• Dr. Lawrence Afrin, Dr. Tania Dempsey

Ask The MCAS Expert: Mast Cell Activation Syndrome


What is the connection between mast cell disorders, celiac disease and immune deficiencies? Why are people often diagnosed with celiac- go gluten-free and then their mast cells go crazy? I've heard from many who had this experience- first diagnosed with celiac and then MCAS.

Unfortunately, we don't know. In my opinion, we remain in the early days of learning the full range of problems mast cell disease can cause. It is likely that as time goes on and further research is conducted, we will learn about more and more connections between mast cell disease (of one variant or another) and other diseases which feature chronic inflammation, allergic-type phenomena, and abnormalities of growth and development in various tissues/organs/systems. Celiac disease certainly is a chronic inflammatory disease, and its cause is unknown. It therefore is "possible" that some particular variant(s) of mast cell disease may be some of the (primary) causes of celiac disease, but, again, this is just conjecture at this point; the research needed to prove or disprove this conjecture has not been done. One could say the same of just about every other chronic inflammatory disease. It's also possible, of course, that something other than mast cell disease is at the root of celiac disease, but once celiac disease arises, normal mast cells may "secondarily" or "reactively" activate in response to that disease. Although it's usually helpful to identify what the true "primary" or "root" cause of a disease/illness is, sometimes it's possible to help the patient (to some degree, at least) by treating symptoms -- such as symptoms of mast cell activation -- regardless of whether what's being treated is the primary problem or a secondary problem.

Do immune deficiencies cause the mast cells to overreact to compensate for the deficiency?

There are a great number of different "immune deficiency" diseases. Some of these diseases clearly result in increased mast cell activation, but for most such diseases, we don't understand yet the impact they have on mast cells.

What is the cause of nerve pain in mastocytosis?

That's a great question. There likely are multiple causes. In general, though, most of these causes probably revolve around the inappropriate release from mast cells of certain mediators which then directly or indirectly stimulate activation of pain-sensing nerves. Sometimes these mediators don't have to travel very far at all to get from the originating mast cell to the destination nerve cell because we know that mast cells and nerve cells physically abut one another in many places throughout the body, and these pairs of cells seem to be engaged in constant mediator "cross-talk."

A study suggested starving the mast cells (fasting for 3-4 days) with only bone broth. This would reboot the body and generate new cells. It only lasts about 4-6 months and then you would have to do it again to continue a type of remission. You would also have to continue on a low histamine diet, avoiding major triggers like mold. What do you think about this study?

I'm not sure as to which research study this question refers. Many mast cell disease experts agree that "Step 1" in managing inappropriate mast cell activation in most patients is identifying the patient's triggers as precisely as possible and then doing one's best to avoid those triggers. Therefore, if histamine exposure or mold exposure is a trigger, then avoidance of such a trigger as much as possible is a good strategy to be employed early in trying to gain control over inappropriate mast cell activation. As to the other part of this question, I'd like to first point out that "bone broth" is certainly not a standardized product, so it's quite unclear that what one patient would be getting exposed to with a "bone broth" preparation is likely different from what another patient would be getting exposed to with a "bone broth" preparation, so it’s difficult to generalize from what might be making one patient react to bone broth to what might be making other patients react to bone broth. Furthermore, fasting most certainly puts the body into a state of stress, and in some mast cell patients, stress can trigger a flare of symptoms, so it's not at all clear to me that fasting to any extent would be a good general recommendation for mast cell patients. I think it's important to understand that mast cell disease is an extraordinarily variable disease from one patient who has it to the next patient who has it, and it has been observed that the treatments which help one mast cell patient often are quite different from the treatments which help the next mast cell patient. Until we have a much better scientific understanding (through research!) of the distinctions between different patients' assorted variants of mast cell disease and can then routinely run tests in the clinical laboratory which identify these distinctions, it will be difficult to make general treatment recommendations for the whole mast cell disease population.

Is this study correct? Is this something you have tried with your patients? I am asking because I am a patient of his and was unable to eat for months surviving on just plain Greek organic yogurt was highly malnourished and became reactive to it, leaving me with nothing to eat until my Dr. put an NJ tube in. I was able to tolerate the formula they used even though I was allergic to corn and soy. I tried to drink it and my throat itched. I became asthmatic, and couldn't drink it.

