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Acid – suppressing drugs and gastro-esophageal reflux disease as risk factors for acute pancreatitis – results from a Swedish Case-Control Study.

Sundström, A. (författare)
University Hospital, Stockholm, Sweden
Blomgren, KB. (författare)
Mälardalens högskola,Institutionen för vård- och folkhälsovetenskap,University Hospital, Stockholm, Sweden
Alfredsson, L. (författare)
Karolinska Institutet
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Wiholm, B-E. (författare)
University Hospital, Stockholm, Sweden
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 (creator_code:org_t)
2006
2006
Engelska.
Ingår i: Pharmacoepidemiology and Drug Safety. - : Wiley. - 1053-8569 .- 1099-1557. ; 15:3, s. 141-9
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • PURPOSE: To study risk factors for acute pancreatitis, here with emphasis on gastro-intestinal diseases and their treatments. METHODS: Population based case-control study covering four areas in Sweden encompassing 2.2 million inhabitants. Included were 462 incident cases of acute pancreatitis aged 20-85 years, hospitalized from 1 January 1995-31 May 1998, and 1,781 unmatched controls randomly selected from the study base using a population register. Information was captured from medical records and structured telephone interviews. RESULTS: Current use of H(2) antagonists starting within 6 months of index-date was associated with acute pancreatitis with an adjusted OR of 4.9 (95% confidence interval (CI) 1.6-15), and current use of proton pump inhibitors (PPIs) with an adjusted OR of 3.2 (95%CI 1.4-7.4). For both drug classes, the ORs tended to be higher at higher doses. Gastritis/gastro-esophageal reflux disease (GERD) within the last 12 months not treated with PPIs or H(2)-antagonists and inflammatory bowel disease (IBD) not treated with anti-inflammatory or immunosuppressive drugs were associated with development of acute pancreatitis with adjusted odds ratios (OR) of 1.9 (95%CI 1.2-3.0) and 5.1 (95%CI 2.0-13) respectively. CONCLUSIONS: Current IBD without treatment and gastritis/GERD without treatment were found to be associated with increased risks to develop acute pancreatitis but the nature of the latter association needs to be further evaluated. On balance, we judge that the observed associations between current use of H(2)-antagonists and PPIs and increased risk of acute pancreatitis are unlikely to be explained by bias.

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