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Background. A number of studies have reported a possible association between use of selective serotonin reuptake inhibitors (SSRIs) and serious upper gastrointestinal bleeding (UGB). We conducted this case--control study to assess if Helicobacter pylori ( H. pylori) potentiates the risk of serious UGB in SSRI users. Material and methods. A population-based case--control study was conducted in the county of Funen, Denmark. Cases were 53 SSRI users with serious UGB whose H. pylori status on their bleeding date could be established. Controls ( n == 723) were selected among subjects who participated in a population H. pylori screening study, and who were users of SSRIs. Data on drug exposure and medical history were retrieved from a prescription database and the county's patient register. Confounders were controlled for by unconditional logistic regression. Results. H. pylori infection increased the risk of serious UGB in patients using SSRI with an adjusted odds ratio (OR) of 2.73 (95% confidence interval (CI), 1.17--6.36). The adjusted OR for serious UGB among users of non-steroidal anti-inflammatory drugs (NSAIDs) and acetylsalicylic acid (ASA) were 3.91 (95% CI, 2.03--7.52) and 3.00 (95% CI, 0.94--9.54), respectively. Conclusion. H. pylori infection increases the risk of SSRI-related serious UGB. [ABSTRACT FROM AUTHOR]

Background/aims: Publications on etiology of chronic pancreatitis (CP) are infrequent. Etiologies today encompass genetic disorders. We wanted to describe etiologies of today and identify patients with genetic disorders like hereditary pancreatitis (HP), mutations in Serine Protease Inhibitor Kazal type1 (SPINK1), and the Cystic Fibrosis Transmembrane Conductance Regulator gene (CFTR) among patients formerly considered to have idiopathic CP.Methods: Data on patients diagnosed with first-time CP < 30 years of age in Denmark identified in the Danish National Registry of Patients were retrieved. Patients previously considered to have idiopathic pancreatitis were offered genetic counseling and evaluation for HP, SPINK1, and CFTR mutations.Results: In the period 1980-2004, 580 patients < 30 years of age presented with CP, the standardized prevalence ratio of CP increased from 11.7 per 100,000 person years in 1980-1984 to 17.0 per 100,000 in 2000-2004 (p < 0.001). The odds ratio (OR) having gallstone-related CP increased in the latter time period, especially in women, that of alcohol-induced CP decreased over time. OR having idiopathic CP increased in the latter period; 50% of patients with idiopathic pancreatitis accepted genetic reevaluation; 28 patients had a genetic mutation that totally or partly could explain their pancreatitis, nine of these had two, and 11 patients had HP.Conclusion: The prevalence of CP, especially in women, increased over time. Genetic causes that partly or totally could explain the CP were found in 54.90% (95% CI (40.45-68.62)) of those with idiopathic CP, as a minimum estimation 1.9% (95% CI (1.00-3.47)) of the total cohort had HP. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Although symptoms of reflux are common, our knowledge of the epidemiology and natural history of gastroesophageal reflux disease is sparse. The risk of esophageal adenocarcinoma is increased among patients with acid reflux, but the contribution of Barrett's lesions is unknown. METHODS: With the aim to estimate the incidence of diagnosed endoscopic esophagitis lesions and the risk of esophageal adenocarcinoma among patients with previously diagnosed esophagitis, we extracted data on endoscopies, esophagitis diagnoses, and gastroesophageal cancer diagnoses from five population-based databases covering the period from 1974 to 2002, and covering all citizens in Funen County (population 470,000). RESULTS: In 2002, the incidence of esophagitis lesions was 2.4 per 1,000 person-years (95% confidence interval 2.3–2.6), 18.3 per 1,000 persons (17.9–18.7) had previously diagnosed esophagitis. Incidence increased by calendar year and age, was higher among males than among females, and was closely related to rate of endoscopy. Among 11,129 patients with previously diagnosed esophagitis, 15 had esophageal adenocarcinoma during 58,322 person-years of follow-up (26 per 100,000 person-years). The expected number was 2.79 and the standardized incidence ratio was 5.38 (3.01–8.87). Ten of the 15 patients with esophageal adenocarcinoma had previously diagnosed Barrett's esophagus. CONCLUSION: The risk of esophageal adenocarcinoma is increased fivefold in patients with previously diagnosed esophagitis, but most of the adenocarcinomas occurred among patients with Barrett's esophagus. [ABSTRACT FROM AUTHOR]