The ILADS 2018 event was my 13th ILADS annual ILADS event.  About 600 people attended which was a little smaller than the prior year but still an amazing turnout and MUCH larger than my first event in 2006 which may have had 75-100 people.  

Much of my time at this event was spent networking, talking with potential future podcast guests, and talking with people in the exhibit hall.  As a result, I did not get to attend as many of the lectures as I have in past years, but I wanted to share the information I learned from those I was able to attend. I think you will be impressed with some of the upcoming podcasts that will result from connections made at the event as well.

Disclaimer: Nothing in this text is intended to serve as medical advice. All medical decisions should be made only with the guidance of your own personal licensed medical authority.

Disclaimer: This information was taken as notes during the conference and may not represent the exact statements of the speakers. Errors and/or omissions may be present.

Note: As this information may be updated as any errors are found, I kindly request that you link to this single source of information rather than copying the content below. If any updates or corrections are made, this will help to ensure that anyone reading this is getting the most current and accurate information.  

Lawrence Afrin, MD spoke on "Mast Cell Activation Disease: Foundation and Application in Tick Borne Disease Management" and shared:

  • Mast Cell Activation Syndrome (MCAS) may be the primary effector of many symptoms of tick-borne disease and infectious diseases.
  • A complex case of Polycythema vera and another with pure red cell aplasia and another with burning mouth syndrome ultimately mast-cell associated and improved with treatment.
  • Chromogranin elevation in a burning mouth syndrome patient could have led some to explore cancer, but this is also produced by mast cells.
  • The bulk of mast cell diseases are allergic diseases.
  • 20% of the human population may have a mast cell issue; the numbers are increasing in our modern era due to genetic and environmental factors.
  • Mast cell proliferation is seen in mastocytosis; in MCAS they mast cells may be more activated but the number of mast cells is not generally increased as it is in mastocytosis.
  • KIT gene mutations are dominant in mast cell regulatory issues; found in almost every case of mastocytosis.
  • Neoplasia in mastocytosis is a problem for a very small subset; everyone else with mast cell disease has a problem with activation of the mast cells, not the number of mast cells.
  • Mastocytosis is the tiny top tip of the iceberg where substantial mast cell proliferation exists; in mast cell activation syndrome the problem is activation. Mastocytosis, cutaneous mastocytosis, uticarias/angioedema, then allergies and anaphalaxis are huge below the water line in MCAS.
  • Cells originate in the marrow, circulate, reside in vascular tissues with predominance in the environmental interfaces such as the skin, GI tract, and blood vessels. They synthesize a huge array of chemicals called mediators; many more mediators are produced beyond tryptase and histamine.
  • KIT is expressed on the surface of the mast cell ten times more than any other cell in the human body.
  • There can be many different triggers for MCAS including pressure, trauma, heat, cold, UV, and many others.
  • Many different mediators can be released such as pro-inflammatory cytokines, chemokines, proteases, growth factors (including TGFb1), vascular permeability and vasodilation substances, platelet aggregation and thrombosis substances, heparin, chondroitin sulfate, SOD, serotonin, and many others.
  • Far more patients symptoms suggest mastocytosis, but they do mot find mastocytosis when looking.
  • May be diagnosed as CFS, POTS, old age, demyelinating polyneuropathy, Fibromylagia, or many other conditions similar to several blind people being asked to describe an elephant.
  • Proposed criteria for MCAS includes a history consistent with chronic or recurrent aberrant mast cell mediator release, rise in tryptase within 4 hours of a flare (not easy to test and capture), and a response to mast cell-targeted therapy. It is a constellation of symptoms combined with lab evidence.
  • Estimated that 1-17% of the world's population is impacted; closer to 17% is probably the reality.
  • Increasing mast cell involvement in IBS, CFS, Fibromyalgia, diabetes mellitus, obesity, depression, and atherosclerosis.
  • Only one KIT mutation (D816V) can be tested for commercially at present. 
  • Mast cells are 0.02% of the leukocyte population.
  • Mast cells produce more than 200 mediators.
  • There are multiple KIT mutations involved in MCAS; multiple mutated genes.
  • Each mediator has a unique array of direct and indirect, local and remote effects.
  • Inflammation is the universal constant with or without an allergic phenomenon.
  • It is multi-system and often perplexing.
  • Tryptase is not generally high (85% of those with MCAS have normal tryptase).
  • It is easy to get false negative test results; lots of nuances in testing.
  • Mast cell symptoms are over and over inflammation, inflammation, inflammation.
  • You can experience crumbling of the teeth with the best possible dental hygiene.
  • In terms of MCAS and tick-borne diseases (TBDs), he shared:
    • TBDs are absolutely epidemic.  
    • Infections of any type can trigger mast cells.
    • Infection can trigger a major escalation of MCAS which can be permanent
    • TBDs can trigger MCAS normally and abnormally/aberrantly.
    • TBDs can drive a worsening of MCAS even if the insighting stressor has been resolved; MCAS may continue indefinitely.
    • Some may have just MCAS and not an infection to begin with.
    • Infection-induced MCAS or escalated MCAS with or without chronic, active infection can exist.
  • It is more likely that there is one explanation at the root of these conditions rather than 50 different issues.
  • In terms of prognosis, most do well in the long run, have a normal lifespan.
  • There are many helpful treatments available for MCAS.
  • Treatment consists of identifying the triggers and avoiding them.
  • Drugs cannot gain control of the MCAS with persistence of exposure to the trigger.

Bob Mozayeni, MD spoke on "Mast Cells: Considerations in the Lyme or Bartonella Patient" and shared: 

  • Disease results from the host response to the germ.
  • Chronic infections don't directly damage our systems.
  • Borrelia can trigger mast cell activation syndrome.
  • It can activate and then return to normal or remain in an activated state.
  • Mast cells are rare in the blood. They are inside the lymphatics, capillaries, gut, and skin.
  • Bartonella is associated with blood vessels and lymphatics.
  • Bartonella "tracks" is a better term for striae or what look like stretch marks.
  • Ehlers-Danlos Syndrome and Mast Cell Activation Syndrome can occur together.
  • He shared a paper with Bartonella and acquired-EDS type III which resolved with treatment.
  • Aspects of a "Herxheimer" may be mast cell activation.
  • Before implementing antibiotics, consider MCAS treatments such as H1 and H2 blockers.
  • Desloratadine may be helpful for Borrelia; even though it is antihistamine, it also is a manganese transport inhibitor and mast cell activation inhibitor. It penetrates connective tissue.
  • Ketotifen is being used to treat malaria.
  • Mast cells and microbes synergistically support one another.
  • Mast cells play a large role in the diseases that patients have.
  • Simple treatments may reduce inflammation.
  • Mast cell issues can be the primary problem or a reason for symptom persistence.  

Disclaimer: While I attempted to accurately represent the statements of the various speakers, it is possible that the above contains errors or inaccuracies. If you have any corrections to the content listed above, please Contact Me.

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