Page Synopsis: Rituximab is a monoclonal antibody as well as an immunomodulator

For CFS patients it reduces inflammation

Though the clinical trial of Rituximab for chronic fatigue syndrome was deemed unsuccessful, it did alleviate symptoms in a third of trial subjects

Skill Level  3

Relevance:3 Technical Level:2


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For those it has helped it has led to full remission


                              ImmunomodulatorsBalance the Immune System (Th1/Th2
 Written by Carol Sieverling, this issue's articles are based on tapes of her October 2000 visit. Dr. Cheney gave permission to share this information, but has not reviewed or edited it. Articles on other topics will be in the April 2001 newsletter and will soon be available on our website in the section on Dr. Cheney. These articles likely apply also to FMS patients experience cognitive difficulties in addition to pain and fatigue, since Dr. Cheney believes they may also have CFIDS. CFIDS patients are Th2 activated. This means they over-respond to toxins, allergens, normal bacteria and parasites, and under-respond to viruses, yeast, cancer and intracellular bacteria. Dr. Cheney suggests six products that can help rebalance the immune system. Dr. Cheney explained that the immune system has two different modes of attack, based on the type of invader. One is Th1 (T Helper 1). It goes after organisms that get inside our cells ‚ intracellular pathogens. It is also known as cell-mediated immunity. The other is Th2 (T Helper 2). It attacks extracellular pathogens ‚ organisms that are found outside the cells in blood and other body fluids. Some call this humoral or antibody-mediated immunity. A healthy immune system is dynamic, able to switch back and forth as needed, quickly eradicating one threat and then resting before responding to the next. (Dr. Cheney began this conversation by drawing a large inverted "V". At the top point he wrote "Th0", which he called "Th naught". The left arrow pointed down to "Th1" and the right arrow to "Th2". The arrow on the right was much darker and thicker, indicating that CFIDS patients are Th2 activated.) Th0 are the naive, or unformed, cells of the immune system. They are resting, just waiting for an invader. When infection occurs, they convert to either Th1 or Th2, depending on the type of threat. When the resting cell is exposed to a virus, cancer, yeast, or intracellular bacteria (like mycoplasma or chlamydia pneumonia), the Th1 response is initiated. (Dr. Cheney wrote these organisms beside the left arrow.) The weapons of the Th1 system include cytotoxic T cells and Natural Killer (NK) cells. (Cheney drew these below "Th1".) On the other side are normal bacteria, parasites, toxins, and allergens. (Likewise written beside the right arrow.) These trigger a predominately Th2 response. Its weapons include eosinophiles (Eos), polymononuclear cells (PMN), and antibody secreting cells (Ab). (Likewise written below "Th2".) How does the naive cell know which pathway to take? It depends on the cytokine information received. The presence of any organism from the left side triggers production of a cytokine called Interleukin 12. IL-12 causes the Th0 cell to move down the Th1 path. On the other hand, organisms on the right side trigger the production of Interleukin 10 (IL-10), which causes the Th0 cell to move down the Th2 path. (Cheney added small vertical dotted lines on each side, pointing upward to "IL-12" on the left and "IL-10" on the right. He then drew horizontal dotted arrows from "IL-12" and "IL-10", each pointing inward toward the "Th0", indicating that these cytokines determine whether it will become Th1 or Th2.) Cheney said this is the point where it gets very interesting. Viruses, especially herpes viruses like EBV, CMV and HHV6, make proteins that mimic IL-10. The virus deceives the immune system into thinking that the threat is coming from the opposite side! So the immune system shifts from the Th1 mode that attacks viruses to the Th2 mode that does not. The virus increases its chances of survival by diverting the immune system. It is now thought that many, if not most, pathogens have this ability. (To represent this effect, Cheney drew a horizontal arrow about half way down the inverted "V", originating from the left side and pointing toward, but not quite touching, the right side. The line was labeled "IL-10 like peptides". Below it he drew a similar arrow from the right side that almost reached the left side. It was labeled "IL-12 like peptides".) Researchers have demonstrated that most CFIDS patients end up stuck in Th2 mode. This has several consequences. When the Th2 system activates, it blocks the Th1 system. This suppresses the Th1 weapons, particularly NK function. Accordingly, there is also an increase in the Th2 weapons - the white cells and antibodies. Most notable is increased antibody production. Dr. Cheney said that if you measure antibodies to anything a CFIDS patient has ever been exposed to, they will very likely be elevated. (At this point he drew small arrows beside the "weapons": They pointed down on the left side to indicated suppression / lower levels; and they pointed up on the right side to indicate activation / higher levels.) Cheney notes that other problems ensue. Patients get into trouble on both sides: they overreact to things on the right side and under-react to those on the left. When they are Th2 activated, they no longer have the defense mechanisms to keep dormant all the things they caught in the past. They cannot suppress or control them anymore, and the EBV, chlamydia pneumonia, CMV, etc. reactivate. The yeast also begins to appear. The only defense against being eaten alive at this point is RNase L. (For more information about RNase L, see The Three Phases of CFIDS and other articles in the Cheney section of our website.) RNase L cannot kill any of these things. It only stops them from reproducing. According to Cheney, "It's a line in the sand saying 'No more replication', and it waits for Th1 to come and kill them. But Th1 never comes. RNase L sits there and grinds away, possibly going up and down as the pathogens