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Rituximab for MCS and CFS

Discussion in 'Rituximab: News and Research' started by kyzcreig, Jul 30, 2017.

  1. kyzcreig

    kyzcreig Senior Member

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    I am currently 3 weeks into Rituximab for CFS and MCS (multiple chemical sensitivity). I am seeing a 25% reduction in symptoms, greater than any therapy I have tried. I will periodically update with how I am doing.

    According to Fluge and Mella case studies CFS patients that respond see benefits as early as 2 weeks, most notice something after 5-6 weeks. Reduction in symptoms continues up to the 14th week, afterwhich there is remission or a gradual return of symptoms. (R)

    What Have I Noticed So Far?
    Since my illness began I have had chronic fatigue, PEM, and a growing list of environmental and food sensitivities. If I ate the wrong food or breathed air with cigarette smoke I could suffer a migraine, palpitations, lassitude and asthma-like symptoms for hours after. Immunosuppressant treatments helped. My go-to remedies were breathing oxygen, IV ozone and high dose vitamin C. I have been managing fatigue with supplements and nutritional IVs.

    Since the second week post-infusion I have noticed my symptoms are increasingly less severe and shorter in duration. At first it was subtle but now in the third week it is significant. Many foods I couldn't tolerate before I no longer have problems with. This includes supplements, many of which I saw significant benefits from but had to discontinue.

    About Me
    Before trying Rituximab I had markers of autoimmune illness. My ANA had been elevated since onset, so had Sjogren's Syndrome Antibody B, and C3 was chronically low. At one point my ANA titer was 1:1280 Homogeneous, the highest the lab can measure, typically only seen in severe autoimmune illnesses. I did not have clinical manifestations of Sjogren's or any other characterized autoimmune illness and did not respond to Plaquinol. (R1, R2)

    I had other less clinical markers, including elevated IL-6 and IL-17 in PBMCs, elevated NO, elevated Nitrotyrosine, low NADPH, low ATP, low GSH, elevate lipid peroxides, dysregulated methylation cycle, dysregulated redox enzymes in RBC. (R1, R2, R3, R4, R5)

    There was more. I spent hundreds of thousands of dollars on testing, treatments, supplements and countless hours reading scientific literature. You can see some of this in the link provided down below. As mentioned I respond strongly to immunosuppressants, including corticosteroids, HBOT, Ozone IV, nutritional IVs, anti-inflammatory herbs, sunshine, exercise, FTIR sauna. But none produced a lasting or significant improvement in environmental sensitivity. They were palliatives at best.

    As I am sure many of you have, I was told there was nothing wrong with me, insinuated I was a hypochondriac, that I was stressed or some other nonsense palaver. Unfortunately, that is the FDA authorized response. As my knowledge of medicine and biochemistry grew this gave way to "I don't know enough to help you", "we don't know everything". I had to be more knowledgeable and kidglove (downplaying my non-specific symptoms) to be taken seriously. I was referred to both UCLA and Stanford and heard more of the same there. I have seen Dr. Rea in Dallas, OMI in Mountain View and plenty of other "experts".

    On the flip side I have known people who claimed to be very unwell and then completely "recover" after DNRS...

    My illness began after using Accutane for 6 weeks when I was 18 years old. Accutane is associated with autoimmune illnesses including Crohn's and IBD, as well as changes in DNA transcription and methylation patterns in T-cells. The latter can be long lasting. (R) Epigenetics is a burgeoning field with many autoimmune diseases expressing similar patterns in epigenetic control mechanisms e.g. DNA methylation, histone acetylation, miRNA. (R) For example, drug induced lupus and systemic lupus erythematosus express an identical DNA methylation pattern with no significant genetic difference to controls. But the former disappears as soon as the offending drug is discontinued. This is an important thread to unravel.

    You can read about my symptoms, testing, illness onset and supplement regiment here.

    How Did I Get Rituximab?

