Case Presentation: We present the case of a 62-year-old Caucasian female with angioedema suspected to be secondary to Olmesartan use, which was relieved with tranexamic acid. Of note, this was the third time she had presented to the hospital with angioedema symptoms within in the past 6 months. Before this period, she states she had never had any angioedema like symptoms. On this hospitalization, it was noted that she was on Olmesartan for Hypertension and had been on it for many years. She had never been on an ACE-inhibitor prior to this. Her vital signs upon arrival were within normal limits, and her only initial laboratory values that were of note were leukopenia at 3.3 K/ul and hyponatremia at 134 mmol/L. A C1 esterase protein inhibitor was also ordered, to assess for possible heredity angioedema, and was slightly elevated at 42 mg/dL. Upon admission, Olmesartan was not restarted. She was started on steroids and given antihistamines with improvement in her symptoms. On second day of hospitalization she was kept for observation, with plans for discharge the next day due to her clinical improvement. That night, she developed angioedema and was treated again with IV steroids and antihistamines. Despite these IV medications, patient endorsed only stabilization but not full resolution of symptoms. It was then decided to try Tranexamic acid, as it has been reported to work for ACE-inhibitor induced angioedema. After administration, she had subsequent improvement of her symptoms but with better response than steroids and antihistamines alone.
Discussion: ARB-induced angioedema has a significantly lower incidence than ACE-inhibitor induced [1]. As with ACE-inhibitors, the management beyond removal of the offending agent is not clear, and there are no specific guidelines. Studies have shown that tranexamic acid may be used in emergent situations to provide treatment for these included angioedema episodes [2]. Tranexamic acid works by blocking the activation of plasminogen to plasmin, which in turns leads to down-regulation of bradykinin which is implicated in angioedema [3]. This case highlights Tranexamic acid use in ARB-induced angioedema not previously reported to the authors’ knowledge. Given the relatively low incidence of ARB-induced angioedema, no studies have been conducted to assess any clinical utilization of treatment other than stopping the offending agent. Reports have shown use of tranexamic acid in use in idiopathic angioedema along with its potential use as a maintenance regimen for prophylaxis [4, 5].
Conclusions: We postulate that tranexamic acid can be utilized in ARB-induced angioedema and is a viable option for angioedema resistant to steroids and antihistamines alone.