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INCREASING INCIDENCE OF ANGIOEDEMA WITHOUT URTICARIA – CLINICAL FEATURES

ASJA STIPIĆ MARKOVIĆ ; Odjel za kliničku imunologiju, pulmologiju i reumatologiju, Klinika za unutrašnje bolesti Medicinskog fakulteta Sveučilišta u Zagrebu, Klinička bolnica Sveti Duh, Zagreb, Hrvatska
MARTINA JANŽEKOVIĆ ; Lječilište Topusko, Topusko, Hrvatska


Puni tekst: hrvatski pdf 239 Kb

str. 119-127

preuzimanja: 1.103

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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.

Ključne riječi

angioedema; bradykinin; C1Inh deficiency

Hrčak ID:

87891

URI

https://hrcak.srce.hr/87891

Datum izdavanja:

1.4.2011.

Podaci na drugim jezicima: hrvatski

Posjeta: 1.830 *