Review: 'Through the Shadowlands’ describes Julie Rehmeyer's ME/CFS Odyssey
I should note at the outset that this review is based on an audio version of the galleys and the epilogue from the finished work. Julie Rehmeyer sent me the final version as a PDF, but for some reason my text to voice software (Kurzweil) had issues with it. I understand that it is...
Discuss the article on the Forums.

My experience with MCAS, and Xolair (Omalizumab)...

Discussion in 'Mast Cell Disorders/Mastocytosis' started by Amelie, Jun 6, 2016.

  1. Hi, my name is Amélie, and I’m also the person that Kati was referring to in her post here.

    I chose to start another thread so it could be put in the Mast Cell Disorders/Mastocytosis section – since I’m giving more information regarding what MCAS can look like, at least in my case, and not just addressing my specific treatment! I hope you guys don’t mind!

    Basically, I was diagnosed with ME/CFS and fibromyalgia back in 2009.

    However, in late 2015, I was seen by an internist in clinical immunology and allergology here in Montreal who (following a few tests, his clinical observations, the description of my symptoms and list of usual triggers, seeing a few pictures of skin lesions I’d brought him, as well as my current response to treatment) finally diagnosed me with Mast Cell Activation Syndrome (MCAS) in April this year.

    I also have multiple associated environmental and food allergies (so I had very elevated IgE antibody levels on top of MCAS), and am allergic to Benadryl (Diphenhydramine), Aspirin (ASA), and Dilaudid (Hydromorphone).

    As a child, I used to suffer from asthma and recurrent pneumonia (last crisis was when I was 12 y.o.), but didn’t suffer from any known allergies. Then, I developed eczema, an allergy to cats, and a pollen-food (or oral allergy) syndrome later in my teens.

    Things remained fairly stable until 2004, a little before I turned 23, when I had a bout of shingles.

    From there, I started suffering from recurrent URTI, fatigue, headaches, night terrors…

    Then, in 2006, now aged 25, I had a mononucleosis. I did partially recover and was able to return to work, but I kept falling ill on and off with either URTI or a few mysterious, unspecified, “viral infections” (at least, that’s how the doctors diagnosed them. Basically, it just looked like I’d caught “some bug”, but they had no clue which one. Lol!).

    I also began experiencing more and more health issues, such as:
    - Crushing and persisting fatigue with post-exertional malaise and muscle weakness;
    - Sleep disorders (sleep paralysis with lucid hypgnogogic and hypnapagogic hallucinations, idiopathic hypersomnia with morning drunkenness...);
    - Skin lesions that came and went (little tender nodes on both ankles, small itching and bald patches on my scalp, red plaques on my chest when I take a bath, “rosacea” on my cheeks, small ulcers in my nose, etc.);
    - Lower body oedema;
    - Stiffness and aches, especially in the joints (causing more discomfort than real pain though – a bit like when you have the flu);
    - Dysphagia;
    - Gastrointestinal issues (nausea, cramps, vomiting, diarrhea alternating with constipation, abdominal bloating…);
    - Frequent earaches and sore throats (but with no other sign of upper respiratory tract infections);
    - Headaches;
    - Swollen glands;
    - More severe dysmenorrhea;
    - Tremors;
    - Palpitations;
    - Excessive sweating, especially at night;
    - Hyperventilation;
    - Vertigo;
    - Strong working memory issues, inability to concentrate, intense « brain fog »;
    - Nosebleeds;
    - Rectal bleeding;
    - Occasional tinnitus;
    - Sensory overload phenomenon. Inability to tolerate intense and/or multiple stimuli: especially noise, movement, lights, vibrations (ex: of the car), etc.;
    - Body temperature regulation issues (often feels too cold or too warm);
    - Bluish / pales extremities (feet especially, hands can get pale, but not white nor bluish); that can later become warm and a little red;
    - Gradual emergence of new multiple food and/or environmental allergies and intolerances;
    - When tired, especially, I often felt like the skin of my face was on fire, and it was indeed very warm to the touch (as if I was running a fever), but it didn’t really “flush” per say (i.e. didn’t become red);
    - And so forth!

