Faculty Bibliography

Drugs are a relatively rare cause of acute pancreatitis, with an estimated incidence of 0.1-2%. Many drugs have been suspected of causing pancreatitis, but the true incidence is not known as the evidence is derived mainly from random case reports. Case reports with the strongest evidence are those that clearly diagnose pancreatitis and exclude common aetiologies, provide the dose and time interval between the start of treatment with the suspected drug and the development of pancreatitis, document response to withdrawal of the drug, and demonstrate recurrent pancreatitis upon rechallenge with the drug. Few data exist on the mechanisms of drug-induced pancreatitis. Certain subpopulations such as children, women, the elderly and patients with advanced HIV infection or inflammatory bowel disease may be at higher risk. The diagnosis of drug-induced pancreatitis is often challenging because there are no unique clinical characteristics to distinguish drugs from other causes of pancreatitis. The majority of cases are mild, but severe and even fatal cases may occur, thus making identification of the offending agent critical. Management of drug-induced acute pancreatitis requires withdrawal of the offending agent and supportive care. Prevention of drug-induced pancreatitis requires an up-to-date knowledge of drugs that have the strongest evidence linking their use to the development of pancreatitis as well as the proposed mechanisms through which they may cause the reaction. In this paper, the epidemiology, diagnosis, management and prevention of drug-induced pancreatitis is reviewed. Drugs and classes of drugs strongly implicated as causing acute pancreatitis, based on well documented case reports, are discussed in detail.

OBJECTIVE:We sought to develop a simple yet accurate prognostic scoring system to determine the severity of acute pancreatitis at admission. SUMMARY BACKGROUND DATA/BACKGROUND:Because acute pancreatitis has a variable and frequently unpredictable course, identifying individuals at greatest risk for significant, life-threatening complications and stratifying their care appropriately remain a concern. Previous prognostic scoring systems predict severity reasonably well but are limited by time constraints, are unwieldy to use, or both. METHODS:Data from the international phase III trial of the platelet-activating factor receptor-antagonist Lexipafant were used to develop a 4-variable prognostic model. We then compared the model's ability to predict the severity of acute pancreatitis with the Ranson, Glasgow, and APACHE II systems. RESULTS:The model (BALI), which included BUN >or=25 mg/dL, Age >or=65 years, LDH >or=300 IU/L, and IL-6 >or=300 pg/mL, measured at admission, was similar to the Ranson, Glasgow, and APACHE II systems in its ability to identify increased mortality from acute pancreatitis. The receiver operating characteristic curve area for the BALI model was >or=0.82 +/- 0.03 (mean +/- SD) versus 0.75 +/- 0.04 (Ranson), 0.80 +/- 0.03 (Glasgow), and 0.79 +/- 0.03 (APACHE II). Furthermore, at a prevalence of 15%, the positive and negative predictive values for increased mortality were similar for all systems. CONCLUSION/CONCLUSIONS:The prognostic ability of the BALI 4-variable model was similar to the Ranson, Glasgow, and APACHE II systems but is unique in its simplicity and ability to accurately predict disease severity when used at admission or anytime during the first 48 hours of hospitalization.

The direct measurement of pancreatic function remains the best tool for diagnosing chronic pancreatitis, especially if imaging tests are normal or inconclusive. The most effective means of measuring pancreatic function is the standard hormone stimulation test using secretin. Traditionally, direct pancreatic function testing involves the fluoroscopic placement of an oroduodenal tube and collection of duodenal fluid containing pancreatic secretions after administration of a standardized dose of secretin and/or CCK. The test is time-consuming and tedious to perform, and placement of the oroduodenal tube is often difficult for the person performing the test and uncomfortable for the patient. Bicarbonate concentration typically has been measured by back-titration, requiring specialized equipment no longer found in most hospital clinical chemistry laboratories. For these reasons, the direct testing of pancreatic function after secretin stimulation has become a much admired but rarely performed test, currently done in only a few centers in the United States. In this issue of the Journal, Stevens et al. report on a cross-over study of secretin-stimulated endoscopic pancreatic function test (ePFT) and dreiling tube pancreatic function test (D-PFT) in healthy subjects and demonstrate that the accuracy of the ePFT is comparable to that of the D-PFT (17). They have demonstrated the relative simplicity and reliability of ePFT, bringing it closer to the diagnostic armamentarium of the practicing physician. We may have lost the Dreiling tube but, in its place, gained a "gold standard" which will be more widely used.