Fatal Acute Pancreatitis in a Patient Chronically Treated with Candesartan

Abstract

VOLUME 21 I J PHARM TECHNOL 79This report describes the case of an elderly man who succumbed to severe acute pancreatitis, for which the most plausible cause was his use of the angiotensin II receptor blocker (ARB) candesartan. Case ReportA 75-year-old previously healthy white male presented to an area hospital after several hours of severe, sharp, right upper-quadrant abdominal pain radiating to his back, accompanied by severe nausea, vomiting, and dizziness.His past medical history was notable for hypertension and nephrolithiasis, for which he was treated with candesartan 32 mg/day and potassium citrate, respectively, and prostate cancer, for which he had undergone transuretheral resection of the prostate several years earlier. He had no prior history of gallstone or biliary tract disease and did not abuse alcohol. He had been taking candesartan 32 mg/day for over one year, apparently without ill effect. Prior to that, his hypertension had been treated with verapamil. He had not taken any other ARBs or angiotensin-converting enzyme (ACE) inhibitors prior to starting candesartan.Objective: To summarize a case of acute pancreatitis in a patient receiving the angiotensin II receptor blocker (ARB) candesartan.Case Summary: A previously healthy 75-year-old white man presented with acute pancreatitis complicated by anuric renal failure, respiratory failure, circulatory collapse, and died within 24 hours despite resuscitation efforts. He had been receiving candesartan 32 mg/day for more than one year with no apparent adverse effects. Discussion:In recent years, angiotensin-converting enzyme (ACE) inhibitors have been linked with sporadic cases of acute pancreatitis. Recent case reports suggest a similar association between pancreatitis and the related drug class of ARBs. Animal data indicate that the renin-angiotensin system plays an important role in pancreatic hemodynamics and exocrine function and is activated in the setting of acute pancreatitis. Because both ARBs and ACE inhibitors affect angiotensin II, we hypothesize that a common pathophysiologic mechanism might apply to both ARB-and ACE inhibitor-induced pancreatitis. Conclusions:Although acute pancreatitis appears to be a rare complication of both ARBs and ACE inhibitors, the catastrophic outcome in this case mandates that clinicians be aware of this adverse effect. Further research into the role of the renin-angiotensin system in the pathogenesis of acute pancreatitis appears warranted.