Mast cell reactivity - two examples

I often describe some post-treatment lyme effects to patients in that certain components of the immune system have developed a "habit" of inflammation that needs to be re-educated and forgotten, if possible. Not really an autoimmune disease per se, but rather symptoms that could be attributed to inflammation that improve when we find the right control.

A complex example is mast cell activation, which sometimes fits the criteria of mast cell activation disorder, and sometimes does not. It rarely fits the criteria for mastocytosis, an increase in the actual number of mast cells versus their activity.

Mast cells are an immune cell that release a host of mediators, including allergic type mediators such as histamine, and flu-sensation mediators like various cytokines. 


I had one patient who responded very well to IV ceftriaxone (an antibiotic) alongside concurrent treatment for bartonella (with oral antibiotics). However, she developed a reactivity of the immune cells that caused mottling rashes, abdominal cramping, and respiratory distress at different times. There was no significant history of "allergies" prior to the lyme treatment (which was quite effective for pain) and it was not a simple post-treatment candida type situation. This responded very well to treatment for mast cell activation syndrome, in this case managed with antihistamines and mast cell stabilizers.

Another patient was from another province and had seen some very good physicians in the states for treatment of lyme. Unfortunately, she had not responded to IV antibiotics nor oral antibiotics for lyme and had sought another opinion from myself. She was a very difficult case, trying in her earnest to get well, but had not responded to months, near a year of various antibiotic treatment. I had worked up her adrenal glands, thyroid hormones, heavy metals, mycotoxins - all the usual "roadblocks" to getting well - but nothing was significant. The only significant hint was a severe facial rash, whenever her cognitive fog would flare alongside other symptoms.

As her rash worsened as we waited for investigations, we trialled cromolyn sodium to stabilize the mast cells alongside loratadine and famotidine. At follow up after 4 weeks - the patient was conversing again with her parents, and starting to even become more social as her brain fog and energy improved, alongside her rash. I was quite surprised at this as previously, anthistamines did not change her rash at all.

Both cases showcase how often there can be a persisting immune system activation, but not really autoimmune disease, that occurs after lyme. It can persist and respond after what appears to be successful treatment for lyme, and also after treatment that has not been effective for lyme.