    Without a well characterized illness you will have a hard time getting treatment in the West. So, I flew to Taiwan. A friend walked me through the medical system. It is ranked best in the world, it would be top of the WHO rankings if it was recognized as a sovereign nation (One China Policy).

    The trip was hard on my health. Even with all my amenities I can't control the environment and get exposed to something (perfumes, foods, etc.). Fortunately my friend arranged everything in advance, the hotel didn't smell like mold or cleaning chemicals, the food was plain and I didn't react.

    It took about a day to get an appointment with one of the top rheumatologists at the top hospital in the country. I brought my friend to translate but the doctor (and apparently every doctor) spoke English. We spoke for 30 minutes in a 10 minute appointment. Afterwards he asked to see me when his shift ended at 5:30pm. We spoke for an additional 90 minutes. Never was I disbelieved or disrespected. When I mentioned scientific literature they asked to see the paper, to evaluate the impact factor of the journal, etc. When I showed blood work they weren't skeptical implying only their lab was valid. It was refreshing. I made a case to try Rituximab. It was in Phase III trials, 66% of patients responded, I had responded to immunosuppressant treatments and my blood work suggested autoimmunity. I was going to pay out of pocket. The doctor agreed to try it if I was comfortable with the risks.

    After additional blood work and two days later I received my first 1000mg infusion, two weeks later I received the second, as per the Phase II study's protocol. (R) Each infusion, including necessary screening, blood work and hospitalization, was ~$4000USD. The Rituximab itself was $1200 per 500mg. During the first IV I had a mild infusion reaction of urticaria which happens ~30% of the time and dissipated with corticosteroids. (R)

    The first two weeks I noticed nothing or only subtle improvements. I also noticed transient side effects, like aches and itches. This is not mentioned in the medical literature but anecdotal reports corroborate it. After the third week it was difficult to deny I was seeing significant improvements.

    How Does Rituximab Work?
    The following paper discusses Rituximab's MOA in Rheumatoid Arthritis, you can extrapolate to autoimmune illnesses in general. I have included excerpts below.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3392126/

    While time will tell whether this major alteration of the immune system has other consequences, it is remarkable that drastic reduction of B-cell numbers over the long term is tolerated so well, and that it maintains efficacy in RA therapy.

    The mechanism of action of rituximab in RA remains controversial but is unlikely to be simply from decreased humoral immunity. Rituximab treatment results in a rapid fall in all mature B-cell subsets, with the exception of plasma cells [9]. Antibody levels (*and autoantibody) are unchanged or fall modestly [10], probably reflecting an incomplete depletion of B cells in the spleen, lymph nodes and marrow [11].

    *According to Jonathan Edwards autoantibody levels fall in proportion to the reduction of inflammatory markers e.g. CRP, which are affected by B-cell depletion.
    It seems probable that the mechanism of B-cell depletion in autoimmune diseases such as RA in part reflects the role of B cells as a source of cytokines, or as antigen-presenting cells [11,15]. Additional mechanisms are possible, such as a role for B cells in influencing dendritic cells or T cells [16], or effects on a small CD20+ T-cell population that may be more prevalent in RA patients [17].

    The most alarming rituximab-associated opportunistic infection is reactivation and neurologic infection by JC virus, causing progressive multifocal leukoencephalopathy (PML). There have been only limited case reports in RA patients treated with rituximab. A few of these reports are confounded by treatment with other immunosuppressive agents and, in one case, chemotherapy and radiation therapy after rituximab and a few months prior to onset of PML [36,37]. The incidence of PML in RA has been estimated at 0.4 per 100,000 versus 0.2 per 100,000 in the general population, so there is a suggestion of increased risk with rituximab-treated RA patients. There have been more cases and probably more risk of PML in systemic lupus erythematosus patients and hematologic malignancy patients treated with rituximab.

    In summary, with the notable exception of hepatitis B, and not including the remote risk of PML, there is little evidence that patients whose B cells are chronically depleted are at any higher risk of infection.
    -​
    Is Rituximab Safe?
    Side effects are "rare but there", please read the following paper:
    http://www.tandfonline.com.sci-hub.cc/doi/full/10.1080/10428190902934944
     
    Last edited: Aug 1, 2017
  2. Hip

    Hip Senior Member

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    That's fantastic that you appear to be responding so quickly; I hope the improvements keep coming.