    My family doctor back then gave me a diagnosis of ME/CFS, and I was evaluated just a few months later with a rheumatologist who gave me a fibromyalgia diagnosis.

    In March 2012, Dr. Byron Hyde took over my medical investigations.

    In November the same year, I made a short trip to Ithaca College (New York) to be evaluated by Dr. Betsy Keller (2 days CPET test protocol developed by Stacy Stevens).

    Like most people diagnosed with ME/CFS, the results were that I had a very low anaerobic threshold (2.1 METS, roughly the effort needed to wash your hands), and my VO2Max dropped from 6.2 METS to 5.7 METS if asked to perform the same effort at a 24 hours’ interval.

    While this should have convinced me that I was, indeed, a ME/CFS patient, I still felt the need to continue digging (and thankfully, Dr. Hyde was all too happy to oblige! Lol!), because I really needed to do all I humanly could to understand why this was happening to me.

    Other significant diagnosis I’ve received since 2009 (not already named) include:
    - Attention deficit / hyperactivity disorder (ADHD), predominantly inattentive type*;
    - Dysautonomia;
    - Hyperinsulinism with insulin resistance;
    - Irritable bowel syndrome;
    - Dermographism.

    *Note: I’ve had ADHD since I was a child, but it had simply never been diagnosed since I was a bit of an overachiever at school, and very quiet in class (the kind of kid that doesn’t listen to what the teacher is saying, is unable to prepare for an exam in advance, but will somehow manage to study the night right before the exam in a panic and still get the top grades of her class!). At home, my parents compensated for most of my deficits – my mother, especially, who was a bit overinvolved in every aspect of my life. Plus, I’d developed a few personal coping strategies that involved doing everything at the very last minute when under a good rush of stress and adrenaline to be able to focus on the task (needless to say that being a nurse is probably one of the very best jobs for someone with ADHD given the high level of accountability and stress!). Obviously, the sudden lack of high energy reserves took all those instinctive coping strategies away since I could no longer rely on my ability to do everything all at once like I used to. ADHD + pacing and planning things in advance, and then especially EXECUTING said planning, doesn’t quite match! Lol!

    The MCAS diagnosis obviously came as a great relief (and explained so much!!!), and was a source of hope since my doctor assured me that, although MCAS can be very difficult to treat, a few of his patients did manage to reach a very decent level of recovery, and were able to reintroduce some of the activities they loved into their lives!

    Before my current treatment, I was virtually homebound (except for when I needed to go out for medical appointments). Otherwise, I could manage going to the movie theater about 4 times a year on a really “good day”, and/or the occasional family dinner with my partner’s family (thankfully, they are EXTREMELY respectful and understanding towards my illness, made special meals that wouldn’t trigger my symptoms, and allowed me to go rest in a quiet bedroom for as long as I needed during and/or after any family event).

    I usually stayed strictly inside the house with very opaque curtains, because direct and/or indirect sunlight is one of my very worst triggers (this, combined with some of my skin lesions, made us think that I might have lupus at some point. However, my adverse response to sunlight is systemic rather than cutaneous, and I didn’t meet enough criteria for the diagnosis). Sunlight made me feel dizzy, nauseated, shaky… Actually, the best comparison would probably be that I felt as if I was highly inebriated or intoxicated each time I was exposed to just a bit of sun.

    I could wash myself and walk a bit around the house on my own most days, but my partner needed to take care of all other tasks. He’s the one who took care of all the cooking at home (he prepared full meals for me in advance, that I only needed to heat in the microwave for lunch… Actually, he still does that! Lol!).

    Like Kati was explaining, in January this year, I began receiving Xolair (Omalizumab) injections, 300mg every 4 weeks.

    Xolair is an anti-IgE antibody from the monoclonal antibodies family (same family as Rituxan (Rituximab), Remicade (Infliximab), etc.). However, it seems that MCAS patients have been responding positively to it regardless of whether they had elevated IgE levels pre-treatment or not! So the exact reason why it seems effective with some MCAS patients when MCAS itself (except secondary MCAS) is not supposed to be IgE dependant is not quite well understood.

    It is given subcutaneously by nurses (you can't bring the medication back home and give it to yourself, or have a family member do it for you), in a medical clinic where there is at least one doctor present in case of an adverse reaction. For the first 3 injections, you must remain under supervision for 2 hours following the injection in order to make sure it is well tolerated.

