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Increased C‐reactive protein in ACE‐inhibitor‐induced angioedema
Author(s) -
Bas M.,
Hoffmann T. K.,
Bier H.,
Kojda G.
Publication year - 2005
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.2004.02268.x
Subject(s) - angioedema , medicine , c reactive protein , fibrinogen , pathophysiology , ace inhibitor , inflammation , angiotensin converting enzyme , acute phase protein , retrospective cohort study , gastroenterology , immunology , blood pressure
Aims This study was designed to identify new factors which may contribute to angiotensin‐converting‐enzyme‐inhibitor (ACEI)‐induced angioedema. Methods In a retrospective cohort study we examined 25 patients who used an ACEI and presented at our emergency room with acute angioedema as well as 18 patients with unknown cause of angioedema and a total of 21 patients on ACEI‐therapy without previous angioedema. We measured markers of inflammation such as acute‐phase proteins (C‐reactive protein, fibrinogen), leukocyte count and body temperature. Results The mean interval between initiation of ACEI treatment and first manifestation of angioedema was 35.8 ± 5.3 months. During symptomatic angioedema, mean plasma levels of C‐reactive protein and fibrinogen were significantly increased by 7.3‐fold and 1.5‐fold, respectively, while leukocyte count and body temperature were normal. These changes disappeared after successful treatment of angioedema and were not found in patients with angioedema of unknown cause and those receiving ACEI without having experienced angioedema. Conclusion Our findings demonstrate for the first time that ACEI‐induced angioedema is associated with strongly increased plasma levels of CRP. We suggest that CRP is involved in the pathophysiology of ACEI‐induced angioedema.