I'm not sure as to which research study this question refers, so I can't say whether "this" is something I have tried on my patients. If I understand the rest of the question correctly, it's describing a patient who was unable to tolerate oral ingestion of a particular feeding formula but who then tolerated the formula OK when it was administered via a nasojejunal (NJ) tube, effectively bypassing the mouth, esophagus, stomach, and duodenum. Yes, I have seen that scenario many times, and it highlights well the fact that not every mast cell in a mast cell patient's body is dysfunctional, and not every dysfunctional mast cell in a mast cell patient's body is dysfunctional in the same fashion. It can easily be the case that only mast cells in one place, or a few select places, in the body are dysfunctional, and it also can easily be the case that dysfunctional mast cells in one part of the body are dysfunctional in ways which are considerably different from how the dysfunctional mast cells in another part of the body are dysfunctional. In the example in this question, it would appear the mast cells in the lining of the GI tract at one or more points from the mouth through the duodenum are abnormally reactive to some component of the formula, while the mast cells in the lining of the GI tract from the jejunum on down are not abnormally reactive and are tolerating all the components in the formula just fine. This variability in behavior of dysfunctional mast cells from one part of the body to another should not be surprising since it mirrors the *normal* behavior of mast cells. Normal mast cells *normally* behave differently in different parts of the body (for example, with regard to the triggers they normally respond to and the mediators they normally produce and release). Furthermore, in those patients in whom mutations in the regulatory genes in the mast cells (and thus also in such mast cells' precursor cells in the marrow) are what's at the root of their mast cell dysfunction, it's always possible that *additional* mutations might develop at any point in time, but it's also easily possible that *different* additional mutations might develop over time in *different* precursor cells, leading to differently mutated populations of mast cells and thus different patterns of dysfunction and misbehavior in these differently mutated mast cell populations. It would seem like every time we think we've come to grasp the full range of complexity of the disease, we then learn of yet another layer or dimension of complexity. There's so much complexity and variability here that it really shouldn't be a surprise to anyone that only in the last decade or so has the medical profession even *begun* to appreciate the existence of mast cell activation disease, let alone have a truly good understanding of it.

I see a genetics doctor as I have EDS "spectrum" and MCAS. They said that they have seen a lot of patients with an EDS like spectrum disorder co-existing with MCAS and that they don't know whether the MCAS is causing the issues with collagen/connective tissue or if it is part of EDS. My question is can MCAD cause issues directly with collagen synthesis and how? I have a vertebral artery dissection and was wondering if there was a plausible correlation.

We do know that normal mast cell function is needed for normal growth and development of most tissues throughout the body, so it is possible that abnormal mast cell function might be able to cause abnormal connective tissue development of the sort seen in hypermobile EDS. hEDS is the most common type of EDS and the only type of EDS in which no mutation in any connective tissue protein has yet been commonly found. However, "possible" and "might be" don't add up to "definite" and "is." The bottom line is that a lot of research needs to be done to truly prove (or disprove) whether MCAS (or at least certain variants of MCAS) is really at the root of hEDS.

Now that Xyzal is OTC would it be more effective than Zyrtec in the current Zantac Zyrtec protocol those with suspected mast cell activation issues try?

It's not presently possible to predict which drugs are more likely to help which mast cell patients. We can't even yet predict which drugs are most likely to help which symptoms in which mast cell patients, and it can well be the case that a given drug helps quite different symptoms in different patients. Again, it's an extremely complex and variable disease. In my experience, most mast cell activation patients who try the different H1 blockers (like Xyzal and Zyrtec) come to find that one particular H1 blocker or another clearly serves them better than the other H1 blockers. The H1 blocker which serves one patient best might well be different from the H1 blocker which serves another patient best. For example, some patients feel that levocetirizine (name-brand Xyzal and other formulations) works best for them, while other patients feel that cetirizine (name-brand Zyrtec and other formulations) works best for them. There are still other patients who feel that loratadine (name-brand Claritin and other formulations) or fexofenadine (name-brand Allegra and other formulations) works best for them. Considering that mast cell activation patients likely will be on antihistamines for a very long time to come -- it seems reasonable for each mast cell patient to take some time to try the different available H1 blockers (preferably the non-sedating ones, given that the disease so commonly causes fatigue) to identify for sure which particular H1 blocker serves him/her better than the other H1 blockers.

If you have additional questions on Mast Cell Activation Syndrome (MCAS), be sure to leave them on our Facebook page here. We will be putting out a new blog post every Friday answering a batch of randomly selected questions posted on our Facebook page.

If you would like to see a NY Mast Cell Activation Disorder specialist, Dr. Lawrence Afrin is now seeing patients in a private practice setting at our office in Armonk, NY. To make an appointment with Dr. Afrin, please call the office or contact us here

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