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
 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
 Yip, J., Cunliffe, W.J. (1992). Hormonally exacerbated hereditary angioedema. Australas.J.Dermatol, 33(1), 35-8
 Kumar, M.A., Gupta, C. (2005). Acquired angioedema secondary to hormone replacement therapy. Indian J.Med.Sci, 59(10), 451-4
 André, C., André, F.,Veysseyre-Balter, C., Rousset, H. (2003). Acquired angioneurotic edema induced by hormonal contraception. Presse Med, 32(18), 831-5
 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.
 Binkley, K.E., Davis, A.E. (2003). Estrogen-dependent inherited angioedema. Transfus.Apher.Sci, 29(3), 215-9.
 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.
 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.
 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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