The AACT toxicology question of the day for yesterday: What is the pathophysiology of ACE-inhibitor associated angioedema? Scroll down for the answer. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The cited reference notes that the exact pathophysiology of ACE-inhibitor angioedema is considered to be controversial. However, the authors point out that conventional wisdom believes decreased degradation of bradykinin (a strong vasodilator capable of increasing blood vessel permeability) is the primary pathophysiologic process for ACE-inhibitor angioedema. They go on to point out that “C1-inhibitor abnormalities, carboxyalkyl dipeptide N, urinary kallikrein and inflammatory mediators such as interleukin-1 and tumor necrosis factor have also been proposed as mediators for ACE-inhibitor angioedema.” (Winters ME et al. Emergency department management of patients with ACE-inhibitor angioedema. 2013 J Emerg Med 45(5): 775-780)
Posted on: Thu, 14 Nov 2013 16:03:45 +0000
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