Helicobacter pylori, acid and gastrin.
ABSTRACT Before the discovery of Helicobacter pylori, duodenal ulcers were thought to be caused by excessive acid secretion. Duodenal ulcer patients have more parietal cells than controls. In addition, they cannot suppress their acid secretion when the gastric lumen is empty or acidic. These changes, plus an increase in the release of gastrin were attributed to a paucity of the inhibitory peptide somatostatin in the gastric mucosa. It has now been established that the paucity of somatostatin and the failure to suppress acid secretion are actually the result of H. pylori infection. In patients without duodenal ulcers H. pylori infection is often associated with decreased acid secretion. This occurs on first infection and also later because H. pylori gastritis predisposes to gastric atrophy.
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ABSTRACT: There is a large literature showing that unemployment has a negative effect on mental health, but little evidence exists on how mental illness affects the unemployeds’ chances of re-employment or the risk of labour market exit. We study how purchase of pharmaceutical products for severe mental illnesses during unemployment affects re- employment and labour market exit probabilities. Within the framework of a multivariate duration model we apply the ‘timing-of-events’ method, which explicitly makes use of the information that pharmaceutical treatment can begin at different points of time during an unemployment spell. In the absence of instrumental variables this method allows for causal inference in presence of unobserved heterogeneity, but at the cost of strong assumptions. The basis for our analysis is state-of-the-art register-based data, which gives insight on the timing, type, and volume of drug purchase as well as labour market histories for a random sample of the Danish population. We find a significant and strong negative effect of periods with drug treatment on the employment chances. During the treatment with drugs, the job-finding rate is reduced substantially relative to what it would have been in absence of a drug treated mental illness. Importantly, our results not only show that drug treated mental illness prolongs the unemployment duration, but it also increases the labour market exit rate.SSRN Electronic Journal 07/2010; DOI:10.2139/ssrn.1672026
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ABSTRACT: Background. The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood.Aim. To evaluate whether antral lymphocyte density could play a role in this alteration.Methods. A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy. Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment.Results. Antral lymphocyte density (5464±1328 and 5635±1186 vs 2267±557 lymphocytes/mm2; p<O. 001 and p<O. 001, respectively) and gastrin levels (66.7±14.1 and 60.4±21.7 vs 40:7±7.8 pg/dl, p=0:004 and p=0:02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and nonulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0:77; p=0:003) and in non-ulcer dyspepsia (r=0. 75; p=0.03) patients, while no correlation was found in controls (r=0: 12; p=0:8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0:027), but disappeared in those successfully cured.Conclusions. These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.Digestive and Liver Disease 11/2000; 32(8-32):676-681. DOI:10.1016/S1590-8658(00)80329-1 · 2.89 Impact Factor
Article: Helicobacter pylori infectionThe Lancet 02/1997; 349(9047):265-9. DOI:10.1016/S0140-6736(96)07023-7 · 39.21 Impact Factor