Abstract
Purpose: Angiotensin-converting enzyme (ACE) inhibitors are routinely used in antihypertensive therapy, chronic kidney disease and in congestive heart failure. Tens of millions of patients worldwide use this class of medications. Angioedema, which most commonly affects the oropharynx and airway, is a well known adverse effect of ACE inhibitors. 0.1-0.2% of patients on ACE-inhibitors develop angioedema. Twenty-one cases of visceral angioedema associated with ACE inhibitor use have been described in the literature. We present a case of small bowel angioedema secondary to ACE inhibitor use to increase awareness of this serious adverse effect. Case: 46 year old female with newly diagnosed hypertension presented to the emergency room with 4 days of severe, periumbilical abdominal pain. She also developed nausea, vomiting and mild diarrhea. No fevers, chills, rashes, tongue or facial swelling, shortness of breath, wheezing, urticaria, history of atopy, vasculitis, vasculopathy, autoimmune disease, or history of angioedema. No family history of angioedema. Her first dose of lisinopril and hydrochlorothiazide was 12 hours prior to developing pain. She was afebrile and vital signs were within normal limits. Her abdomen had normal bowel sounds and was firm, slightly distended, with tenderness to palpation in the mid-abdomen, particularly in the periumbilical region. She had guarding but no rebound. White blood cell count was slightly elevated with a normal differential. Hemoglobin, platelets, comprehensive metabolic panel, amylase and lipase were all normal. CT scan revealed diffuse thickening of the jejunum and ileum, consistent with angioedema, and ascites. She discontinued lisinopril and had resolution of her pain. C1 esterase level is pending. Discussion: Angioedema is an adverse effect of ACE inhibitors and may affect the GI tract without involvement of the oropharynx or airway. The most common presenting symptoms are diffuse abdominal pain and vomiting. Diagnosis is based on history and clinical findings. There is no specific test for confirmation. Treatment involves stopping the ACE inhibitor. Patients who develop angioedema from ACE inhibitors should not be given angiotensin II receptor blockers as they may also precipitate angioedema. Although the number of reported cases of visceral angioedema is small compared to the number of patients using ACE inhibitors, this may reflect under diagnosis. A high degree of suspicion is necessary to quickly make the diagnosis and stop the medication without subjecting the patient to unnecessary invasive diagnostic procedures.
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