3183 Clinical Efficacy of Recombinant Human C1 Inhibitor in Patients with Acute Hereditary Angioedema Attacks

Tuesday, 6 December 2011: 13:15 - 13:30
Gran Cancún 5 (Cancún Center)

Avner Reshef, MD , Head of Allergy and Immunology, Sheba Medical Center, Angioedema Center, Tel Aviv, Israel

Marc Riedl , Clinical Immunology and Allergy, UCLA - David Geffen School of Medicine, Los Angeles, CA

Dumitru Moldovan, MD, PhD , University of Medicine and Pharmacy, Mures County Hospital, Tirgu Mures, Romania

Richard F. Lockey, MD , Division of Allergy & Immunology, University of South Florida and James A. Haley Veterans' Hospital, Tampa, FL

Vincenzo Montinaro , Azienda Ospedaliera Policlinico Consorziale di Bari, Bari, Italy

Daniel Suez , Allergy, Asthma & Immunology Clinic, P.A., Irving, TX

Anurag Relan, MD , Pharming Technologies BV, Leiden, Netherlands

Marco Cicardi, MD , Scienze Cliniche "Luigi Sacco", Universitŕ di Milano, Ospedale L.Sacco, Milano, Italy

Bruce Zuraw , Medicine, University of California, San Diego, La Jolla, CA

Background: Recombinant human C1 Inhibitor (rhC1INH) has been approved in Europe for the treatment of acute hereditary angioedema attacks. The efficacy of rhC1INH was demonstrated in two randomized-controlled trials. Open-label extension studies, where patients could be treated for subsequent HAE attacks, demonstrated continued efficacy for repeated rhC1INH treatments.

Objective: To review the integrated efficacy data of rhC1INH for treatment of acute HAE attacks.

Methods: Efficacy was assessed using patient-reported HAE-specific visual analog scales.  The primary endpoint was time to onset of relief of symptoms (VAS decrease ≥ 20mm), and the secondary efficacy endpoint was time to minimal symptoms (VAS < 20mm at all locations). Other endpoints included clinical response (relief achieved within 4 hours) and relapse (recurrence of symptoms within 24 hours following initial improvement). Subgroup analyses by attack location were also performed.  

Results: The dataset included 141 HAE patients treated for 403 attacks. Median times to the onset of symptom relief for attacks treated with 100 U/kg, 50 U/kg and 2100 U rhC1INH were 66, 60, and 61 minutes, respectively, compared to 495 minutes in the placebo-treated group. Median times for time to minimal symptoms were 266, 240 and 241 minutes for the 100 U/kg, 50 U/kg, and 2100 U rhC1INH-treated attacks respectively compared to 1210 minutes for the placebo-treated attacks.

High clinical response rates were observed for the rhC1INH-treated groups (93%, 96% and 88% for the 100 U/kg, 50U/kg, and 2100 U respectively) compared to the placebo group (41%).

None of the rhC1INH-treated attacks relapsed.

Subgroup analysis by attack location showed that abdominal attacks had the fastest median time to onset of symptom relief (50, 36 and 60 minutes for 100 U/kg, 50 U/kg and 2100 U doses respectively), followed by oro-facial-pharyngeal-laryngeal attacks ( 70, 65 and 120 minutes), and peripheral attacks (75, 84 and 121 minutes)

 No drug-related serious adverse events or hypersensitivity reactions were observed.

Conclusions:

RhC1INH has demonstrated efficacy for the treatment of repeated HAE attacks for all doses tested (100 U/kg, 50 U/kg and 2100 U). Controlled studies did not show additional benefit with doses greater than 50 U/kg.  RhC1INH was generally safe and well tolerated.