    But, afterwards, the appointments take roughly 15 minutes, since you can leave right after receiving it.

    It can also take a few doses (3 to 4) before you start noticing its effect. Personally, the medication really started to make an important difference for me after the 3rd injection in March.

    A small correction to Kati’s initial post: I am not the one who suffered from headaches as a side effect of the medication, but a few other MCAS patients I had the chance to speak with.

    I do feel SLIGHTLY more tired on the day I receive the injections, but otherwise I’m perfectly fine! Xolair is extremely well tolerated in my case.

    My doctor initially wished for me to receive 375mg every 2 weeks, but my insurance company refused. He’s now trying to push for 450mg every 4 weeks, with the hopes of being able to increase the dose to 600mg every 4 weeks. But there again, my insurance company has been pretty firm on the fact that they will only agree to pay for 300mg every 4 weeks.

    In Canada, Xolair is only recognized for two clinical applications: allergic asthma and urticaria.

    Thankfully, I do have urticaria, so he’s allowed to prescribe it. But the maximum dose officially recognized by Health Canada in order to treat urticaria here is 300mg every 4 weeks, so my insurance company won’t accept to cover for anything more than that (at least, thus far).

    Still, given the current results, I do feel rather fortunate to be able to receive it at all!

    Because I have been responding rather amazingly well to that treatment (in my humble opinion! Lol!).

    Last Friday, for example, I was able to walk 0.5 mile (800m) from my home to a local restaurant to enjoy a wonderful meal outside in the sun on the terrace with my boyfriend! I was able to drink a nice glass of wine, too, without any issues!

    My legs were aching (but I believe it is more from lack of use over those 7 years), but the fatigue I felt when getting there (and later coming back home) was overall “normal”, I think, and not accompanied by any other specific discomfort.

    From what I can tell, it was just the overall feeling of having provided a significant physical effort that my body is no longer quite used to provide, that was then relieved by sitting down and enjoying our meal.

    I was also able to start reintroducing a few foods (even those that cause true allergic reactions as opposed to an intolerance) in my diet. Alcohol (in very small quantities), chocolate, poultry, SOY (One of the most annoying allergies to have! There’s soy virtually everywhere! You can’t escape it!)… All things I can safely eat again!

    The foods I’m most allergic to will be reintroduced a little later, once (or if) I’ve continued to improve.

    And later today, I plan on going to have lunch at the food court of our local mall, and doing a tiny bit of shopping.

    I’m still highly deconditioned, and have good bouts of brain fog every now and then, but it’s much less severe than it used to be!

    I can try to slowly push back my limits without fear of “crashing” the next day (or the day after) and making my illness worse!

    If I’ve been pushing myself too hard, a day or two of “taking it easy” will be enough to make me return to my previous level of functioning.

    Please note that not all the people I’ve spoken with (on a MCAS forum on Facebook) had positive results with Xolair. Like most medications, having a matching diagnosis does not guarantee that two patients will respond the exact same way to treatment.

    But I still wanted to share my own experience so that you guys know that this treatment option exists (and is occasionally used for MCAS patients) somewhere out there!

    Not sure if I should put disclaimers, but beyond being a patient that receives the treatment I have no personal affiliations with the company that produces Xolair. Lol! I've just been extremely lucky that it's been helping me get parts of my life back thus far...
     
    anni66, Wonko, Gingergrrl and 12 others like this.
  2. Sidereal

    Sidereal Senior Member

    Messages:
    3,097
    Likes:
    17,177
    Thank you for taking the time to post this extremely informative post, @Amelie. I can relate to almost everything in your history. There is a subset of us with MCAS and it's very frustrating how this has been totally neglected in ME/CFS research. In my experience, most immunologists don't even accept that MCAS is a real condition.

    (Tagging @Gingergrrl and @justy as I think they'll find your post very interesting.)
     
    Wonko, Gingergrrl, Misfit Toy and 2 others like this.
  3. My pleasure! :)

    I was actually seen by two other immunologists (including another one who was also an internist in clinical immunology and allergology), and both of them completely missed it!