activate and reactivate. But they never get wiped out. RNase L holds the line, waiting for the cavalry that never arrives." While it is valiantly trying to hold the line, it is also chewing up human messenger RNA, inhibiting all the enzymes in the body, disrupting protein synthesis, and generally making patients miserable. As RNase L grinds away, it eventually shifts into "after-burner" desperation mode - the more powerful and deadly low molecular weight form discovered in CFIDS patients by Suhaldonik. Cheney commented "RNase L is a very good anti-cancer defense. So as long as you're involved in this scenario, you don't get cancer. But a lack of growth hormone will wipe out RNase L, and we now know there is profound loss of growth hormone in CFIDS. Growth hormone is responsible for protein synthesis, and RNase L is a protein. So if you lose growth hormone, you lose protein synthesis, including RNase L. That may explain why, as the disease wears on and you get more injury, you stop seeing high levels of RNase L. You can't make it anymore." He believes this is a very scary situation. Patients are Th2 activated and Th1 suppressed. The things on the left come out and there is nothing to stop them. There is no Th1, and eventually no Rnase L. He also believes patients need to balance the immune system - to push it a little more towards Th1. That way they will lose some of the overreaction on the right and gain some control on the left. Cheney recommends the following to help shift the immune system from one mode to another. They are called "right to left shifters". Three of them are published, or near publication. 1) Kutapressin (published, prescription) Kutapressin is an immune modulator and a broad spectrum anti-viral. Dr. Cheney has found that it is most effective when the dose is varied or "pulsed". The dose should vary from 1 to 4 cc daily; see the section on Isoprinosine for this theory. Dr. Cheney strongly suspects Ampligen is a right-to-left shifter also. He has said in the past that Kutapressin is rather like a weak form of Ampligen. 2) Isoprinosine (published, prescription) Published for use in CFIDS, this anti-viral enhances NK function. Dr. Cheney believes it would also be good against intracellular bacteria since it is a Th2 - Th1 shifter. It appears to raise IL-12 and lower IL-10, which turns off Th2 and turns on Th1. It is also called Imunovir and is very nontoxic, very safe. It has been approved in Europe and Canada for just about any viral infection for 18 years. It is not approved in the US (for political reasons, not safety concerns) but is easy to get from Ireland with a prescription. Contact Newport Pharmaceuticals at 353-1-890-3011, fax them at 353-1-890-3016 or email them at [email protected] Week one, take 6 tablets a day, Monday through Friday, and none on the weekend. Week two, take 2 tablets a day, Monday through Friday, and none on the weekend. Repeat this cycle. But do not treat every month. Do two months on and then one month off of this "pulsing" dose. This medicine works best when you do not treat regularly. If you treat continuously at the same dose, it stops working. It is an immune modulator, and Dr. Cheney suspects all immuno-modulators are like this. If taken continuously they stop working. The dose must vary so the immune system never knows what to expect. 3) Pine Cone Extract (supplement, Cheney said, "They make a tea from this in Southern Japan and they have significantly reduced cancer rates. It's thought to work at the gene level in lymphocytes, where it turns on IL-12. It also shuts down IL-10 at the gene level, and that causes a shift towards Th1. Pine Cone extract is expensive, but at just 10 drops a day (in the morning), of all the possibilities, it's probably the cheapest per day." It is called PineExtra, and 1 oz is about $60, but it lasts a long time. 4) Earth Dragon Peptides (supplement,, Earth Dragon is round worm peptides. It causes a shift to the left, and is believed to be very similar to IL-12. There has been a huge surge in the use of ED peptides to treat Inflammatory Bowel Disease, specifically Crohn's Disease. One professor at UNC treats all his Crohn's Disease patients with Earth Dragon. It is very non-toxic and safe. This is a good choice for those who want to balance their immune system and also have bowel problems. Earth Dragon is about $36 for 150 caps. The dose is two a day. 5) Heparin (prescription) Heparin is a Th2 - Th1 shifter. One advantage for many patients is that it is also an anticoagulant. Dr. Cheney only recommends this if a patient has a coagulopathy. About half of his patients do, according to the ISAC test. (See or "Blood Related Disorders in CFS/FM.") 6) Formula 560 Transfer Factor (to be published, supplement, Formula 560 is an immune modulator. Dr. Cheney likes this product. It reportedly works against HHV6 and Lyme Disease, as well as other problems. It costs about $585 for the first three months, then the dose drops one-third. It averages out to about $130 a month for the first six months, and $65 thereafter. (The cost of this product has reported dropped since this was first published.)NOTE: Pro Health is an additional source for the Transfer Factor products (we carry the Formula 560 as well as the exact same product and from the same manufacturer that we call Transfer Factor 6000 and sell it for less). Which should you use? Cheney recommends that you pick one and see what it does to your NK function. It is a question of whether it will work and how much it costs. NK levels will rise if there is a shift from Th2 towards Th1. Before beginning one of these products it is best to get a baseline on NK function. Then test again after having been on the product for one to three months. Dr. Cheney uses the lab of Mary Ann Fletcher, an NK specialist and colleague of renowned researcher Nancy Klimas, at the University of Miami. Her lab is no more expensive than commercial labs, and is top quality. Cheney emphasizes that you must have a quality lab do this test: do not use just any lab. For test information, phone 305-243-6288 or fax 305-243-4674. The test is called "Natural Killer Cell Function Assay" and costs $350 

