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.07/2010;
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ABSTRACT: Although several duodenal ulcer disease-specific abnormalities in gastric function have been described (e.g. exaggerated gastrin releasing peptide-stimulated acid secretion and an abnormal sensitivity of the parietal cells to gastrin), none has withstood careful examination. We describe here the critical nature of the duodenal acid load in precipitating and washing out bile salts, which inhibit the growth of Helicobacter pylori (H. pylori) in the development of duodenal ulcer disease. The risk of duodenal ulcer is enhanced by infection with proinflammatory H. pylori (e.g. with an intact cag pathogenicity island). Progressive damage to the duodenum promotes gastric metaplasia, resulting in sites for H. pylori growth and more inflammation. This cycle results in an increasing inability of the duodenal bulb to neutralize acid entering from the stomach until changes in duodenal bulb structure and function are sufficient for an ulcer to develop. Cure of the H. pylori infection results in a sustained fall in duodenal acid load as well as a marked (and continuing) reduction in inflammation, which results in the cure of chronic ulcer disease.Baillière' s Best Practice and Research in Clinical Gastroenterology 03/2000; 14(1):97-107. · 3.16 Impact Factor
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ABSTRACT: Helicobacter pylori causes specific ultrastructural changes to the gastric mucosa. In developing countries a high percentage of infants acquire this infection, which initially causes a transient drop in stomach acid and thus allows transit of lower bowel pathogens, with consequent diarrhea and malnutrition. When infection occurs at an early age, the acid-producing cells of the stomach are involved in the inflammation, and the lifelong reduced acid output means a duodenal ulcer rarely develops. However, lifelong gastric inflammation leads in due course to atrophy, and in the presence of other factors gastric cancer may develop. People infected with H. pylori on average are of shorter stature than uninfected people. Adherence of H. pylori to the gastric mucosa is a prerequisite for infection, and a new binary model of adherence has been shown recently. Chaperonins of H. pylori induce macrophages to secrete cytokines, which leads to an immunologic cascade and inflammation.Clinical Infectious Diseases 12/1997; 25(5):1017-9. · 9.37 Impact Factor