    (Actually, I was evaluated / followed by a grand total of 24 different doctors over the course of 7 years! Lol! So a few medical specialties have tended to repeat themselves.)

    The thing is, for those few doctors who are aware that MCAS exists, I think they tend to make the connection when the patient suffers from more dramatic anaphylactoid reactions that require hospitalization, and/or when they present the more classical cutaneous manifestations of the syndrome.

    When the manifestations are more (multi)systemic - and/or if you've already received a ME/CFS diagnosis (which sadly tends to provide the perfect excuse for certain doctors to avoid investigating further, when they don't believe that they are in front of a patient with a somatic symptom disorder!) - I'm not sure that they will realize that mast cells might be involved. At least, not unless they have a specific interest in MCAS and mastocytosis.

    I'm at the point right now where I think almost every single patient who were given a ME/CFS diagnosis at some point in their lives should get screened for MCAS and mastocytosis.

    Not that I think they are the exact same entity per say. But MCAS is such a recent diagnosis that I'm fairly sure a large majority of the patients that would fit the MCAS criteria today were diagnosed as having ME/CFS in the past.

    Plus, I imagine that being able to isolate that particular subgroup and put those patients together would definitely help with ME/CFS research.

    When I hear about drug trials for ME/CFS patients that don't have a high enough success rate with the patients to get approved (ex: Ampligen) for treatment, I can't help but wonder if one of those reasons might be because what causes the ME/CFS-like manifestations is too diverse in the patients that were selected to participate to the study.
     
    ScottTriGuy, PhoenixDown and halcyon like this.
  4. Vasha

    Vasha Senior Member

    Messages:
    119
    Likes:
    376
    Hi @Amelie -

    Thanks for sharing your story! If you don't have it, you might want to get Dr. Afrin's new book, "Never Bet Against Occam" about MCAS. It's long and case-history based. He talks about a lot of different medications he tries with patients including omalizumab -- but also others if you end up considering trying additional things.

    -Vasha
     
    Amelie likes this.
  5. ukxmrv

    ukxmrv Senior Member

    Messages:
    4,335
    Likes:
    4,407
    London
    "I'm at the point right now where I think almost every single patient who were given a ME/CFS diagnosis at some point in their lives should get screened for MCAS and mastocytosis."

    Is this a clear diagnosis with simple, available tests?

    (and I am delighted to hear of your progress!)
     
    JaimeS and Amelie like this.
  6. @ukxmrv the answer would be no, yes, and sort of 'yes and no'. Lol!

    Just like with ME/CFS, since MCAS mimics a very large number of other diseases, you also need to rule out other causes behind the multi-systemic symptoms.

    However, given that all patients with ME/CFS should already have been thoroughly investigated for other disorders and diseases (since ME/CFS is still considered in very large part an exclusion diagnosis), that part of the process should already have been completed.

    Another tricky thing is that some of the tests can come back negative if the patient is not experiencing their symptoms at the moment where the samples are taken. So there might be a need for retest, especially serum tryptase in the case where Systemic Mastocytosis is suspected, if I remember correctly.

    "A MCAS diagnosis is made if the patient meets those criteria:
    • Recurrent or chronic symptoms of mast cell activation.
    • Laboratory results showing evidence of mast cell activation (eg, a transient rise in serum tryptase (>15 ng/mL but <20 ng/mL) or urinary N-methyl histamine, or the histamine metabolites prostaglandin D2 and prostaglandin F2-alpha.
    • Response of clinical symptoms to anti-mediator therapy."
      (Source)
    In my particular case, my serum tryptase levels came back normal (something very common for MCAS patients), but the urinary histamine metabolites prostaglandin D2 and prostaglandin F2-alpha were elevated.

    There was also a number of other blood tests that were done in order to rule out other disorders involving the immune system, I think... I could give you the list, but I'm not sure if it is entirely complete because some of the tests had already been done by Dr. Hyde, I think, and I'm not sure that my immunologist has repeated those.

    Obviously, the blood tests and 24 hours urine sample collection themselves are fairly simple!

    But the urinary N-methylhistamine and/or 11β-prostaglandinF2α tests aren't available here in Canada. So we had to send my urine sample to the Mayo Clinic in the USA in order for it to be analyzed.

