AMelioration of Angiotensin Converting Enzyme Inhibitor Induced Angioedema Study
|ClinicalTrials.gov Identifier: NCT01154361|
Recruitment Status : Completed
First Posted : June 30, 2010
Last Update Posted : December 23, 2011
This is a multicenter study recruiting patients with angioedema induced by ACEI.
Open-label treatment with subcutaneous Icatibant compared to a historic group of 47 patients with ACE inhibitor induced angioedema which the investigators have been previously treated in the investigators centers with current "standard" therapy (250 mg methylprednisolon and 2 mg clemastine).
In cases with fast progression of edema after application the study-drug, a second application with icatibant could be necessary. Rescue medication and intervention.
|Condition or disease||Intervention/treatment||Phase|
|Angioedema||Drug: Icatibant (subcutaneous) and plazebo (intravenous) Drug: Cortisone + Clemastin (intravenous) and plazebo (subcutaneous)||Phase 2|
Sudden occurrence of subcutaneous or submucosal non-itchy swelling, so-called angioedema, is a well known side effect of angiotensin-converting enzyme inhibitors (ACEi), which may become life-threatening if the upper airway is involved. To be note, ACEi induced angioedema were always located in the head and neck region.
The pathophysiology of ACE inhibitor (ACEi) induced angioedema most likely resembles that of hereditary angioedema (HAE), i.e. it is mainly mediated by bradykinin induced activation of vascular bradykinin B2 receptors (BKR-2). In contrast to an increased bradykinin generation in HAE, treatment with ACEi decreases the bradykinin degradation in plasma and increases the biological activity of bradykinin.
The current pharmacotherapy of ACEi induced angioedema is not satisfactory. Antihistamines and corticosteroids may be effective in the treatment of urticaria with cutaneous edema and itchy, but are theoretically ineffective and hence superfluous in bradykinin induced angioedema. However, glucocorticoids still belong to the standard treatment of angioedema.
We hypothesized that the BKR-2 antagonist icatibant might be an effective therapy for ACEi-induced angioedema.
Patients with ACEi induced angioedema, located in the upper aero-digestive tract will be randomized and treated either with icatibant and plazebo or cortisone with clemastin and plazebo.
|Study Type :||Interventional (Clinical Trial)|
|Intervention Model:||Parallel Assignment|
|Masking:||Triple (Participant, Investigator, Outcomes Assessor)|
|Official Title:||A Multicenter Study, Randomized, Double-blind With 2 Groups as Prove of Concept for the Treatment of ACEI Induced Angioedema With Subcutaneous Icatibant|
|Experimental: Arm A||Drug: Icatibant (subcutaneous) and plazebo (intravenous)|
|Active Comparator: Arm B||Drug: Cortisone + Clemastin (intravenous) and plazebo (subcutaneous)|
- Time to complete resolution of angioedema
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01154361
|Klinikum rechts der Isar Hals-Nasen-Ohrenklinik der TUM|
|Munich, Bavaria, Germany, 81675|
|Principal Investigator:||Murat Bas, Dr.||Klinikum rechts der Isar, Hals-Nasen-Ohrenklinik, Ismaninger Str. 22 81675 München|