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In Reply: We agree with Dr. Khan that the duration of ACE inhibitor therapy should never be used to rule out ACE inhibitor-associated angioedema. In an Italian study of 85 cases of angioedema with ACE inhibitor therapy, the mean ACE inhibitor exposure was a full 12 months before angioedema was diagnosed.1 More disturbing was the fact that another 12 months elapsed before the ACE inhibitor actually was discontinued. This would indicate that neither the patient nor the physician related the angioedema to ACE inhibitor therapy. In patients with visceral angioedema, since the diagnosis is unusually challenging, even a further delay can be expected.
Angioedema has been reported with aliskiren, but the 0.04% incidence reported by White et al2 may reflect very simply that physicians are more alert and on the lookout now more than they ever were when ACE inhibitors were first available. Obviously, greater awareness will lead to more frequent diagnosis. As Dr. Khan points out, there is no known mechanism by which aliskiren should cause angioedema, whereas there is fairly solid evidence that ACE inhibitor-associated angioedema is mediated by bradykinin.3,4
- Zingale LC, Beltrami L, Zanichelli A, et al. Angioedema without urticaria: a large clinical survey. CMAJ 2006; 175:1065–1070.
- White WB, Bresalier R, Kaplan AP, et al. Safety and tolerability of the direct renin inhibitor aliskiren: a pooled analysis of clinical experience in more than 12,000 patients with hypertension. J Clin Hypertens (Greenwich) 2010; 12:765–775.
- Molinaro G, Cugno M, Perez M, et al. Angiotensin-converting enzyme inhibitor-associated angioedema is characterized by a slower degradation of des-arginine(9)-bradykinin. J Pharmacol Exp Ther 2002; 303:232–237.
- Cunnion KM Wagner E, Frank MM. Complement and kinin. In: Parlow TG, Stites DP, Imboden JB, editors. Medical Immunology, 10th Ed. New York, NY: Lange Medical Books; 2001:186-888.
In Reply: We agree with Dr. Khan that the duration of ACE inhibitor therapy should never be used to rule out ACE inhibitor-associated angioedema. In an Italian study of 85 cases of angioedema with ACE inhibitor therapy, the mean ACE inhibitor exposure was a full 12 months before angioedema was diagnosed.1 More disturbing was the fact that another 12 months elapsed before the ACE inhibitor actually was discontinued. This would indicate that neither the patient nor the physician related the angioedema to ACE inhibitor therapy. In patients with visceral angioedema, since the diagnosis is unusually challenging, even a further delay can be expected.
Angioedema has been reported with aliskiren, but the 0.04% incidence reported by White et al2 may reflect very simply that physicians are more alert and on the lookout now more than they ever were when ACE inhibitors were first available. Obviously, greater awareness will lead to more frequent diagnosis. As Dr. Khan points out, there is no known mechanism by which aliskiren should cause angioedema, whereas there is fairly solid evidence that ACE inhibitor-associated angioedema is mediated by bradykinin.3,4
In Reply: We agree with Dr. Khan that the duration of ACE inhibitor therapy should never be used to rule out ACE inhibitor-associated angioedema. In an Italian study of 85 cases of angioedema with ACE inhibitor therapy, the mean ACE inhibitor exposure was a full 12 months before angioedema was diagnosed.1 More disturbing was the fact that another 12 months elapsed before the ACE inhibitor actually was discontinued. This would indicate that neither the patient nor the physician related the angioedema to ACE inhibitor therapy. In patients with visceral angioedema, since the diagnosis is unusually challenging, even a further delay can be expected.
Angioedema has been reported with aliskiren, but the 0.04% incidence reported by White et al2 may reflect very simply that physicians are more alert and on the lookout now more than they ever were when ACE inhibitors were first available. Obviously, greater awareness will lead to more frequent diagnosis. As Dr. Khan points out, there is no known mechanism by which aliskiren should cause angioedema, whereas there is fairly solid evidence that ACE inhibitor-associated angioedema is mediated by bradykinin.3,4
- Zingale LC, Beltrami L, Zanichelli A, et al. Angioedema without urticaria: a large clinical survey. CMAJ 2006; 175:1065–1070.
- White WB, Bresalier R, Kaplan AP, et al. Safety and tolerability of the direct renin inhibitor aliskiren: a pooled analysis of clinical experience in more than 12,000 patients with hypertension. J Clin Hypertens (Greenwich) 2010; 12:765–775.
- Molinaro G, Cugno M, Perez M, et al. Angiotensin-converting enzyme inhibitor-associated angioedema is characterized by a slower degradation of des-arginine(9)-bradykinin. J Pharmacol Exp Ther 2002; 303:232–237.
- Cunnion KM Wagner E, Frank MM. Complement and kinin. In: Parlow TG, Stites DP, Imboden JB, editors. Medical Immunology, 10th Ed. New York, NY: Lange Medical Books; 2001:186-888.
- Zingale LC, Beltrami L, Zanichelli A, et al. Angioedema without urticaria: a large clinical survey. CMAJ 2006; 175:1065–1070.
- White WB, Bresalier R, Kaplan AP, et al. Safety and tolerability of the direct renin inhibitor aliskiren: a pooled analysis of clinical experience in more than 12,000 patients with hypertension. J Clin Hypertens (Greenwich) 2010; 12:765–775.
- Molinaro G, Cugno M, Perez M, et al. Angiotensin-converting enzyme inhibitor-associated angioedema is characterized by a slower degradation of des-arginine(9)-bradykinin. J Pharmacol Exp Ther 2002; 303:232–237.
- Cunnion KM Wagner E, Frank MM. Complement and kinin. In: Parlow TG, Stites DP, Imboden JB, editors. Medical Immunology, 10th Ed. New York, NY: Lange Medical Books; 2001:186-888.