Helicobacter pylori Infection in Peptic Ulcer Disease

Berstad, K; Berstad, Arnold

doi:10.3109/00365529309096088

Cited by 43 publications

(17 citation statements)

References 68 publications

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“…This is in contrast to observations in patients with uncomplicated peptic ulcer, in whom a Hp infection is present in a majority of the patients [1,2,14], Further evaluation of this difference is warranted to provide infor mation regarding etiology, treatment and follow-up of patients who suffer from this rare but potentially fatal complication of peptic ulcer disease [6]. Whether Hp serology is clinically useful and cost-effective in this con text remains to be shown.…”

Section: Discussioncontrasting

confidence: 45%

“…Although the understanding of various causes of peptic ulcer disease in general has improved [1,2], and the rationale for utilization of different treatment options has been refined [2], the complete explanation why some ulcers perforate remains unknown [5, 10. 13, 14], The number of these select patients treated annually in a single institution is usually low.…”

Section: Discussionmentioning

confidence: 99%

“…The role of Helicobacter pylori (Hp) in the pathogene sis of chronic duodenal ulcer disease is now well estab lished [1,2]. Recently, an increased risk of gastric cancer [3] and gastric lymphoma [4] has been linked to the pres ence of Hp-induced gastritis.…”

Section: Introductionmentioning

confidence: 99%

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<i>Helicobacter pylori </i>Status after Treatment for Perforated Gastroduodenal Ulcer

1997

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This cross-sectional study was performed to evaluate the Helicobacter pylori (Hp) status as measured by serology (i.e. IgG antibodies against Hp) in patients surgically treated for perforated gastroduodenal ulcer. Of 104 consecutive patients, 67 (64%) males and 37 (36%) females with a median age of 68 (range 16-89) years and diagnosed between 1987 and 1993, 72 patients (69%) were available for long-term follow-up, of whom 56 (78%) patients completed a questionnaire, and 43 patients (60%) also provided a blood test for measurement of IgG antibodies. A positive serology (i.e. elevated IgG antibodies) was found in 61% of the patients at follow-up. The frequency of symptoms at follow-up in Hp-positive and Hp-negative patients was similar. A significantly higher proportion of Hp-positive patients were smokers (p < 0.01). Although not statistically significant, Hp positivity was associated with higher age and male gender. Our study provides interesting findings at follow-up regarding Hp status in patients surgically treated for this potentially fatal complication of ulcer disease. Further evaluation of the usefullness of Hp serology, and the possible clinical consequences of Hp positivity found during follow-up in this group of patients, remain to be shown in longitudinally studies.

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Section: Discussioncontrasting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

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<i>Helicobacter pylori </i>Status after Treatment for Perforated Gastroduodenal Ulcer

1997

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“…Colonization of H. pylori causes chronic active gastritis in man and an association with duodenal and gastric ulcer, stomach carcinoma and gastric malignant lymphoma has been reported [1,14,19,20]. Several studies have investigated the virulence factors of H. pylori and the mechanisms leading to gastric epithelial lesions and dysregulation of gastrin secretion in H. pyIori infection [3,5,7].…”

Section: Introductionmentioning

confidence: 99%

Antigastric autoantibodies in Helicobacter pylori gastritis: prevalence, in-situ binding sites and clues for clinical relevance

Faller

Steininger

Eck

et al. 1996

Vichows Archiv A Pathol Anat

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Colonization of human gastric mucosa with Helicobacter pylori leads to chronic active gastritis and induces the occurrence of an acquired mucosa-associated lymphoid tissue (MALT) in the stomach. This remodelling of the gastric mucosa together with chronic antigen persistence may induce autoimmune reactions. The aim of this study was to investigate humoral autoimmune reactions to human gastric mucosa in H. pylori gastritis and their clinical relevance. Sera from patients with dyspeptic symptoms were tested for presence of IgG immunoglobulins against H. pylori. Gastric infection with H. pylori and alterations of gastric mucosa were demonstrated by histological examination of gastric biopsy specimens. All sera were tested for reactivity against human gastric mucosa by immunohistochemistry. Two different in-situ binding sites of antigastric autoantibodies were observed. Binding to canalicular structures within parietal cells was significantly correlated with antibodies to H. pylori, elevated basal gastrin levels and atrophy of gastric corpus glands. Our data indicate that autoimmune reactions to antigens in the human gastric mucosa occur in H. pylori gastritis and that they may play a role in the pathogenesis of the disease.

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“…This still holds true after the identification of Helicobacter pylori as the major pathogen in gastric and duodenal ulcer disease [5,6]. The main stimulus for gastric acid secretion in man is histamine [7,8], and therefore H 2 -receptor antagonists constitute a well recog- nized therapeutic principle.…”

Section: Introductionmentioning

confidence: 99%

Animal Pharmacology of Reversible Antagonism of the Gastric Acid Pump, Compared to Standard Antisecretory Principles

Kromer¹,

Postius²,

Riedel³

2000

Pharmacology

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To define the basic antisecretory profile of a potassium-competitive antagonism of the gastric acid pump relative to other classes of acid-inhibitory drugs, they were compared to each other against all three major stimuli of acid secretion. Pumaprazole is an imidazo-pyridine derivative that was used in this investigation as an example of reversibly binding acid pump antagonists (APAs). It differs from covalently binding proton pump inhibitors (PPIs), such as omeprazole, both with respect to chemical structure and mode of interaction with the gastric H⁺/K⁺-ATPase (i.e., the acid or proton pump). The present data show that a single dose of pumaprazole is able to elevate intragastric pH in the dog with gastric fistula under pentagastrin or carbachol stimulation from pH 1 to about pH 7 while still displaying a dose-dependent, well-controlable duration of action of a few hours. Ranitidine at the same oral dose also shows a short duration of action, but combined with a far lower efficacy. By contrast, a single oral dose of the PPI omeprazole elevates intragastric pH for a longer time period, but this pH elevation is far lower compared to that of the APA. Regarding the less stringent parameter of inhibition of total acid output in the Heidenhain pouch dog, the modified Shay rat or the Ghosh-Schild rat, pumaprazole is, overall, slightly more efficacious than ranitidine. The M₁-muscarinic antagonist pirenzepine is ineffective (against histamine stimulation) or far less effective than pumaprazole (against pentagastrin-stimulation), but as effective as pumaprazole against carbachol stimulation in the Ghosh-Schild rat. Basal acid output in the same model is more effectively inhibited by pumaprazole than by ranitidine. In conclusion, our data demonstrate the exceptional ability of a reversibly binding APA to elevate intragastric pH up to neutrality even upon a first administration while still displaying a limited, dose-dependent duration of action.

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Helicobacter pylori Infection in Peptic Ulcer Disease

Cited by 43 publications

References 68 publications

<i>Helicobacter pylori </i>Status after Treatment for Perforated Gastroduodenal Ulcer

<i>Helicobacter pylori </i>Status after Treatment for Perforated Gastroduodenal Ulcer

Antigastric autoantibodies in Helicobacter pylori gastritis: prevalence, in-situ binding sites and clues for clinical relevance

Animal Pharmacology of Reversible Antagonism of the Gastric Acid Pump, Compared to Standard Antisecretory Principles

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