Examination of baseline levels of carboxypeptidase N and complement components as potential predictors of angioedema associated with the use of an angiotensin-converting enzyme inhibitor

Angioneurotic Edema

“…Other causes include nonsteroidal antiinflammatory drugs, 10 codeine, morphine, radiocontrast agents, and acquired C1 esterase inhibitor deficiency; angioedema may also be idiopathic or hereditary 1 . Immunosuppressed cardiac and renal transplant patients, 11 as well as individuals with a history of idiopathic angioneurotic edema, 12 are more likely to develop ACE inhibitor‐associated angioneurotic edema 11 . The duration of ACE inhibitor treatment at the onset of angioedema ranges from 1 day to 8 years, 13 and most cases occur within the first 6 months of therapy.…”

“…Although the exact mechanisms are uncertain, the condition is thought to be secondary to increased bradykinin levels 14 . In one study that compared 22 ACE inhibitor‐treated patients with angioneurotic edema and 48 matched controls, the mean levels of carboxypeptidase N (kininase I) and C1 esterase inhibitor were significantly lower in the patients than in the controls, but were within normal laboratory ranges 12 …”

ACE Inhibitor‐Related Angioedema: Can Angiotensin‐Receptor Blockers Be Safely Used?

“…An additional study has reported decreased levels of carboxypeptidase N and C1 esterase inhibitor in affected patients treated with an ACE inhibitor 36 . More recently, low levels of aminopeptidase P and dipeptidyl peptidase IV, enzymes known to catabolize bradykinin, have been suggested as predisposing factors for development of angioedema in patients treated with ACE inhibitors 37,38 .…”

PGX: Pharmacogenomics During Generation X

“…Now, we appreciate that the differential effect of hydralazine on patients is genotypically attributable to human, hepatic arylamine N-acetyltransferase 2 activity. 1 Arylamine N-acetyltransferase 2 single nucleotide polymorphisms (SNPs) determine acetylation status, with rapid acetylators requiring greater drug exposure for efficacy. Approximately an eighth of individuals possess the rapid acetylation phenotype, a third the slow phenotype, and the remainder with an intermediate phenotype.…”