Causes of death in duodenal and gastric ulcer.
ABSTRACT An analysis has been made of 235 deaths that occurred among 1905 patients with peptic ulcer who constituted a random sample of the occurrence of ulcer disease in an area of Denmark comprising half a million inhabitants. The disease itself, according to the death certificate, was considered the primary cause of death in 10% of the cases; half of these had been operated on immediately before death. The other patients died more frequently than expected from the following causes: chronic bronchitis, pulmonary emphysema, cancer of the lung, cirrhosis of the liver, and cancer of the pancreas. Although the comorbidity with chronic bronchitis and emphysema was especially pronounced in patients with gastric ulcer, the association with liver cirrhosis and cancer of the pancreas occurred only in patients with duodenal ulcer. In women the mortality rate attributable to cardiac and vascular diseases was lower than expected. No excess coincidence of suicide was found. Berkson's fallacy is considered to be of much less importance as a possible explanation of the comorbidity found in the present study than in the majority of publications concerned with this question.
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ABSTRACT: Peptic ulcer disease has been associated with an increased risk of pancreatic cancer, but findings on this topic are inconsistent. We investigated the association between pancreatic cancer and the occurrence of gastric or duodenal ulcer in a large US cohort. We analyzed data collected from 51,529 male health professionals in a prospective cohort study. History of peptic ulcer disease was assessed at baseline in 1986 and updated biennially thereafter. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models adjusting for smoking, body mass index, diabetes, and physical activity. During 18 years of follow-up evaluation, we observed 274 incident pancreatic cancer cases. Compared with those with report of no peptic ulcer disease, men with gastric ulcer had an increased risk of pancreatic cancer (RR, 1.83; 95% CI, 1.13-2.97). Although the risk was highest for those with a diagnosis of gastric ulcer that was close in time to the cancer diagnosis (RR, 3.66; 95% CI, 1.45-9.24), the risk remained significantly increased 10-19 years after the gastric ulcer diagnosis (RR, 2.89; 95% CI, 1.26-6.64). In contrast, duodenal ulcer was not associated with pancreatic cancer risk (RR, 1.15; 95% CI, 0.78-1.71). Gastric ulcer increases the risk of pancreatic cancer, whereas there does not appear to be an association between duodenal ulcers and pancreatic cancer.Gastroenterology 10/2009; 138(2):541-9. · 12.82 Impact Factor
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ABSTRACT: Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N-nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3-38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10-40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10-110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4-3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer.International Journal of Cancer 02/2007; 120(2):368-72. · 6.20 Impact Factor
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ABSTRACT: Helicobacter pylori (HP) infection may cause extradigestive manifestations directly or indirectly, by potential mechanisms. HP infection triggers a marked local inflammatory response and a chronic systemic immune response. Some of the mediators that are thought to be possibly involved in the pathogenesis of extradigestive diseases caused by HP infection include IL-1, TNF-alpha, interferon (IFN)-gamma, leukotriene C4 and platelet-activating factor. Previous epidemiological and serological case control studies have revealed that HP infection might have a role in the development of chronic bronchitis, bronchiectasis, lung cancer and tuberculosis. However HP infection does not appear to have a role in the development of bronchial asthma. Considering the importance and prevalence of respiratory system diseases, it may be time to conduct well-designed sets of studies to clarify whether there is an association with HP infection and respiratory system diseases, and to answer questions that have been posed regarding the patterns of histology, genotypes of HP, and the effects of eradication therapy. The aim of this review was to analyze the possible association between HP and respiratory disease and provide a critical review of the relevant literature.Respiratory Medicine 03/2007; 101(2):203-9. · 2.59 Impact Factor