QOTW: “What is the difference between food allergies and food triggers for HAE?”
Dec 2, 2015
Dr. C:The simple answer to the question is that a true food allergy is the result of the immune system recognizing the structure of food as an allergen and making allergic antibodies (IgE) to that food. With exposure to what should be a harmless material (food) the sensitized individual will unleash a firestorm of activation of the cells that contain histamine (mast cells) by the network of specific IgE molecules. The release of histamine during these reactions will cause a myriad of symptoms including itching, hives, at times respiratory distress, gastrointestinal symptoms, possible collapse and even death.
The second part of the question posed by our reader is more difficult. Attacks of swelling do not relate to histamine but rather the generation of bradykinin. Often the attacks are unpredictable—by nature we always want a reason for something that happens. As the one thing we are always doing is eating it can certainly coincide with an attack. The issue is whether it is truly causal or coincidental. Our reader’s question highlights a concern by many patients that there is a link between their diet and swelling. We actually do not have any data that can answer the question. I have had patients tell me that alcohol can be a trigger and others express concern about a variety of foods. I am left with simply telling patients that it is OK to avoid something if it seems to make the swelling worse.
I have been teaching allergy fellows for over 30 years. One of my favorite bits of wisdom to pass on is ‘listen to the patient and they will tell you the answer’. I think that we have finally started to ‘listen’ about this dietary issue. Bruce would you like to tell our readers about the FAMISH study?
I’m happy to do so. I agree that many patients bring this question up, and therefore it’s important to us to obtain solid information about it. The UC San Diego Angioedema Center along with the HAEA Medical Advisory Board is preparing to conduct a study to see if there are any patterns that link dietary practices to HAE severity. We will be using an anonymous one-time online diet questionnaire to collect this information. While most of us are skeptical that there is an actual link between diet and HAE severity, I feel that it’s important not to dismiss the concern and potentially miss this connection if it really exists. Should the diet questionnaire suggest such a link, we would then set up a more rigorous follow-up study that would track the relationship looking forwards (that is, prospectively).
Excellent. We are quite excited to see the data and where it will lead. Marc, what thoughts do you have for our reader on this question?
The concept of specific foods as triggers for HAE attacks is an interesting area that really hasn’t been studied. I certainly hear from some patients that they strongly suspect certain foods are symptom triggers so much so that they’ve eliminated these foods from their diet. Unfortunately, to date, we don’t have any study data to confirm this is a general or predictable trigger in HAE. We also don’t have any known biologic mechanism by which this might occur and therefore no available lab tests to look for this trigger factor in HAE. So this is another area ripe for study. Environmental (in this case food) exposure studies are notoriously difficult to design and conduct in a rigorous fashion, but surveys such as the one being planned at the Angioedema Center could point us in the right direction. Food allergy, on the other hand, is generally a histamine-mediated condition caused by food-specific IgE (allergic antibody) produced by the immune system. Because we better understand the mechanism of these reactions, we have fairly reliable means of identifying this allergic antibody through blood or skin testing. This highlights the importance of distinguishing between the pathways of allergic reactions (IgE-mast cell-histamine) and HAE reactions (C1INH-kallikrein-bradykinin) and recognizing these different types of clinical reactions require different treatments.
Thank you, well stated. Bruce do you have any other comments regarding the likelihood of obtaining helpful data from our investigation?
I agree with what Marc stated, but I’d also emphasize that it’s important to recognize that there may be additional mechanisms at play here. It would be very easy to show that IgE-mediated reactions to foods are not a significant cause of HAE attacks. By taking a very broad and open-minded approach such as the one we proposed for the FAMISH study, we run the risk of finding relationships that turn out to be incorrect. That’s why I believe that positive findings can only be a starting point, and must be followed by controlled prospective studies.
Thank you Bruce and Marc. I do hope that the FAMISH study will lead to better answers. I somehow now have the desire to go eat some leftover turkey…. We look forward to hearing from you and our next ‘Question of the Week’.