Angioedema is a potentially life threatening condition and may be inherited or acquired.According to sporadic reports, hormonal contraceptives can induce or exacerbate symptoms of hereditary angioedema type I or type III or idiopathic angioedema. 

However,  many   women   with   these   diseases   may   use   oral contraceptives without having any effect on their angioedema (1).  The main symptoms include sudden swilling and reddening of the skin which can improve after hormonal contraceptive (HC)  cessation (2).

Although in rare cases,  patients presenting severe abdominal pain and laryngeal oedema can have airway obstruction and even death (3).

It is advisable that clinicians should not administer estrogen-containing   contraceptives   to   women   known   to   have   hereditary angioedema,  in   whom   C1-esterase   inhibitor   (C1   INH)deficiency   was demonstrated. 

In fact,evidence showed a remarkable improvement with increase of C1-INH, after HC discontinuation. Several studies reported that HCs may play an iatrogenic role in the aetiology of chronic angioneurotic oedema or urticaria. (4). 

Hormonal   measurement   demonstrated   that   the   number   of   attacks   is significantly higher in female with high progesterone levels;while,a significantly lower attack frequency, during 1-year follow-up,  in patients with a higher (40 nmol/ l) SHBG level (5).

Recurrent angioedema is biochemically characterized by reduced C1 inhibitor level and/or function ,and genetically by a heterogeneous group of mutations in the C1 inhibitor gene that have an autosomal dominant mode of trasmission (6).

Recently, a new type of hereditary angioedema(type 3) has been reported. This occurs only in women and is characterized by normal C1-INH   levels   and   severe   attacks   of   angioedema,which   are   clinically indistinguishables from the classic form (7,8,9). 

Acquired forms of angioedema are estrogen (both endogenous and exogenous)dependent, although it seems that progesterone-only-contraceptives may also induce attacks of this disease (2,8).

Rosa Sabatini and Giuseppe Loverro
Dept. Obstetrics and Gynecology,
General Hospital Policlinico-University of Bari, Italy


[1]  Bork,  K.,  Fischer,  B.,  Dewald,  G.  (2003).  Recurrent episodes of skin angioedema   and   severe   attacks   of   abdominal   pain   induced   by   oral contraceptives or hormone replacement therapy. Am. J.Med, 114(4), 294-8
[2]  Yip,  J.,  Cunliffe,  W.J.  (1992).  Hormonally   exacerbated   hereditary angioedema. Australas.J.Dermatol, 33(1), 35-8
[3]  Kumar,  M.A.,  Gupta,  C.  (2005).  Acquired angioedema secondary to hormone replacement therapy. Indian J.Med.Sci, 59(10), 451-4
[4]  André,  C.,  André,  F.,Veysseyre-Balter,  C.,  Rousset,  H.  (2003). Acquired angioneurotic   edema   induced   by   hormonal   contraception. Presse   Med, 32(18), 831-5
[5]  Visy, B., Fust, G.,Varga, L., Szendei, G., Takàcs, E., Karadi, I., Fekete, B., Harmat,  G.,  Farkas,  H.  (2004).  Sex hormones in hereditary angioneurotic oedema. Clin.Endocrinol, 60(4), 508-15. 
[6]  Binkley,  K.E.,  Davis,  A.E.  (2003). Estrogen-dependent   inherited angioedema. Transfus.Apher.Sci, 29(3), 215-9.
[7]  Van der Klooster,  J.M.,  Schelfhout,  L.J.,Grootendorst,  A.F.,  Zweers,  P.G. (2002).  Recurrent attacks of angioedema ascribed to the use of estrogen preparations   and   a   pregnancy(hereditary   angioedema   type 3). Ned. Tijdschr. Geneeskd, 146(34), 1599-602.
[8]  André,  F.,Veysseyre-Balter,  C.,  Rousset,  H.,  Descos,  L.,  André,  C. Exogenous oestrogen as an alternative to food allergy in the aetiology of angioneurotic oedema. Toxicology, 2’‘3, 185(1-2), 155-60.
[9]  Bettoni,  L.  (2005).  Influence of ethinyl estradiol on C1inhibitor: a new etiopathogenesic mechanism of angioedema:case report.  Eur.  Ann.Allergy Clin.Immunol, 37(2), 49.

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