    Will you have to fly back to Taiwan in a few months for the maintenance infusions? In the Fluge and Mella phase II trial, they gave 2 initial infusions in the first two weeks, then maintenance infusions at 3, 6, 10 and 15 months.

    Does your ME/CFS satisfy the strict CCC definition of ME/CFS (see page 2), by the way?
     
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  3. kyzcreig

    kyzcreig Senior Member

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    I will play subsequent infusions by ear. I would have to fly back. I am of course trying not to get my hopes up but I have seen remarkable improvement already and even if I return to baseline next week it would have been worth sharing/experiencing.

    I have a list of therapies I would still consider trying e.g. DMARDs like Cyclophosphamide and some of the more advanced Mast Cell disorder drugs. The best evidence we have for environmental sensitivities relates to Mast Cells.

    I have skimmed the document you linked. CFS is a poorly characterized constellation of symptoms, a diagnosis by exclusion. This makes research and comparing experiences difficult. I tried to be comprehensive in the symptoms and history document I linked above. If my case resonates with you then you might respond like I do. But it's likely nobody's case is exactly the same.

    At one point or another I experienced every symptom in the CCC's definition. If there's a particular excerpt you want me to respond to please let me know. With supplementation and lifestyle modifications the list got shorter, to the point where I could manage my life spending hundreds of dollars on supplements and other therapies. Except for the environmental sensitivities. Nothing ever helped with that until now.

    My illness onset followed accutane, if you google around you'll find similar anecdotal reports. Sadly.
     
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  4. Hip

    Hip Senior Member

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    Your medical self-description was very useful and clear, and it does help characterize your illness. But knowing whether a patient satisfies the Canadian Consensus Criteria is also of value, as the CCC one of the strictest ME/CFS definitions. By contrast, the CDC definition is quite a loose one.

    It just that whenever one sees an account of a patient either responding to rituximab, or not responding, it's nice to know whether they fit into the typical "ME/CFS mold" or not, and the CCC is most precise and widely used definition.

    It's the 7 boxed criteria on page 2 that you have to satisfy in the CCC definition (although you can still satisfy the CCC if you don't have criteria 4, the pain symptoms).



    An Accutane trigger a new one for me. Is the illness triggered by Accutane usually considered to be ME/CFS in the anecdotal reports you have read? Or is the illness just considered to be a fatiguing syndrome of unknown type?
     
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  5. kyzcreig

    kyzcreig Senior Member

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    Re: CCC Criteria
    IMO this is still very non-specific criteria. But yes I qualify on all 7 categories. I could get much more detailed. For example:
    • Muscle pain is short and transient, I will feel pains in my heart, arm or hand. But not the pins-and-needles neuropathy type of pain. I do get severe migraines.
    • PEM is worse for resistance based exertion (e.g. lifting something) versus walking or running. Arthralgia follows running so I don't do it, even if I have the wherewithal. I used to run 5 miles a day.
    • Early on I experienced POTS but this went away when I got a HEPA filter and changed my diet to plainer foods
    • I have cold intolerance, transient cold extremities, run low body temperature and blood pressure. These symptoms are responsive to stress.
    • I have transient tender lymph nodes, transient malaise and a growing list of sensitivities (hopefully not for long)
    In some cases the Accutane reports tangent into CFS and PhoenixRising: http://www.acne.org/messageboard/topic/295030-repairing-the-long-term-damage-from-accutane/?page=329
     
    Last edited: Jul 30, 2017
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  6. Hip

    Hip Senior Member

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    What sort of criteria would better capture all ME/CFS patients, while trying as much as possible to exclude diseases having similar symptoms. That's the basic idea of ME/CFS defining criteria.
     
