Angioedema - Twitter summary from 2012 #AAAAI meeting

This summary was compiled from the tweets posted by the following allergists/immunologists who attended the 2012 annual meeting of the American Academy of Allergy Asthma and Immunology (AAAAI): From Sakina Bajowala, M.D ‏@allergistmommy and David Fischer, MD ‏@IgECPD4. The tweets were labeled #AAAAI. The text was edited and modified by me.

Dr. Bruce Zuraw discussed angioedema practice parameters.

The big question in angioedema is: hereditary or acquired?

Hereditary angioedema (HAE)

Hereditary angioedema (HAE) is often triggered by trauma, stress, estrogens. Extremities and abdomen are common sites. HAE does not skip generations, and is autosomal dominant. Genetic mutation in HAE: SERPING1

HAE Type I can also be a new mutation so family history is not always helpful for ruling out the condition.

50% of HAE patients develop swelling before the age of 10 yrs. Currently, diagnosis time from onset of symptoms is 9-10 yrs! HAE nearly always presents before age 20.

Diagnosis of type I and type II angioedema is fairly straightforward. Type III HAE is more complicated from a diagnostic standpoint (many allergists doubt that HAE type III even exists). There is no reliable way of distinguishing HAE III and idiopathic AE. Type III angioedema has normal complement indices and it is difficult to sort out from idiopathic angioedema. The Factor XII gain of function mutation as a cause of HAE III has not really panned out. It is not advisable to order this analysis.

At which age can we begin screening for HAE with C4? Age 1 year.

There are 2 ways to measure C1 inhibitor function: ELISA and chromogenic assay. If ELISA is normal, consider the chromogenic assay.

Acquired angioedema

Acquired angioedema is associated with underlying cause (organic disease). Acquired angioedema patients should be worked up for hematological malignancy, including bone marrow examination.


There was a huge increase in therapeutic modalities for angioedema in the last decade. Many are targeting the bradykinin cascade.

Treatment for HAE: C1-inhibitor, ecalantide, icatibant. Use prophylaxis for known triggers, provide on-demand therapy, and preventative therapy if needed. Long-term HAE prophylaxis includes C1 inhibitor and androgens.

Although labs are normal, C1 inhibitor replacement still helps patients with HAE III. Type III HAE seems bradykinin-dependent, therefore Icantibant (bradykinin inhibitor) may work best.

Exercise caution in using C1 inhibitor in acquired HAE, as many patients have Auto-Ab.

For children, Dr. Zuraw recommends C1 inhibitor as therapy. As a native human protein replacement, there are fewer long-term safety concerns. Dr Zuraw is still most comfortable with blood-derived C1 inhibitor in pediatric population with HAE.

Allergists achieved highest use of social media by any specialty

During the 2012 AAAAI meeting, the allergists achieved the highest use of social media by any specialty. There are more than 100 allergists on Twitter and 30 of them posted simultaneously from the annual meeting, broadcasting thousands of tweets tagged with #AAAAI. The annual AAAAI meeting was attended by approximately 5,000 people. In comparison, the 30 allergists on Twitter reached 250,000 people (measured by on 03/04/2012).

This summary was compiled from some of the tweets posted by  Sakina Bajowala, M.D ‏@allergistmommy and David Fischer, MD ‏@IgECPD4. I would strongly encourage you to post updates on Twitter from the CME conferences that you are planning to attend in the future. Here is how to do it: Twitter for Physicians: How to use Twitter to keep track of the latest news and scientific meetings, and share information with colleagues and patients.

Disclaimer: The text was edited, modified, and added to by me. This is one of a series of posts that will be published during the next few weeks.


What are treatment options for idiopathic angioedema? Some success with HAE therapies, omalizumab, tranexamic acid

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