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

被引:34
作者
Capurso, G.
Schuenemann, H. J. [1 ]
Terrenato, I.
Moretti, A.
Koch, M.
Muti, P.
Capurso, L.
Delle Fave, G.
机构
[1] Italian Natl Canc Inst Regina Elena, Dept Epidemiol, Rome, Italy
[2] Univ Roma La Sapienza, Sch Med 2, Digest & Liver Unit, Rome, Italy
[3] S Filippo Neri Hosp, Dept Gastroenterol, Rome, Italy
关键词
LOW-DOSE ASPIRIN; CYCLOOXYGENASE-2; EXPRESSION; COLORECTAL-CANCER; COHORT; CARCINOGENESIS; INHIBITOR; WOMEN; INFLAMMATION; ASSOCIATION; NIMESULIDE;
D O I
10.1111/j.1365-2036.2007.03495.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 (I-2 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.
引用
收藏
页码:1089 / 1099
页数:11
相关论文
共 41 条
[1]   Cyclooxygenase-2 expression associated with severity of PanIN lesions: A possible link between chronic pancreatitis and pancreatic cancer [J].
Albazaz, R ;
Verbeke, CS ;
Rahman, SH ;
McMahon, MJ .
PANCREATOLOGY, 2005, 5 (4-5) :361-369
[2]  
Anderson KE, 2002, J NATL CANCER I, V94, P1168, DOI 10.1093/jnci/94.15.1168
[3]   What now for aspirin and cancer prevention? [J].
Baron, JA .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2004, 96 (01) :4-5
[4]   Do nonsteroidal anti-inflammatory drugs affect the risk of developing ovarian cancer? A meta-analysis [J].
Bonovas, S ;
Filioussi, K ;
Sitaras, NM .
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 2005, 60 (02) :194-203
[5]   Long-term use of aspirin and nonsteroidal anti-inflammatory drugs and risk of colorectal cancer [J].
Chan, AT ;
Giovannucci, EL ;
Meyerhardt, JA ;
Schernhammer, ES ;
Curhan, GC ;
Fuchs, CS .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2005, 294 (08) :914-923
[6]  
Coogan PF, 2000, CANCER EPIDEM BIOMAR, V9, P119
[7]   Low-dose aspirin in the primary prevention of cancer the women's health study: A randomized controlled trial [J].
Cook, NR ;
Lee, IM ;
Gaziano, JM ;
Gordon, D ;
Ridker, PM ;
Manson, JE ;
Hennekens, CH ;
Buring, JE .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2005, 294 (01) :47-55
[8]   Protective association of aspirin/NSAIDs and esophageal cancer: A systematic review and meta-analysis [J].
Corley, DA ;
Kerlikowske, K ;
Verma, R ;
Buffler, P .
GASTROENTEROLOGY, 2003, 124 (01) :47-56
[9]   Frequency of use of acetaminophen, nonsteroidal anti-inflammatory drugs, and aspirin in US women [J].
Curhan, GC ;
Bullock, AJ ;
Hankinson, SE ;
Willett, WC ;
Speizer, FE ;
Stampfer, MJ .
PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, 2002, 11 (08) :687-693
[10]  
Eibl G, 2005, CANCER RES, V65, P982