  7. kyzcreig

    kyzcreig Senior Member

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    A unique diagnostic marker is needed. The discovery work being done on PDH (carbohydrate metabolism) is in the right direction. Unfortunately this won't capture everyone. The list of illnesses that can present like the criteria you linked is long and multifactorial. It's likely CFS encompasses many different etiologies.
     
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  8. Gingergrrl

    Gingergrrl Senior Member

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    Wow, @kyzcreig, you have had improvements from Ritux after only three weeks?!! I did not even realize that this was possible. I will be having my second Ritux infusion in two days which will be exactly two weeks from the first infusion. I am continuing to have improvements as well but in my case, I have done a full year of IVIG (and am continuing with IVIG through Dec) and I believe my current improvements are from the IVIG and that it is too early for the Ritux to be doing anything in my case. My doctor felt we'd probably know if I am a responder by the three month mark but did not expect me to know anything by three weeks. Your case is very inspiring for me to read and thank you for sharing it.

    I plan to do the maintenance infusions (at my dose which is 600 mg per infusion per the autoimmune formula/protocol). Three months will be the very beginning of Nov so we will have to get insurance approval since we could only ask for the initial two infusions on this Auth. If we can present that I am responder, we think they will give me the month 3 maintenance infusion. Next year I will have a new insurance so when it is time to get an Auth for the month 6 maintenance infusion, we will be starting from scratch.

    I tend to agree with this and there are doctors today who would swear on a bible that my diagnosis is "CFS" and my auto-antibodies, POTS, muscle weakness, shortness of breath, etc, does not mean anything. But I feel like you, that it is a diagnosis of exclusion and no two people's cases are alike. So my doc just says I have a B cell autoantibody driven disease until science can give me an exact label. I have MCAS but it remains in remission from IVIG and last night I was able to eat (gluten-free) pizza with absolutely no reaction and this is a very high histamine food that would have killed me back in 2015 (pre-IVIG).

    The very first trigger of my illness was a neurotoxic reaction to Levaquin that also severely injured my right triceps tendon. So I completely understand what you mean (even though I have never taken accutane).

    Please keep updating this thread and I will follow it closely! Best wishes to you 100 million percent!
     
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  9. Hip

    Hip Senior Member

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    What you are saying would imply that all ME/CFS research studies on patients are a complete waste of time, including Fluge and Mella's, because you think there could be any number of different diseases in the patient cohort.

    So if Fluge and Mella publish their phase III study and it shows a high percentage of their cohort improve or go into remission, your view would be that this result is meaningless and proves nothing, because their cohort might contain all sorts of disparate diseases.
     
  10. kyzcreig

    kyzcreig Senior Member

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    I apologize I don't mean to undermine that effort. What I meant was many illnesses present chronic fatigue, not just the unexplained one(s) that are associated with CFS. That CFS is unexplained is partly what defines it. If a biomarker is discovered for Rituximab responders how will we refer to non-responders that still need treatment? Head cases? There's likely something physiologically wrong with them like there was for responders. But their etiology is different and medical science would differentiate between them. Even among responders there might be different flavors of illness, as there is for RA.

    I have spoken to academics about this and the consensus opinion is that kind of criteria is not sufficiently specific or "objective" to define an illness. In their eyes it is too dependent on self reporting. Preposterous I know. But here we are. I agree it's the best we have and I am not criticizing the practice of using that criteria to screen stories like mine. It seems productive.

    I could have been diagnosed with a few illnesses based on symptoms if I had the right biomarker or pushed for it e.g. MCAS. So many illnesses are clinical diagnosis. But insurance companies will weasel out of obligations if it's only based on self reporting. And in any case all the treatments I would be interested in are off-label. So, practically, the academics are right. Amusingly, if not surprisingly, these doctors almost always tried to diagnose me with Sjogren's because of my positive SS-B despite nothing being wrong with my lachrymal glands.

    So in summary, I thank those wonderful researchers for their work. And my impression is most people will never see treatment until there is an academically accepted, "objective" diagnostic criteria. That doesn't mean progress can't be made or recoveries can't happen until then.
     
