Syed M. Fehmi

A meta-analysis of rectal NSAIDs in the prevention of post-ERCP pancreatitis

Background: Several pharmacological agents for the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) have been studied. Clinical trials evaluating the protective effect of non-steroidal anti-inflammatory drugs (NSAIDs) have yielded inconclusive results. Aim: To perform a meta-analysis of studies evaluating the effect of prophylactic rectal NSAIDs on PEP. Methods: By searching Medline, Embase, meeting abstracts and bibliographies, two independent reviewers systematically identified prospective randomised controlled trials (RCTs) examining the effect of rectally administered prophylactic NSAIDs on the incidence of PEP pancreatitis. A meta-analysis of these clinical trials was performed. Results: Four RCTs, enrolling a total of 912 patients, have been published. Meta-analysis of these studies demonstrates a pooled relative risk for PEP after prophylactic administration of NSAIDs of 0.36 (95% CI 0.22 to 0.60); patients who received NSAIDs in the periprocedural period were 64% less likely to develop pancreatitis and 90% less likely to develop moderate to severe pancreatitis. The pooled number needed to treat with NSAIDs to prevent one episode of pancreatitis is 15 patients. No adverse events attributable to the use of NSAIDs were reported in any of the clinical trials. Conclusion: In this meta-analysis, prophylactic NSAIDs were effective in preventing PEP. Widespread prophylactic administration of these agents may significantly reduce the incidence of PEP, resulting in major clinical and economic benefit. Given current scepticism regarding the efficacy of any prophylactic medication for ERCP, additional multicentre studies are needed for confirmation prior to widespread adoption of this strategy.

Hypercalcemic Pancreatitis Triggered by Pregnancy With a CYP24A1 Mutation.

To the Editor: W e report the first case of hypercalcemic pancreatitis as a result of a CYP24A1 mutation. In 2011, loss-of-function mutations in the CYP24A1 gene were discovered to be a cause of idiopathic infantile hypercalcemia (Online Mendelian Inheritance in Man No.143880). The CYP24A1 gene encodes 25-hydroxyvitamin D 24hydroxylase, which is a key enzyme in the degradation of 1,25 dihydroxyvitamin D. Patients with loss-of-function mutations in CYP24A1 can develop hypercalcemia due to high levels of 1,25 dihydroxyvitamin D.