    My immunologist also needed to wait to see how I was responding to treatment before concluding that I was indeed a MCAS patient. So this would obviously cause some delay for the patient to receive the diagnosis, especially if the first treatment chosen doesn't produce any positive results.

    As for Mastocytosis, the tests involved in its investigation and diagnosis criteria can be found here. As you can see, it is a much clearer diagnosis to make, and one that doctors are generally more familiar with.

    For the few doctors who are familiar with Mastocytosis, once the serum tryptase levels come back normal and they've ruled out that possibility, they don't typically think to consider MCAS as well!

    (Thank you so much! :) )
     
    ScottTriGuy and ukxmrv like this.
  7. Thank you for the suggestion @Vasha ! I'll be sure to look into it! :)
     
  8. Jesse2233

    Jesse2233 Senior Member

    Messages:
    1,724
    Likes:
    4,339
    Southern California
    Hi @Amelie

    So happy to read about your success. Gives us all hope

    When you were working with Dr Hyde, did he ultimately diagnose you with ME? And did he find stomach enteroviruses and brain hypoperfusion?
     
  9. Hi @Jesse2233!

    No, Dr. Hyde used to call me his "mystery girl", because I hadn't been exposed to any enteroviruses, and most of the clinical findings did show that there was something "not quite right" happening with me, but they failed to fit any specific diagnosis.

    Until Mast cell activation syndrome, that is. ;) But even there, all it really means is that my mast cells are hypersensitive to virtually anything and everything and hyperesponsive, but we've got absolutely no clue why!

    A lot more helpful than CFS as a diagnosis, because it allows my immuno-allergologist to use mast cell stabilizers to help me get significant relief from my symptoms and at the very least we understand some of what's happening...

    But why? i.e. What triggered the MCAS, and/or what's currently causing the dysfunction? No idea!

    And previous SPECT scans showed dissociation between certain areas of the brain + signs of dysautonomia, but I don't think there was hypoperfusion.

    I am, however, supposed to do another brain SPECT scan in Ottawa in the very near future (referral has been sent, but I don't have the date for my appointment yet) to get a better view of what's going on in there.

    Basically, the first SPECT scans were done with an old machine, and Dr. Hyde wants to have a SPECT scan done with a more modern and precise one, and then send the data to Chile, because they have one of the best computer programs to analyze the data over there, I think.

    I'll try to remember to keep you guys updated if we find something interesting that might either further differentiate me from ME patients, or show similarities between what's happening in the brain of a ME patients v.s. a patient with MCAS of unknown cause (idiopathic).
     
    ScottTriGuy likes this.
  10. Jesse2233

    Jesse2233 Senior Member

    Messages:
    1,724
    Likes:
    4,339
    Southern California
    Thanks for the thorough explanation!

    Interesting on the SPECT scan. Did Dr Hyde say your results were in any way consistent with ME patients? And is POTS still present with omalizumab?
     
  11. Jesse2233

    Jesse2233 Senior Member

    Messages:
    1,724
    Likes:
    4,339
    Southern California
    Also @Amelie

    What were your Prostaglandin F2alpha levels? Mine are 555 with a ref of 80-240
     
  12. Gingergrrl

    Gingergrrl Senior Member

    Messages:
    9,543
    Likes:
    24,660
    USA
    I agree and I do not know how I missed this thread last year and never realized that I had been tagged!

    Thanks for tagging me (even though I did not see it at the time)!

    I agree except that there are so few MCAS specialists in the U.S. (and in the world) that it would be very hard for people to be tested. Although at least there are actual tests that can be run that serve as markers (like histamine, prostaglandins, tryptase, etc) unlike in ME/CFS.

    I agree and do not think they are the same entity but there is lots of overlap.

    It's the weirdest thing, @Jesse2233 re: my Prostaglandin F2 Alpha levels. In my most recent test (March 2017), they were 1,452 (also with the 80-240 reference range) yet I have not had an allergic reaction to a food or smell in over one year. I can eat the highest histamine foods (soup from a can, spices, red tomatoes, citrus, yogurt, leftovers, etc, with no limitations or reactions) and I can eat without food including in restaurants without taking a whole shit-load of MCAS meds 30 min prior to eating.

