Angioedema caused by angiotensin-converting enzyme inhibitors is an unpredictable adverse event with potentially life-threatening consequences. The reported incidence of angiotensin-converting enzyme inhibitor-related angioedema is about 0.1% to 0.5% [1, 2]. Although angioedema usually occurs within 1 week after the drug is started, it has been reported in some patients after several months of therapy [3]. Angioedema usually involves the face, lips, and tongue but may also include the hands, feet, and genitalia, as well as the mucous membranes of the mouth and upper respiratory and gastrointestinal tracts [2]. Matsumura and colleagues [4] described a patient with abdominal visceral edema probably related to captopril. We report a new case associated with lisinopril.

A 29-year-old woman was treated for hypertension with lisinopril (20 mg/d) and hydrochlorothiazide (12.5 mg/d) since February 1993. She experienced two episodes of peritoneal effusion in June and December 1993, respectively. Each episode began with severe abdominal pain and swelling. She had no diarrhea, vomiting, or fever. Coelioscopic surgery done during the first episode showed ascites. Peritoneal fluid was a sterile inflammatory exudate with 85% lymphocytes (1500 G/L). Her genitourinary system was normal, and no definite diagnosis was made. During the second episode, an abdominal echogram showed a peritoneal effusion in the rectovaginal cul-de-sac. These two episodes resolved spontaneously, but the patient reported continuous bloating sensations. She was eventually hospitalized for a third episode of acute abdominal pain and swelling in January 1994. Routine biological measurements were normal. Hereditary angioedema was excluded on the basis of normal complement and complement 1-esterase inactivator levels. An abdominal echogram was normal. The patient had no history of idiopathic angioedema. Abdominal visceral angioedema caused by angiotensin-converting enzyme inhibitors was nevertheless suspected, and therapy with lisinopril was discontinued. The patient had no further episodes of abdominal pain during 6 months of follow-up.

Patients with hereditary or acquired deficiency of complement 1-esterase inactivator (angioneurotic edema) may present with acute abdominal pain and ascites [5]. Because angioedema induced by angiotensin-converting enzyme inhibitors shares clinical and pathophysiologic features with hereditary angioneurotic edema [2], and because acute abdominal pain probably related to these inhibitors has been reported [4], we believe that drug-induced visceral angioedema should be considered in cases of unexplained abdominal pain in patients receiving the inhibitors.