how is hereditary angioedema treated?

 

If left untreated, hereditary angioedema (HAE) attacks gradually worsen over 12 to 24 hours and typically subside in 1 to 5 days. Treatment for HAE should be individualised to your patient’s needs and lifestyle to help reduce the burden of disease by preventing or attenuating attacks.1,2

 

According to the 2017 World Allergy Organization (WAO)
Treatment Guideline, HAE can be managed with:

WAO/EAACI recommendations:

"We recommend that all attacks are:

  • Considered for on-demand treatment. We recommend that any attack affecting or potentially affecting the upper airway is treated.
  • Treated as early as possible.
  • Treated with either C1-INH, ecallantide*, or icatibant."3

WAO/EAACI recommendations:

"We recommend that all attacks are:

  • Considered for on-demand treatment. We recommend that any attack affecting or potentially affecting the upper airway is treated.
  • Treated as early as possible.
  • Treated with either C1-INH, ecallantide*, or icatibant."3

WAO/EAACI recommendation:
“We recommend short-term prophylaxis before procedures that can induce an attack.”3

WAO/EAACI recommendation:
“We recommend short-term prophylaxis before procedures that can induce an attack.”3

WAO/EAACI recommendation:
“We recommend that patients are evaluated for long-term prophylaxis at every visit. Disease burden and patient preference should be taken into consideration.”3

WAO/EAACI recommendation:
“We recommend that patients are evaluated for long-term prophylaxis at every visit. Disease burden and patient preference should be taken into consideration.”3

Availability of therapies differs by country.

 

*Only available in the US.

HAE management guideline fact sheet

See the latest WAO/EAACI recommendations on how to manage your patients’ HAE.

Watch and learn:
New Views on Prevention & On-Demand Therapy: Highlights from the 2017 WAO/EAACI Guideline

Watch Dr Marcus Maurer review some updates to the treatment guideline.

 

Please note that current treatment guidelines are for patients with Type 1 and Type 2 HAE only; the pathogenesis of other forms of HAE is not well-characterised, and therefore, therapeutic options may not be similarly effective.3