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Bradykinin-mediated angioedema

The first step is to identify and eliminate triggers for the patient’s swelling attacks, insofar as this is feasible. Examples of common triggers include:

  • Emotional stress
  • Excessive heat or cold
  • Pharmaceutical preparations containing oestrogens (oral contraceptives, hormone replacement)
  • Certain medications

In many cases, however, no triggers can be identified. In very rare cases, angioedema may be associated with another underlying disorder. This, of course, must also be addressed by your doctor.

Hereditary angioedema

Although hereditary angioedema (HAE) is incurable, the swelling attacks can be very effectively controlled with medication.The use of medications to control angioedema attacks should be discussed in a comprehensive consultation with your doctor. Acute therapy, which refers to treatment during an angioedema attack, may be recommended in the following circumstances:

  • Severe to life-threatening angioedema attacks (e.g. swelling affecting the larynx)
  • Painful swelling during angioedema attacks involving the gastrointestinal tract
  • Swelling that, because of its severity or location, severely interferes with activities of daily life

Patients can also be offered the option of short-term prophylaxis, consisting of a time-limited treatment with medication aimed at reducing the risk of swelling associated with known triggers of angioedema, such a dental treatments or surgical procedures.

Patients in whom swelling attacks occur very frequently may benefit from a long-term prophylaxis with medications known to reduce the risk. When considering long-term use of medication, however, one must not forget the possible side effects, which, under certain circumstances, can also be significant.

There are two currently available options for the treatment of acute angioedema attacks:

  • Icatibant (bradykinin B2-receptor antagonist):
    Bradykinin, which increases the permeability of the vascular wall for fluid, is present in abnormally high quantities in patients with HAE. Icatibant blocks the bradykinin B2 receptors on the cells of the blood vessel walls, which in turn prevents the swelling caused by the actions of bradykinin. The medication is injected into the subcutaneous adipose tissue in a manner similar to that of an insulin injection.
  • C1-esterase inhibitor (C1-INH) concentrate:
    Patients with HAE have too little C1-esterase inhibitor (C1-INH) or the C1-INH present in their systems does not function correctly. Because of this deficiency, the body produces excessive amounts of bradykinin, with the result that they are at risk of swelling of the skin and mucous membranes. C1-INH concentrate is either injected into a vein or administered as an intravenous infusion. It temporarily replaces the body’s own deficient C1-esterase inhibitor.

Beside these options, there are other treatment concepts still in the developmental stage. These include a recombinant C1-esterase inhibitor and ecallantide. Recombinant C1-INH is obtained from the milk of transgenic rabbits, substitutes the deficient natural C1-INH. It is useful in acute therapy of HAE attacks and reduces the suddenly-developing angioedema. Ecallantide is a recombinant kallikrein inhibitor, which interrupts the kallikrein-kinin cascade and blocks the release of bradykinin.

IMPORTANT: Antihistamines and corticosteroids (cortisone) are ineffective in the treatment of hereditary angioedema (HAE).