    Last edited: Jul 30, 2017
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  11. ebethc

    ebethc Senior Member

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    It makes me cry to read this... What would it cost in the US?? And on top of the (relatively) reasonable prices you're actually treated w respect? I can't even imagine.. I think the US pays back all the R&D costs w the sky-high medical costs here, then the rest of the world pays the sensible rate because they have advocates to negotiate lower prices on drugs...
     
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  12. ebethc

    ebethc Senior Member

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    I understand that there's no biomarker for RTX responders, but isn't is generally a drug for ppl w autoantibodies? I have an underactive immune system, not an overactive (AI) immune system, so I'm not sure I should get my hopes up... Of course, I will discuss it w Kaufman if/when I can ever afford to see him..
     
  13. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    I think it may be important for people to remember that members may have different illnesses. I would be cautious about attributing fatigue associated with an ANA of 1/1280 low C3 and Anti-La to 'CFS', or indeed ME.

    CFS is defined as a fatiguing illness where there is no specific explanation for the fatigue. We take an ANA of 1/1280 and low complement as quite adequate explanation for all sort of things like nephritis, rash, pleurisy and fatigue when people have several problems. There is no particular reason not to do the same for isolated fatigue, or indeed other features. Old fashioned groupings like lupus and Sjogren's are not that helpful. Now that we have explanations for immunological effector mechanisms and statistical data about natural history rational management has much more to do with the specific immunology than clinical syndromes. The presence or absence of salivary gland problems is really just an old fashioned clinical sign. It was never the main issue in what got called primary Sjogren's which was the association of certain antibodies to nucleoproteins and systemic features like fatigue.

    Unfortunately, there s an ever increasing disconnect between lab immunologists working on mice who know nothing about human disease and physicians working in clinics who know next to nothing about immunology. Most rheumatologists do not even understand the different roles played by immune complexes in lupus and RA.

    An illness with an ANA of 1/1280 and anti-La and low complement falls within the general category of lupus-spectrum ANA mediated autoimmune disease and we know that rituximab can be very helpful in that situation, although fatigue itself has been one of the less rewarding targets.

    I would also be cautious about interpreting any reports of early improvement in CFS following rituximab. The Norwegian phase II trial show no difference between rituxmab and placebo up to three months. Only at six months did there seem to be a difference, and we still do not know if that is meaningful.
     
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  14. Gingergrrl

    Gingergrrl Senior Member

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    This is my understanding from talking with my doctors but I could be wrong.
     
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  15. ebethc

    ebethc Senior Member

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    and IVIG is for both ppl w autoantibodies and low immune function from what I understand... is that you're understanding? (I will discuss w kaufman when/if I can ever afford to go..)
     
  16. perovyscus

    perovyscus

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    Thank you for sharing. You mentioned OMI, is there a reason other than fiscal you did not go this route?
     
  17. kyzcreig

    kyzcreig Senior Member

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    I am still seeing them, it's just slow. Given the opportunity to do the same treatments for less money, I did.

    @Jonathan Edwards gives an accurate and level-headed perspective. To add color, since onset I have had autoimmune markers, for the first few years ANA never topped 1:160. This was dismissed as not specific or significant enough. Not being familiar with immunology I took this for granted.

    Fatigue is a well documented phenomena in autoimmune diseases like lupus, sjogren's, etc. with characterized immunological origins. (R) But if your symptoms and clinical markers are "non-specific" no rheumatologist can treat you without the looming threat of losing their license.

    If you have non-specific autoimmune markers like I did e.g. positive ANA, ENA or low complement complexes, I would encourage you to look into autoimmune treatments (corticosteroids, DMARDs, IVIG, Rituximab) with a forward thinking physician. Your best bet might be a clinic like OMI but this can be slow and cost prohibitive. Their protocols are designed to (1) protect them from litigation, (2) substantiate your case to an insurance company, (3) depend on insurance approval because of the heavy drug markup in the USA.

