Many mast cell disease patients have allergy tests that come back negative, myself included, for things we are 100% sure are triggering our “allergies”.
It can be really frustrating for doctor and patient.
It wasn’t until a few hours after I went home that three of my food allergy skin prick test spots formed hard, raised, itchy welts. They went away and then came back again the next day, in the same three spots. I mentioned this to my doctor and nurse at my follow up appointment (the one where he would ask me if I’d ever been tested for mast cell disease) but they hadn’t heard of that happening.
So technically my food allergy tests were all negative, despite this apparent anomaly. Does this mean I don’t have “real” food allergies? It’s complicated, I’m learning.
Here is an article from PubMed that addresses this topic. It talks about the development of allergic inflammation and while it’s very long it does have a lot of good information, like:
In addition, several effector mechanisms that are independent of IgE may also contribute to the pathology of allergic inflammation. In a mouse model of chronic asthma, mast cells can substantially influence features of chronic allergic inflammation and tissue remodelling (including expansion of the number of goblet cells), independently of mast-cell signalling through either IgE–FcεRI or antigen–IgG1–FcγRIII. Thus mast cells have the potential to drive important features of allergic inflammation independently of IgE.
So this research shows exactly how and why mast cell disease can cause us to have what looks like an IgE-mediated food (or other) allergy when it isn’t. It still can be just as dangerous, though!!
It can be extremely complex, too, and may go beyond involvement of just our mast cells:
Moreover, in mouse models, allergic inflammation of the airways can be induced in mice that lack mast cells or B cells. This underscores the important point that the coordination of chronic allergic inflammation may reflect complex and partly redundant pathways involving interactions between mast cells, T cells, eosinophils, basophils, neutrophils, monocyte–macrophage lineage cells, platelets and natural killer T cells, as well as a large and growing list of cytokines (including IL-4, IL-5, IL-12, IL-13, IL-15, IL-25 and IL-33). However, the relative importance of each of these potential effector or regulatory elements may vary in different disorders or between patients, and many of these interactions may not be markedly affected by IgE.
So it’s pretty clear that we can have a “true” allergic response independent of IgE and our chronic, inflammatory, allergic responses may be far more complicated than we or our mast cell doctors ever realized.
What can we do to manage our chronic, allergic inflammation since, at the end of the day, that’s what really matters?
The two key elements of allergy management are preventing the exposure of sensitized individuals to allergen and treating these individuals with therapeutic agents appropriate to the disorder.
In other words, avoid our triggers and take our medicines.