Bradykinin and the pathophysiology of angioedema☆
Section snippets
Clinical presentation of angioedema
Angioedema is a swelling involving the deeper layers of the skin or submucosal tissue and tends to recur chronically. It is most often located on the lips and face (Fig. 1), hands or feet. If angioedema occurs in the upper airways, particularly at the larynx, it is life-threatening. It may also occur in the gastrointestinal tract, where it can be very painful and can be mistaken for appendicitis, diverticulitis or mesenterial ischemia. It may cause diarrhea or ileus-like symptoms. Angioedema
Etiology of angioedema
Angioedema is caused by various reasons such as allergies, inherited or acquired deficiencies of C1-inhibitor or drug reactions. In many cases of angioedema, the pathophysiology remains undetermined. The clinical response to specific antagonists can provide a good evidence for a particular mediator. Histamine, which can be blocked by anti-histamines, is the best identified mediator [1], [2]. The reaction to an allergen induces the release of histamine and other chemicals. However, at the site
Pathogenesis of angioedema and the kinin system
Theoretically, at least two forms of angioedema may be due to bradykinin-mediated increase in vasopermeability: (1) angioedema due to C1-inhibitor deficiency and (2) ACE inhibitor-related angioedema.
Measurement of plasma bradykinin
We measured plasma levels of bradykinin-(1–9)nonapeptide by radioimmunoassay after liquid phase extraction and high-performance liquid chromatography [26]. Our method enabled us to solve several pre-analytical and analytical problems which have rendered extremely difficult the measurement of plasma kinins in the past [27]. The preanalytical problems consist in the very low concentration of bradykinin (pM), its short half life (seconds) and its easy enzymatic generation and degradation during
Bradykinin in different types of angioedema
During remission between angioedema attacks, plasma bradykinin in 26 patients with angioedema due to C1-inhibitor deficiency (22 hereditary and 4 acquired) was normal or slightly increased (3.9±3.7 and 10.4±1.6 pM, respectively; normal range 0.2–7.1 pM) [26]. During acute attacks of angioedema, in 11 patients plasma bradykinin was increased from 2 to 12 times the upper limit of normal (18.0–90.0 pM) [26], [28]. In two other patients with C1-inhibitor deficiency, we had the opportunity to
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This paper is part of the Proceedings of the 16th International Conference on the Kallikrein-Kinin System (Kinin 2002) which was held in Charleston, SC, May 26–31, 2002 (see International Immunopharmacology Volume 2/13–14)