Increased C-reactive protein in ACE-inhibitor-induced angioedema

被引:44
作者
Bas, M
Hoffmann, TK
Bier, H
Kojda, G
机构
[1] Univ Dusseldorf, Dept Otorhinolaryngol, D-4000 Dusseldorf, Germany
[2] Univ Dusseldorf, Inst Pharmacol & Clin Pharmacol, D-4000 Dusseldorf, Germany
关键词
angiotensin converting enzyme inhibitor; angioedema; C-reactive protein; acute-phase-proteins;
D O I
10.1111/j.1365-2125.2004.02268.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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.
引用
收藏
页码:233 / 238
页数:6
相关论文
共 25 条
[1]   Aminopeptidase P in individuals with a history of angio-oedema on ACE inhibitors [J].
Adam, A ;
Cugno, M ;
Molinaro, G ;
Perez, M ;
Lepage, Y ;
Agostoni, A .
LANCET, 2002, 359 (9323) :2088-2089
[2]   Drug-induced angioedema without urticaria - Incidence, prevention and management [J].
Agostoni, A ;
Cicardi, M .
DRUG SAFETY, 2001, 24 (08) :599-606
[3]   ENALAPRIL AND HYDROCHLOROTHIAZIDE IN HYPERTENSIVE AFRICANS [J].
AJAYI, AA ;
OYEWO, EA ;
LADIPO, GOA ;
AKINSOLA, A .
EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY, 1989, 36 (03) :229-234
[4]   Angioedema and cough in Nigerian patients receiving ACE inhibitors [J].
Ajayi, AAL ;
Adigun, AQ .
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 2000, 50 (01) :81-82
[5]   Recurrent angiotensin-converting enzyme inhibitor-associated angioedema [J].
Brown, NJ ;
Snowden, M ;
Griffin, MR .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1997, 278 (03) :232-233
[6]   Black Americans have an increased rate of angiotensin converting enzyme inhibitor-associated angioedema [J].
Brown, NJ ;
Ray, WA ;
Snowden, M ;
Griffin, MR .
CLINICAL PHARMACOLOGY & THERAPEUTICS, 1996, 60 (01) :8-13
[7]  
CHEN HM, 1993, J BIOL CHEM, V268, P25311
[8]   Angiotensin-converting enzyme inhibitor use is associated with reduced plasma concentration of C-reactive protein in patients with first-ever ischemic stroke [J].
Di Napoli, M ;
Papa, F .
STROKE, 2003, 34 (12) :2922-2929
[9]   C-reactive protein as a regulator of autoimmunity and inflammation [J].
Du Clos, TW .
ARTHRITIS AND RHEUMATISM, 2003, 48 (06) :1475-1477
[10]   Mechanisms of disease: Acute-phase proteins and other systemic responses to inflammation [J].
Gabay, C ;
Kushner, I .
NEW ENGLAND JOURNAL OF MEDICINE, 1999, 340 (06) :448-454