with atrophic body gastritis (2002)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 16 (2002), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Helicobacter pylori infection induces atrophic body gastritis, but the long-term effect of its cure on body atrophy is unclear.Aim : To investigate the long-term effects of H. pylori cure on gastric morpho-functional parameters in patients with atrophic body gastritis.Methods : Forty patients with atrophic body gastritis were cured of H. pylori infection. Gastroscopy with biopsies, gastrin and pepsinogen I levels and basal and stimulated acid secretion were evaluated before and 6–12 months after treatment.Results : At eradication assessment (6–12 months), in eight of the 40 patients, body atrophy was no longer observed, whereas in 32 of the 40 it remained substantially unchanged (2.03 ± 0.12 vs. 1.83 ± 0.15). In the eight patients with reversed body atrophy, gastrinaemia decreased significantly with respect to pre-treatment values (265 ± 59.9 pg/mL vs. 51.8. ± 6.04 pg/mL), and basal and stimulated acid secretion increased significantly after cure. In the 32 patients still presenting body atrophy, gastrinaemia was similar topre-treatment values (457 ± 76.04 pg/mL vs. 335.1 ± 58.8 pg/mL). At follow-up (21–25 and 32–70 months), the eight patients with reversed body atrophy continued with normal gastrinaemia (35.3 ± 10.1 pg/mL vs. 38.5 ± 8.8 pg/mL), but in the 19 patients with continued atrophy, both corporal atrophy and intestinal metaplasia remained substantially unchanged.Conclusions : Following successful treatment in patients with atrophic body gastritis and H. pylori infection, long-term histological investigations are crucial in order to detect reversed body damage or to confirm continued body atrophy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2002.01336.x
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  • 8
    Electronic Resource
    Electronic Resource
    Does the widespread use of proton pump inhibitors mask, complicate and/or delay the diagnosis of Zollinger–Ellison syndrome? (2001)
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 15 (2001), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Proton pump inhibitors are potent acid suppressants which, at normal doses, can result in hypergastrinaemia in patients with idiopathic oesophageal reflux disease and in the control of symptoms in most patients with gastrinomas. Therefore, their use could delay or mask the diagnosis of gastrinoma.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To investigate whether the widespread use of proton pump inhibitors masks or complicates the diagnosis of gastrinoma.〈section xml:id="abs1-3"〉〈title type="main"〉Subjects and methods:Data from two centres with different referral criteria for suspected gastrinomas were analysed (Gastroenterology Unit, Rome, Italy and National Institutes of Health, Bethesda, MD, USA). The number of referrals and the number of new patients with gastrinoma diagnosed in the years prior to the widespread use of proton pump inhibitors (1986–1992) were compared with the numbers since proton pump inhibitors became widely available (1993–1998).〈section xml:id="abs1-4"〉〈title type="main"〉Results:The decrease in referral rate (P=0.0009) and the decrease in the annual rate of gastrinoma diagnosis (P=0.0020) at both centres correlated with the increased use of proton pump inhibitors. At the Italian centre, there was a 62% decrease in annual referrals (P 〈 0.0001) in the post-proton pump inhibitor period, relative to the pre-proton pump inhibitor period, whereas there was an increase in the rate of referral of other gastrointestinal endocrine tumours. The number of new cases of gastrinoma diagnosed decreased by 40%. At the US centre, the referral rate decreased by 28% (P=0.024) in the post-proton pump inhibitor period. There was also a 43% decrease in the number of new cases diagnosed annually in the post-proton pump inhibitor period (P=0.0012). There was a 2.6-fold increase in the post-proton pump inhibitor period in the percentage of referrals with a false diagnosis of gastrinoma as the cause of hypergastrinaemia (P=0.0040).〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:In both referral centres, less patients have been referred with a possible diagnosis of gastrinoma and fewer new patients with gastrinoma have been diagnosed since proton pump inhibitors became widely available. These data support the conclusion that, since proton pump inhibitors have been released, the diagnosis of gastrinoma has been masked and will probably be delayed, with the result that patients with gastrinoma will be diagnosed at more advanced stages in their disease course.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2036.2001.01085.x
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  • 9
    Electronic Resource
    Electronic Resource
    Long-term follow-up in atrophic body gastritis patients: atrophy and intestinal metaplasia are persistent lesions irrespective of Helicobacter pylori infection (2005)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 22 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Long-term outcome of atrophic body gastritis has not yet been defined.Aim : To investigate at long-term follow-up the behaviour of atrophy and intestinal metaplasia and the occurrence of neoplastic lesions in atrophic body gastritis patients.Methods : Overall 106 atrophic body gastritis patients with ≥ 4-year follow-up were studied; 38 were Helicobacter pylori-positive at histology + serology and cured of infection (group A), 36 were positive at serology and not treated (group B) and 32 were H. pylori-negative (group C). Patients underwent gastroscopy with antral (n = 3) and body (n = 3) biopsies for histology according to the Sydney System.Results : At 6.7-year follow-up body atrophy and intestinal metaplasia remained unchanged in all 106 patients irrespective of H. pylori status. Antral atrophy was significantly increased at follow-up only in group C, whereas antral intestinal metaplasia was unchanged in all three groups. During follow-up eight (8%) patients developed neoplastic lesions (one adenocarcinoma, one adenoma with low-grade dysplasia and six low-grade dysplasia without endoscopic lesions). Antral atrophic gastritis was present at baseline in all but one (88%) of the eight patients with neoplastic lesions, but only in 15 (15%) of the 98 patients without (P 〈 0.0001, RR = 26.7).Conclusions : Atrophy and intestinal metaplasia persist at 6.7-year follow-up and atrophic body gastritis patients with panatrophic gastritis are at increased risk of developing neoplastic lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2005.02582.x
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  • 10
    Electronic Resource
    Electronic Resource
    Bombesin effects on human GI functions
    Amsterdam : Elsevier
    Peptides 6 (1985), S. 113-116 
    Details
    ISSN: 0196-9781
    Keywords: Bombesin ; Gastric endocrine secretion ; Gastric exocrine secretion ; Gut hormones ; Motility ; Pancreatic endocrine secretion ; Pancreatic exocrine secretion
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0196-9781(85)90360-2
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