B-lymphocyte Depletion Using Rituximab for CFS and Epstein Barr treatment

"EBV was eliminated from by the treatment of rituximab. This would be consistent with the B cells being infected by EBV being depleted."

OMI treatment center Silicon Valley

The last segment is about a lady who is doing much better about being treated with rituximab at the OMI in Silicon Valley.

From phoenixrising users on 'Does anyone know of any cases in the US where Rituximab has led to remission of CFS/ME?'


"The drug apparently completely cures around ⅓ of ME/CFS patients according to the Kolibri private hospital in Norway


see this post, and according to the OMI

(see this post, and according to Fluge and Mella's published 2015 phase II study which found 11 out of the 29 patient treated were still in full remission 3 years later."


"My doctor who was from OMI but now in his own private practice  OMF is actually the research piece vs. the institute feels that the potential responders are the ones with autoantibodies who have had good responses to IVIG.


User dreampop said:


I also don't buy into someone with long term moderate or severe M.E. not coming onto one of the online forums to rave about it.


I can tell you with 100% honesty that since posting my thread about Rituximab, I have been contacted by multiple people who did Rituximab either through OMI or Kolibri and several had good responses. I was also contacted by one OMI patient over a year ago who had a good response but she did not want to share it on the public board for personal reasons. Since I do not have permission to share any of their names or details, I have to honor that but this is several people and they really do exist.


User dreampop said:


Is it the same protocol - dosage/time/etc.. Only someone who has been on Ritux at OMF can answer this question.


My protocol was the autoimmune protocol which is 375 mg Ritux/BSA  body surface area which for me equals 600 mg per dose vs. in the Fluge and Mella study it is one gram per dose regardless of the BSA formula. My doctor feels that total B-cell depletion is the goal and such a high dose is not needed in many patients  which also decreases the risk of allergic reactions and other side effects.


