Angioedema is a potentially life-threatening disease cate-gorised into several forms such as allergic, hereditary, acquired autoimmune and idiopathic. Allergic angioedema is dependent on histamine release, whereas mutations in the C1-inhibitor and factor XII genes have been described in hereditary angioedema (1, 2). Bradykinin-induced acquired angioedema is often caused by antibodies to C1-inhi...

Background In classic hereditary angioedema, inadequate C1-inhibitor (C1-INH) failing to restrict factor-XII activity leads to increased production of bradykinin, a potent vasodilator and mediator of angioedema. Hereditary angioedema with normal C1-INH (Type-III) manifests with sporadic recurrent angioedema but normal C1-INH concentration and activity. Here, bradykinin accumulation appears depe...

current evidence suggests no absolute contraindication to angiotensin receptor blockers (ARBs) in patients who have had angioedema attributable to an angiotensin-converting enzyme (ACE) inhibitor. However, since ARBs can also cause angioedema, they should be prescribed with extreme caution after a thorough risk-benefit analysis and after educating the patient to watch for signs of angioedema wh...

Dipeptidyl peptidase-IV (DPP-IV) inhibitors decrease degradation of the incretins. DPP-IV inhibitors also decrease degradation of peptides, such as substance P, that may be involved in the pathogenesis of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema. This study tested the hypothesis that DPP-IV inhibition affects risk of clinical angioedema, by comparing the incidence of ...

BACKGROUND Bradykinin is an underestimated mediator of angioedema. One subgroup of bradykinin induced angioedema is angioedema triggered by treatment with angiotensin converting enzyme (ACE) inhibitors. Due to its localization in the head and neck region and its unpredictable course, it is a possibly life-threatening condition. There is not an officially approved treatment for ACE inhibitor ind...

<b>Background</b> Angiotensin converting enzyme inhibitor-induced angioedema is a major cause of angioedema-related hospitalizations each year. Common swelling predilection sites include the face, periorbital skin, lips, pharynx, larynx, and tongue. Involvement airway structures could lead to obstruction ultimately death if not treated promptly. A 62-year-old man presented rural cli...

INTRODUCTION — Acquired deficiency of C1 inhibitor (C1-INH), also called acquired angioedema (AAE), is a rare syndrome of recurrent episodes of angioedema, without urticaria, which is associated with B cell lymphoproliferative disorders in some patients [1,2]. Angioedema typically affects the skin or mucosal tissues of the upper respiratory and gastrointestinal tracts. The swelling is self-limi...

Several types of angioedema exist beyond hereditary angioedema (HAE) types I/II; however, the diagnostic and treatment needs of these conditions are not well understood. Noticeably, there are no licensed treatments available for other forms of angioedema beyond HAE types I/II, and similarly they are unresponsive to conventional antihistamine/glucocorticoid treatment. A group of angioedema exper...

BACKGROUND Angioedema has numerous hereditary, acquired and iatrogenic causes. A number of studies show that angioedema is inadequately assessed and treated during its acute phase as well as in the follow-up period. We present an algorithm for the assessment and treatment of patients with angioedema. KNOWLEDGE BASE: The article is based on a literature search in PubMed, a review of bibliographi...

Bradykinin and substance P have been implicated as mediators in angiotensin-converting enzyme inhibitor (ACEI)-associated angioedema. Studies investigating the metabolism of bradykinin in sera from patients with a history of ACEI-associated angioedema and controls suggest that there is a defect in a non-ACE, non-kininase I pathway of bradykinin degradation, such as the aminopeptidase P (APP)/di...