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. 2007 May 21;13(19):2655–2668. doi: 10.3748/wjg.v13.i19.2655

Table 2.

Pharmacalogical prevention of post-ERCP pancreatitis: targeted mechanisms, drug tested, quality of evidence, and overall results1

Mechanism Drug Evidence Average risk patients High risk patients
Sphincter spasm Ca++ channel blocker Lidocaine (topical) Nitroglycerine B B B Ineffective Ineffective Possibly effective in high dose No data No data Ineffective
Infection Antibiotics B Possible effective No data
Contrast Nonionic contrast A Ineffective Ineffective
Toxicity Corticosteroids A Ineffective Ineffective
Inflammatory Allopurinol B Ineffective Ineffective
PAF inhibitors A Ineffective Ineffective
Cascade IL-10 B Ineffective Ineffective
Heparin derivatives A Ineffective Ineffective
NSAID B Possibly effective No data
Gabexate A Ineffective (≤ 6 h infusion) Ineffective
A Effective (12-h infusion) No data
Pancreatic secretions Octreotide A Ineffective No data
Somatostatin A Ineffective (≤ 6-h infusion) No data
B Possibly effective (12-24 h infusion)

PAF: Platelet activating factor; IL-10: interleukin 10; NSAID: non-steroidal anti-inflammatory drug. The level of evidence was graded by using a system adapted from Cook et al 17 as follows: Grade A supported by two or more randomized trials with P values < 0.05, appropriate methodology, and no conflicting results in the trials; Grade B supported by randomized trials with P values > 0.05, and/or inappropriate methodology, and/or inadequate sample sizes, and/or conflicting results among the trials; Grade C supported by non-randomized trials. 1Adapted from Freeman and Guda[5].