    The only thing I continue to avoid is FD&C food dyes and certain preservatives b/c I don't think the risk is worth taking but for all I know even those are okay now. Back in 2015 when I was in hospital with anaphylaxis to all food but water, my PG F2 Alpha levels were just barely above the normal range! I wish I knew what this all meant. My MCAS doc says the numbers will always fluctuate, and was not overly concerned, and I still take one full set of MCAS meds every day to be safe (and pre-meds for every IVIG). But outside of IVIG, I have not taken my rescue med (Atarax) in over one year.

    I would rather be MCAS symptom free and have the bad numbers than vice versa. I just find it strange! Do you know what this might mean @Amelie?
     
  13. @Jesse2233 , actually, I may have (sort of) failed the test for POTS… Maybe…

    However, I was diagnosed with dysautonomia, given that my blood pressure fails (or used to fail, it’s a bit hart to tell) to increase with physical exercise.

    Actually, I think this might be explaining why my heartrate would raise for more than 40bpm when I went from lying down to sitting; and the same thing occurred when I went from sitting to standing.

    Except when I did the tilt table test, the results came back perfectly normal.

    I don’t think the positioning itself was the issue, but rather the physical effort required to change positions.

    See, histamine is a very potent vasodilatator.

    And the more I moved, the more histamine used to get released into my system.

    So, it makes a lot of sense that, as soon as I’d reached my “degranulation threshold”, my mast cells would start pumping tons of histamine into my body.

    And while the histamine lowered the blood pressure, the physical activity made it rise – so those two opposite forces might have sort of cancelled out each other during the CPET, and the blood pressure values remained the same.

    And, in order, to compensate for the blood pressure dropping / not rising while the level of activity increased, then the heartrate needed to get higher.

    So, I’m thinking it just might be the effort required to change position by myself that made my blood pressure drop and my heartrate increase, as opposed to the change of position itself.

    I went from resting to making the effort to sit. And then from sitting to making the effort to stand. It may not seem like much but that used to require a pretty huge effort.

    But, of course, that’s just my theory.

    And the thing is that I haven’t done another CPET since I started receiving those treatments. We do know they’re working because of the fact that I no longer get triggered as I used to, and my activity levels have dramatically improved.

    But I’m not sure if I still suffer from some level of dysautonomia or not… My pulse can reach sometimes 180 bpm during my bellydancing classes, and that’s quite high. But I don’t get any PEM, and recovery time seems fairly normal, so at least there’s that!

    I was also able to go on this ride this summer:

    I used to have a crazy high tolerance to thrill rides, so usually, I would have been able to do it like 4 times in a row without issues. This time, however, I had to wait about one hour (the time to go drink some juice, eat a bit, and take a rest) before I was able to go on another thrill ride, namely that guy ( ).

    So, for a girl who would get sick just riding 20 minutes as a car passenger before she began receiving treatments, and then would need a few weeks to recover, I think that’s pretty much day and night.

    To know if I still have some level of dysautonomia for sure, then I’d need to do another CPET and watch how my blood pressure responds to physical activity, but I think we can conclude that if I still have any level of dysautonomia at all, I’d be surprised it would be related to passive positioning (because keeping my rear end seated in those rides didn’t make me pass out! Lol!).

    I don’t think Dr. Hyde and I ever really took the time to discus how my tests compared to ME patients… I think that, once the results came back that I hadn’t been infected with an enterovirus, then we just straight out continued to try to figure out what could cause my symptoms.

    After I do my SPECT scan and we get the results, I’ll try to remember to ask him what the differences between my results and those he typically finds in ME patients are.

    I know that some of the SPECT scans we did back in 2012 and 2014 (with less precise imagery) showed something that was associated with dysautonomia, and there were some abnormal findings… Like some cerebellar diaschisis, dissociation between certain areas of the brain, and certain deficits that shift when I’m at rest or tired.

    Otherwise let me check my results…

    My 11 Beta-Prostaglandin F2 alpha levels were 1216 ng/24hrs, reference value < 1000 ng/24hs.
     
    ScottTriGuy, Gingergrrl and Jesse2233 like this.
  14. @Gingergrrl, well, I'd say that depends on what type of MCAS medication you are taking...

