Losartan is a nonpeptide angiotensin II type 1 receptor antagonist that has recently been licensed for the treatment of hypertension in many countries [1]. Its side effects include hypotension, renal dysfunction, and hyperkalemia. Uncommon serious adverse events include worsening heart failure, unstable angina, and myocardial infarction [1-3].

I describe a 39-year-old man who developed acute pancreatitis while receiving losartan. In July 1996, he presented with a 3-day history of nausea, vomiting, and constant pain in the epigastrium that radiated to the flanks. He had been well until 5 months previously, when enalapril, 10 mg once daily, was prescribed for moderate hypertension. One week before admission, enalapril therapy was stopped because of persistent cough attributed to the therapy; losartan, 50 mg once daily, was given instead. The patient denied any previous use of alcohol or other drugs. Apart from a moderately tender abdomen with no bowel sounds, physical examination had otherwise normal results. Laboratory data showed leukocytosis (leukocyte count, 16 x 10⁹/L) with a normal differential and increased serum levels of pancreatic -amylase (732 IU/L [normal, 0 to 115 IU/L]) and lipase (946 IU/L [normal, 0 to 190 IU/L]). Results of serologic tests for Mycoplasma species, viral hepatitis, and other viral infections were negative. Abdominal ultrasonography yielded normal findings, but the pancreas could not be visualized because of excess bowel gas. On computed tomography, the pancreas was apparently normal.

Losartan therapy was discontinued; atenolol, 50 mg once daily, was given instead. Five days after admission, serum -amylase and lipase values returned to normal and the patient was asymptomatic. Eight days after admission, atenolol therapy was stopped and losartan therapy, 25 mg once daily, was reinstituted with the patient's informed consent and under intensive clinical surveillance. Three days later, losartan treatment had to be definitively discontinued because of new clinical and biological evidence of pancreatic injury (nausea, vomiting, abdominal pain, -amylase level of 368 IU/L, and lipase level of 455 IU/L). The patient's serum pancreatic profile returned to normal 3 days later. Atenolol therapy was restarted, and pancreatitis has not recurred 11 months after admission.

The temporal relation, recurrence of symptoms on reexposure, and improvements upon discontinuation of therapy are highly suggestive of losartan-induced acute pancreatitis.