INCREASING INCIDENCE OF ANGIOEDEMA WITHOUT URTICARIA – CLINICAL FEATURES
ASJA STIPIĆ MARKOVIĆ
; Department of Clinical Immunology, Pulmonology and Rheumatology, University Department of Medicine, Sveti Duh University Hospital, Zagreb, Croatia
; Topusko Health Resort, Topusko, Croatia
APA 6th Edition STIPIĆ MARKOVIĆ, A. i JANŽEKOVIĆ, M. (2011). TREND POVEĆANE INCIDENCIJE ANGIOEDEMA BEZ URTIKARIJE – KLINIČKE OSOBITOSTI. Acta medica Croatica, 65 (2), 119-127. Preuzeto s https://hrcak.srce.hr/87891
MLA 8th Edition STIPIĆ MARKOVIĆ, ASJA i MARTINA JANŽEKOVIĆ. "TREND POVEĆANE INCIDENCIJE ANGIOEDEMA BEZ URTIKARIJE – KLINIČKE OSOBITOSTI." Acta medica Croatica, vol. 65, br. 2, 2011, str. 119-127. https://hrcak.srce.hr/87891. Citirano 29.01.2020.
Chicago 17th Edition STIPIĆ MARKOVIĆ, ASJA i MARTINA JANŽEKOVIĆ. "TREND POVEĆANE INCIDENCIJE ANGIOEDEMA BEZ URTIKARIJE – KLINIČKE OSOBITOSTI." Acta medica Croatica 65, br. 2 (2011): 119-127. https://hrcak.srce.hr/87891
Harvard STIPIĆ MARKOVIĆ, A., i JANŽEKOVIĆ, M. (2011). 'TREND POVEĆANE INCIDENCIJE ANGIOEDEMA BEZ URTIKARIJE – KLINIČKE OSOBITOSTI', Acta medica Croatica, 65(2), str. 119-127. Preuzeto s: https://hrcak.srce.hr/87891 (Datum pristupa: 29.01.2020.)
Vancouver STIPIĆ MARKOVIĆ A, JANŽEKOVIĆ M. TREND POVEĆANE INCIDENCIJE ANGIOEDEMA BEZ URTIKARIJE – KLINIČKE OSOBITOSTI. Acta medica Croatica [Internet]. 2011 [pristupljeno 29.01.2020.];65(2):119-127. Dostupno na: https://hrcak.srce.hr/87891
IEEE A. STIPIĆ MARKOVIĆ i M. JANŽEKOVIĆ, "TREND POVEĆANE INCIDENCIJE ANGIOEDEMA BEZ URTIKARIJE – KLINIČKE OSOBITOSTI", Acta medica Croatica, vol.65, br. 2, str. 119-127, 2011. [Online]. Dostupno na: https://hrcak.srce.hr/87891. [Citirano: 29.01.2020.]
Sažetak The causes of angioedema (AE), a self-limited, localized swelling of subcutaneous tissue or mucosa unaccompanied by urticaria, are diverse. The commonly applied label of “allergic” is frequently wrong and standard anti-allergic therapy can be ineffective. Types of AE could be categorized according to mediators which mediate vascular leakage: bradykinin AE (hereditary, acquired, angiotensin-converting enzyme inhibitor (ACEi)-related), histamine AE (allergic etiology), and various mediators mediated AE (pseudoallergic reaction to non-steroidal anti-inflammatory drugs). Idiopathic AE is a poorly understood syndrome. The growing relevance of AE without urticaria has been highlighted; angioedema is the most common cause of hospital admission among all acute allergic diseases. The diagnosis of AE is based on the presence of family history (hereditary), absence of family history with the onset during or after the fourth decade of life (acquired C1Inh deficiency), and treatment with ACEi (ACEi-related angioedema). About 0.1%-0.7% of patients taking ACEi develop angioedema as a well-documented but still frequently unrecognized side effect of drugs. Laboratory diagnosis is enabled by measuring serum levels of C1Inh antigen or C1Inh function. Type 1 (hereditary angioedema (HAE) was diagnosed when both antigenic and functional levels of C1Inh were below 50% of normal, and type 2 when functional levels of C1Inh were low, along with antigenic levels normal or higher. ACEi-related AE is diagnosed when AE recurs during therapy and disappears upon withdrawal. Symptoms may appear several years after therapy introduction. Severe acute attacks should be treated with C1Inh concentrate and icatibant, a selective and specific antagonist of bradykinin B2 receptors. Prophylaxis with attenuated androgens (danazol, stanazolol, oxandrolone) is effective in preventing symptom development.