Q1/2
Is it possible for MCAS to cause the loss of ability to smell?
If so, how would it possible for the ability to taste not to be affected at the same time?
A
I have never heard of that happening but mast cell disease can cause some weird neurologic symptoms. The smell/taste thing could be a couple of the things. It's possible that you have swelling or narrowing of your sinuses so the smell is obstructed from getting to the right place. You could have damage to the olfactory tract, the specific nerve set that transmits smell to the brain. Taste is from two things: your sense of smell and the taste buds on your tongue. So no sense of smell doesn't always block taste.
Q3
Is there a trend towards getting stricter criteria for MCAD diagnosis?
Why?
A
Yes
Q4
I've heard that the immune system naturally down-regulates in males during the ages of 21-24 and in females a few years later leading to a possible suppression of MCAD symptoms. Is there any validity to this theory?
A
I've never heard of it and I know plenty of mast cell patients in those demographics.
Q5/6
Why do mast cell stabilizers like cromolyn and ketotifen often cause a spike in symptoms when first starting, or titrating a dose upwards?
Some doctors say to start at full dose, others say to start low and work up. Is there any evidence about which is really best, as far as keeping the initial symptom flare low AND short?
A
We don't why this happens. There have been studies on cromolyn but not for mast cell disease. Those studies mostly indicate that it's okay to start at the full dose. But most mast cell patients don't tolerate that with cromolyn. Ketotifen doesn't cause symptom spikes like cromolyn as often but it can take time to acclimate to the side effects.
Q7
Are there any statistics on symptom severity or quality of life?
A
Yes, there are. What specifically are you looking for?
Q8/9
Do you have a list of questions you ask before agreeing to medication changes, additional testing, or invasive procedures/surgeries?
If you agree, how do you document your experience? Do you have a template you can share?
A
Not at this point because I've been entrenched in the science of my disease for a long time. This is a good question. I'll do a blog post on this.
Q10/11
Can a Zenkers Diverticulum (age 29) and/or failure to granulate post surgery, be related to Systemic Mast Cell Disease? Or are they just weird, rare happenings?
Also, does untreated mast cell disease confer a greater risk of infections?
A
Zenkers can activate the local GI mast cells and respiratory mast cells. I don't know anyone with mcas secondary to Zenkers but really anything that irritates your GI tract can cause mast cell symptoms.
Failure to granulate can be chronic mast cell activation but it is more often from a relative connective tissue disease like EDS. Mast cell mediators could either interfere with tissue remodeling to heal a wound or cause excessive scarring.
No.
Q12
Why do I have so much skin and nail problems after anaphylaxis/shock?
A
Skin is because so many effects of anaphylaxis affect the skin. You have tons of mast cells in your skin. Hives, rashes and angioedema can further activate them.
I don't know for sure about nails but using epinephrine decrease circulation to the fingers and toes and that can cause nail problems.
Q13/14
When both adrenal insufficiency and mast cell activation are involved, which is primary, or likelier to be primary?
If adrenal insufficiency is primary, how does it trigger development of mast cell activation? If mast cell activation is primary, how does it trigger development of adrenal insufficiency?
A
You can be tested to ascertain if the AI is primary (Addison's Disease) or not. I wrote some very detailed posts about this:
http://www.mastattack.org/2015/02/corticotropin-releasing-hormone-cortisol-mast-cells/
Sorry, I just went looking and can't find it either. Let me see if I made it private or something.
The cortisol interaction series explains the molecular interplay between cortisol level and mast cell activation. You can test for addisons to see if the AI is primary or not. If you have Addisons, the reasonable assumption is that mcas is secondary.
Low cortisol can trigger immune activation and inflammation since cortisol keeps this in check. So AI can directly induce mast cell activation. That's why steroids help us to not be so reactive. On the other hand, chronic inflammation can cause a sort of adrenal burnout where your glands stop producing as much cortisol due to high demand for too long. And then there's the fact that long term use of systemic steroids for mast cell symptoms (or anything) directly causes adrenal insufficiency because your body stops making the hormones to tell your adrenals to make cortisol.
I'll let you know when I find the post.
Q15/16
What are the symptoms of elevated prostaglandin levels?
What are the medical and alternative treatments available to treat elevated levels?
A
Flushing is the big one. High or low BP, tachycardia, excessive sleep.
Anything that is a COX inhibitor will decrease production of prostaglandins. This includes aspirin and NSAIDs. Turmeric and holy basil are both Cox inhibitors.
Q17
What is the efficacy of low dose allergen therapy (LDA) as a treatment for MCAD?
A
“ I know plenty of mast cell patients who have used allergy shots or oral immunotherapy to improve trigger tolerance. I can’t think of any reason why this wouldn’t help if you could safely increase the exposures.”
http://www.mastattack.org/2017/07/mastattack-107-laypersons-guide-understanding-mast-cell-diseases-part-50/
Q18
Why does glucagon help with ending anaphylaxis?
A
“Beta blockers directly block many of the places where epinephrine works to mitigate anaphylaxis. This means that using epinephrine to treat the anaphylaxis may be ineffective. Patients who must take beta blockers may be given a glucagon autoinjector for use prior to using injectable epinephrine. The reason for this is glucagon is the antidote to beta blocker overdose.”
http://www.mastattack.org/2017/03/beta-blockers-epinephrine/
The reason epi treats anaphylaxis is because it binds to the beta adrenergic receptor. This initiates a series of steps that result in cells making more of a molecule called cAMP. Glucagon can bind to another receptor and cause the same increase in cAMP. It's basically a back door.
Q19
Is there any information about mast cell disorders and improving the odds for successful breastfeeding? If not, no worries.