Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: HAE international home therapy consensus document. | Longhurst et al. Allergy Asthma Clinical Immunology 2010 6 22 http content 6 1 22 ALLERGY ASTHMA CLINICAL IMMUNOLOGY REVIEW Open Access HAE international home therapy consensus document I I irr f 1l_I fl c 1 r I 1 r 2 I I V V z L V I z t3 c K I A r i A V Di Ifr I v 4 I I vr o z-xt- L I I Z X5 I o D I Z X r I -S I o r6 Hilary J Longnurst Henriette rarKas Timothy Craig tmel Aygoren-rursun Claire Bethune Janne BjorKander 7 8 9 10 11 12 Konrad BorK Laurence Bouillet HenriK Boysen Anette Bygum Teresa Caballero Marco Cicardi John Dempster13 Mark Gompels14 Jimmy Gooi15 Sofia Grigoriadou16 Ursula Huffer17 Wolfhart Kreuz18 Marcel M Levi19 Janet Long20 Inmaculada Martinez-Saguer21 Michel Raguet22 Avner Reshef23 Tom Bowen24 Bruce Zuraw25 Abstract Hereditary angioedema C1 inhibitor deficiency HAE is associated with intermittent swellings which are disabling and may be fatal. Effective treatments are available and these are most useful when given early in the course of the swelling. The requirement to attend a medical facility for parenteral treatment results in delays. Home therapy offers the possibility of earlier treatment and better symptom control enabling patients to live more healthy productive lives. This paper examines the evidence for patient-controlled home treatment of acute attacks self or assisted administration and suggests a framework for patients and physicians interested in participating in home or self-administration programmes. It represents the opinion of the authors who have a wide range of expert experience in the management of HAE. Introduction Hereditary angioedema HAE is an autosomal dominant condition caused by a partial deficiency of C1 inhibitor C1INH . C1INH controls a variety of local inflammatory pathways. Insufficient regulation of the classical complement pathway causes consumption of the complement component C4 resulting in typical diagnostic abnormalities. Insufficient inhibition of kallik-rein results in .