    Are you taking antihistamines and/or other meds whose job is to block the mast cell's chemical mediators from binding with receptors?

    Or are you taking mast cell stabilizers, supposed to prevent the mast cells from degranulating?

    Because if you're taking meds aimed at preventing mediators from binding with receptors (like antihistamines), that won't change the amount of mediators being released into your body, and therefore it shouldn't influence your PG F2 alpha levels (I think!).

    The mediators are still there, because the meds just prevents them from signalling other cells in the body, and triggering some of the symptoms. They block the messages from being delivered, but they don't kill the messengers! ;)

    While mast cell stabilizers, at least from my understanding, are preventing the onset of mast cell degranulation, so they are essentially preventing the mast cells from giving birth to those messengers in the first place.

    Omalizumab (Xolair) might actually kinda do both, though we aren't 100% clear on how...

    I've seen some people report that there would be an increase of free IgE in the patient's body with Xolair, because Xolair prevents IgE from binding themselves to receptors, but do not inhibit their production.

    IVIG might perhaps bind themselves to receptor sites on the T and B cells and/or monocytes? So that wouldn't necessarily stop the mast cells from being triggered and producing prostaglandins?

    I'd have to look a bit deeper into that...
     
    Gingergrrl likes this.
  15. Gingergrrl

    Gingergrrl Senior Member

    Messages:
    9,543
    Likes:
    24,660
    USA
    So would you say that this is the #1 connection between MCAS and POTS since the two conditions so frequently go hand in hand? I know that histamine makes the membranes more permeable so third spacing occurs but wasn't really thinking about the extent that it is a potent vasodilator. I guess this is why I have always had hypotension (but I did not develop POTS until 2013 and did not develop MCAS until 2015). We believe that a virus triggered the POTS and hardcore mold exposure triggered the MCAS (which was most likely already there but sub-clinical).

    I 2015, I was taking literally everything known to man to try to stop the episodes of anaphylaxis. I have never tried Xolair or Gleevec but short of that, I tried everything in mid 2015 out of desperation until I was put on IV Benadryl in hospital (which I could only tolerate short-term). Once I saw my MCAS specialist in July 2015, we found a plan that worked which ultimately became: Zyrtec, Pepcid, Ketotefin, Quercetin + Vit C, and Daosin. My rescue med was Atarax and at that time, I was having to take it several times per week but now I only take it as a pre-med for IVIG.

    It was not until IVIG that my reactions to food and smells went into remission and have stayed there for over one year. My POTS/dysautonomia, breathing and muscle weakness, and other issues did not go into remission and I remained very functionally impaired (having to use wheelchair 24/7, unable to drive or climb stairs, etc) but the allergic reactions literally stopped and have never returned. My MCAS doctor said he has had many patients achieve permanent remission to MCAS from IVIG but he has never explained the mechanism of how. I want it to be permanent once I stop IVIG but am still not 100% certain that it will be.

    It sounds like you are thinking that IVIG might bind itself to receptor sites of T and/or B cells or monocytes? I just Googled "monocytes" b/c I forgot what they were :D and it sounds like they are a type of WBC? Are they produced by the B cells (if you happen to know)? I am also doing Rituximab, and my B cells are currently at zero, but my remission to MCAS allergic reactions occurred from IVIG at least one year prior to doing the first two infusions of Ritux.

    In dummy terms (for me) it sounds like the IVIG is potentially blocking something and stopping the allergic reactions from being triggered but it does not stop prostaglandins from being produced so my levels are still fluctuating? They are not always as high as they were in the test that I had in March 2017 which to be honest, was shocking to me.

    My main doctor is having me do blood work prior to my next IVIG cycle (which starts 8/31) and amongst a bunch of other stuff, he is testing my histamine, PG D2, PG F2 Alpha, Tryptase, and Chromogranin A levels.

    I would love to hear anything that you learn or hypothesize on this issue! I am having many global improvements from the IVIG and Rituximab and cannot imagine the thought of the allergic reactions coming back once I stop IVIG. I am happy to take MCAS meds for the rest of my life as long as I never return to how bad it was in 2015 when I was hospitalized.
     

See more popular forum discussions.

Share This Page