Meta-analysis: The use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk for different exposure categories

G. Capurso, H. J. Schünemann, I. Terrenato, A. Moretti, M. Koch, P. Muti, L. Capurso, G. Delle Fave

Research output: Contribution to journalArticle

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Abstract

Background: A better understanding of predictors of risk for pancreatic ductal adenocarcinoma (PDAC) could inform preventive efforts against this lethal cancer. While aspirin (ASA) and non-steroidal anti-inflammatory drugs (NSAIDS) might protect against several gastrointestinal cancers, their role in the development of PDAC remains unclear. Aim: To conduct a systematic review and meta-analysis on the relation between ASA/NSAIDs exposure and the risk of PDAC. Methods: We searched Pubmed, Embase, Scopus, Cochrane database of systematic reviews and reference lists of identified papers and included observational (cohort or case-control) studies and randomized controlled trials examining exposure to ASA and/or NSAIDs and the incidence or mortality of PDAC. We defined three categories (low, intermediate, high), based on exposure duration and dose. Results: Eight studies fulfilled our inclusion criteria (four cohort, three case controls, and one randomized controlled trial studies) enrolling 6301 patients between 1971-2004; all but one study took place in the US. The pooled OR were 0.99 (0.83-1.19), 1.11 (0.84-1.47) and 1.09 (0.67-1.75) in the low, intermediate and high exposure groups respectively, with considerable heterogeneity (I2 ranging 60-86%). Sensitivity analysis by ASA use only, study design or sex did not reveal additional important information. Conclusions: This study did not show an association between ASA/NSAIDs and PDAC. The large baseline exposure in controls in North-America may have obscured an association. There is need for additional studies, especially in Europe, to clarify this issue.

Original languageEnglish
Pages (from-to)1089-1099
Number of pages11
JournalAlimentary Pharmacology and Therapeutics
Volume26
Issue number8
DOIs
Publication statusPublished - Oct 2007

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Pancreatic Neoplasms
Meta-Analysis
Adenocarcinoma
Anti-Inflammatory Agents
Non-Steroidal Anti-Inflammatory Agents
Pharmaceutical Preparations
Randomized Controlled Trials
Gastrointestinal Neoplasms
North America
PubMed
Aspirin
Case-Control Studies
Databases
Mortality
Incidence
Neoplasms

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Meta-analysis : The use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk for different exposure categories. / Capurso, G.; Schünemann, H. J.; Terrenato, I.; Moretti, A.; Koch, M.; Muti, P.; Capurso, L.; Delle Fave, G.

In: Alimentary Pharmacology and Therapeutics, Vol. 26, No. 8, 10.2007, p. 1089-1099.

Research output: Contribution to journalArticle

Capurso, G, Schünemann, HJ, Terrenato, I, Moretti, A, Koch, M, Muti, P, Capurso, L & Delle Fave, G 2007, 'Meta-analysis: The use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk for different exposure categories', Alimentary Pharmacology and Therapeutics, vol. 26, no. 8, pp. 1089-1099. https://doi.org/10.1111/j.1365-2036.2007.03495.x
Capurso, G. ; Schünemann, H. J. ; Terrenato, I. ; Moretti, A. ; Koch, M. ; Muti, P. ; Capurso, L. ; Delle Fave, G. / Meta-analysis : The use of non-steroidal anti-inflammatory drugs and pancreatic cancer risk for different exposure categories. In: Alimentary Pharmacology and Therapeutics. 2007 ; Vol. 26, No. 8. pp. 1089-1099.
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AU - Koch, M.

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N2 - Background: A better understanding of predictors of risk for pancreatic ductal adenocarcinoma (PDAC) could inform preventive efforts against this lethal cancer. While aspirin (ASA) and non-steroidal anti-inflammatory drugs (NSAIDS) might protect against several gastrointestinal cancers, their role in the development of PDAC remains unclear. Aim: To conduct a systematic review and meta-analysis on the relation between ASA/NSAIDs exposure and the risk of PDAC. Methods: We searched Pubmed, Embase, Scopus, Cochrane database of systematic reviews and reference lists of identified papers and included observational (cohort or case-control) studies and randomized controlled trials examining exposure to ASA and/or NSAIDs and the incidence or mortality of PDAC. We defined three categories (low, intermediate, high), based on exposure duration and dose. Results: Eight studies fulfilled our inclusion criteria (four cohort, three case controls, and one randomized controlled trial studies) enrolling 6301 patients between 1971-2004; all but one study took place in the US. The pooled OR were 0.99 (0.83-1.19), 1.11 (0.84-1.47) and 1.09 (0.67-1.75) in the low, intermediate and high exposure groups respectively, with considerable heterogeneity (I2 ranging 60-86%). Sensitivity analysis by ASA use only, study design or sex did not reveal additional important information. Conclusions: This study did not show an association between ASA/NSAIDs and PDAC. The large baseline exposure in controls in North-America may have obscured an association. There is need for additional studies, especially in Europe, to clarify this issue.

AB - Background: A better understanding of predictors of risk for pancreatic ductal adenocarcinoma (PDAC) could inform preventive efforts against this lethal cancer. While aspirin (ASA) and non-steroidal anti-inflammatory drugs (NSAIDS) might protect against several gastrointestinal cancers, their role in the development of PDAC remains unclear. Aim: To conduct a systematic review and meta-analysis on the relation between ASA/NSAIDs exposure and the risk of PDAC. Methods: We searched Pubmed, Embase, Scopus, Cochrane database of systematic reviews and reference lists of identified papers and included observational (cohort or case-control) studies and randomized controlled trials examining exposure to ASA and/or NSAIDs and the incidence or mortality of PDAC. We defined three categories (low, intermediate, high), based on exposure duration and dose. Results: Eight studies fulfilled our inclusion criteria (four cohort, three case controls, and one randomized controlled trial studies) enrolling 6301 patients between 1971-2004; all but one study took place in the US. The pooled OR were 0.99 (0.83-1.19), 1.11 (0.84-1.47) and 1.09 (0.67-1.75) in the low, intermediate and high exposure groups respectively, with considerable heterogeneity (I2 ranging 60-86%). Sensitivity analysis by ASA use only, study design or sex did not reveal additional important information. Conclusions: This study did not show an association between ASA/NSAIDs and PDAC. The large baseline exposure in controls in North-America may have obscured an association. There is need for additional studies, especially in Europe, to clarify this issue.

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