    Re: my 3 week response. I would encourage you to read Fluge and Mella's case studies from the first Rituximab trial:
    https://bmcneurol.biomedcentral.com/articles/10.1186/1471-2377-9-28
    Two weeks after single rituximab infusion (500 mg/m2) the diarrhoea vanished, while all the other symptoms remained unchanged. Before treatment he was mostly confined to rest indoors, with very brief walks, usually to and from the garden mailbox once daily. However, approaching six weeks after treatment he started to feel energy. During the next two weeks his activity level and muscle usage increased to the greatest level since the CFS debut. He could take one-hour walks and started to do carpentry on his house. Myalgic pain was markedly reduced. Cognitive functions improved remarkably, and he could now read a whole book without interruption. The hypersensitivity to noise decreased. He and his wife confirmed that family life had improved considerably.​

    So we have evidence some patients see a response as early as 2 weeks. Think critically for a second about why this might not be considered statistically significant but is unlikely to be a placebo. This is why we have case studies. Not everything that can be measured is important and not everything important can be measured. It could be a spontaneous recovery, sure, but again, think critically. Post hoc ergo propter hoc?

    The standards for clinical trials exist to inform policy decisions. They are rigorous and conservative to prevent false positives, because much rests on their sensitivity. The standards for a Bayesian model are considerably less and also less biased. Human beings, Google, DeepMind think like Bayes, not like the FDA.

    I'm not anywhere near cured. I am seeing a significant reduction in environmental sensitivities, where nothing else helped. Again, speaking statistically, knowing what all I have tried, understanding the experimental conditions of N=1, this is unlikely to be a placebo or spontaneous recovery. But from your perspective "man is the measure of all things", so I could be disingenuous or misremembering. I don't discourage that kind of thinking. But if you are like me, if my story resonates with you, then I hope I can help by sharing.
     
    Last edited: Jul 31, 2017
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  18. Gingergrrl

    Gingergrrl Senior Member

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    @ebethc Yes, this is correct and IVIG is used in immune deficiency (low dose) and in autoimmunity (high dose) and everything in between.

    For what it's worth, my ANA is also 1:160, speckled pattern, and the rheumy that I saw felt it was not specific or significant enough. He said that my muscle weakness and breathing problems (which he agreed were present) could not be caused by the auto-antibodies that I had including the "N-type calcium auto-antibody". I asked him point blank, "In your entire career, have you ever had a patient with the N-type calcium channel auto-antibody" and he said "No". So I asked (very politely), "Then how can you be certain that it is not contributing to my muscle weakness?" and he said that he could not.

    But he felt IVIG was too risky for me. All I can say is thank God I did not listen to him. I know I give random examples but to me they are life-changing. I made a b-day party for my niece this weekend and I was able to put the cupcakes and ice-cream on all the plates and lift the plate over my head to someone standing behind me. My sister's jaw dropped and she said, "You can lift things over your head now"?!!! There is no explanation except IVIG b/c in my case it is too early to be from Rituximab (my 2nd infusion is tomorrow morning).

    I don't know if I am an unusual case but my doctor from OMI was able to get both IVIG and Rituximab approved through my insurance and I am just paying the co-pays. My local MCAS doctor was in agreement with this plan and is prescribing it so I can do it at the infusion center at his hospital b/c they are very familiar with mast cell patients and it avoids me having to travel seven hours up to OMI. I spent a tremendous amount of hours dealing with the insurance bureaucracy which helped moved things along but without both doctors, this would never have been possible. Without insurance approval, I would not have been able to do these treatments in the U.S. but the co-pays are manageable.
     
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  19. mariovitali

    mariovitali Senior Member

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  20. kyzcreig

    kyzcreig Senior Member

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    Interesting work, no doubt the future. Though I think we need more data. If we had comprehensive genomic and epi-genomic data we would very quickly get to the bottom of the "what" in syndromes like this. The latter epi-genomic technology is still a few years from reality and much farther from ready availability.

    I think I remember you doing well with TUDCA? I did well with this supplement too. I noticed improved digestion and energy.
     

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