L'angioedema

Abstract

Angioedema is a term which includes various clinical conditions and is defined as the presence of oedema, in deep dermis, subcutaneous and/or submucosal tissue. Angioedema usually has an acute and sudden onset, rapid progression and sometimes a recurrent course. Mucosal involvement is the most important feature for the clinical outcome and can cause systemic symptoms, which may be very severe and life-threatening (e.g., laryngeal oedema). The exact recognition of the clinical forms and the appropriateness of the diagnostic approach are fundamental, considering that the pathomechanisms, and, consequently, the therapeutic management are completely different for the various types of angioedema. Angioedema can be distinguished into distinct groups: histamine-dependent angioedema, which can be a component of urticaria-angioedema syndrome and complement-dependent angioedema which corresponds to C1-inhibitor deficiency, which may be either hereditary or acquired, and is never associated with urticaria. In the former type the development of oedema is strictly mediated by histamine, whereas kinins (e.g., bradykinin) are the most important mediators in the latter form. Other forms include idiopathic angioedema and iatrogenic angioedema. Among the drugs which have been potentially implicated in the development of angioedema, angiotensin-converting enzyme (ACE) inhibitors are the most frequently associated and well-established agents. The mechanism involved in angioedema induced by ACE-inhibitors seems to be mediated by increased levels of bradykinin. Angiotensin receptor (AR) blockers were initially regarded as safe alternatives in patients who developed angioedema with ACE-inhibitors, but some studies have reported the possibility of angioedema during treatment with AR blockers also.