User silky said:


And why would they keep giving their patients an expensive, potentially dangerous drug if there were no responses? I would be inclined to say marketing


My doctor got it covered by my insurance so all I will have to pay is the co-pay. I have to be honest, I find it a little insulting to imply they are doing this for the marketing. Ritux was not even considered for me for over three years of being an OMI patient until I had a life-changing response to high dose IVIG first. No one pushed this decision on me and we discussed it for over a year of IVIG until we reached the decision that I had a good chance of being a responder. I did all possible safety tests  for Hepatitis, TB, JC Virus, etc and coordinated the infusion with my MCAS doctor so it was done locally and as safely as possible. My MCAS doctor is actually the one prescribing it so I can do it at his infusion center without having to travel up to OMI. I am documenting the entire thing in another thread and even if it does not provide remission, or any benefits beyond IVIG, I have zero regrets that I tried it.


Once more patients get the opportunity to try it, there will be more public reports on boards like PR. I was contacted by an OMI patient on FB in my calcium auto-antibody group who believe it or not, had never even heard of PR or that it existed. So, not everyone uses the internet as much as we do especially if they are too ill to post."


You also have Maria Gjerpe who started the crowdfunding MEandYou for the Fluge/Mella Phase 2 study  Not Phase 3 as you state, Phase 3 is not published until 2018. Maria was testing the procedures for the Phase2 study and went from being bedridden to working 80 % in just over half a year.


That the people who had a solid chance of being responders were those with proven B-cell driven auto-antibodies but he did not say that someone without auto-antibodies could not respond. I think there is a just a greater chance of being a responder if you know that you have actual auto-antibodies to knock out.


The Fluge & Mella paper  the one with the 12 authors said that the responders had the beta-adrenergic and anti-muscarinic auto-antibodies, plus anti-thyroid antibodies, plus a positive ANA titer, and I have all of those things. But my assumption is that someone who did not have those things could still be a responder and that I could end up not being a responder. It's a crap-shoot but we felt that I had a decent chance at being a responder.

My Experience with Rituximab for ME


I was given Hydrocortisone, Phenergan and Panadol prior to the infusion. Rituximab is a heavy duty drug and these 3 drugs are aimed at lessening the side effects and improving the tolerability of Rituximab  never before had I taken drugs to prepare for another drug. The infusion starts at a deliberately measured rate to mitigate the chance of side effects. Watching the Rituximab drip into the infusion apparatus was almost hypnotic as it created miniature ripples.


I took regular bathroom trips and it was on one of these trips two hours into the infusion that I caught a glimpse of myself in the mirror. My neck and sides of face had begun to develop a rash. I nonchalantly informed a nurse of the rash, after considering not mentioning it. She examined the rest of my skin and across 75% of my body was a bright red rash that would best blend in amongst a Google image search of “bad rash.” The snails-paced world of the cancer infusion centre was sent into overdrive. I had around 15 nurses swarm around me, phone calls to doctors were made and I was the centre attraction of a grotesque show of sorts.


At this stage the infusion was only 10% complete and my thoughts flickered between “what a waste of money”, “I was really hoping Rituximab was going to cure my ME and that hope is fading” and “I hope this rash isn’t foreshadowing a nasty reaction or death.” After much commotion and discussion I was pumped full of more Hydrocortisone and Phenergan. I pleaded for the rash to go in order for me to continue the infusion. The rash faded and surprisingly I was allowed to continue the Rituximab infusion albeit at a slower rate than before. I overheard a nurse murmur “I think we’ll be here until midnight.”


I tolerated the rest of the infusion and after 8 hours had completed the 1000mg. Upon returning home I experienced shortness of breath which continued the next day before disappearing. Two weeks after the first infusion I returned to the cancer centre for my second and last dose of 1000mg of Rituximab. On this occasion I didn’t develop a rash although I did experience shortness of breath again. During the following few weeks I noticed a persistent tenderness on my arm, separate from the infusion sites and an increase in bowel movements.


The smaller Rituximab studies on ME patients presented remarkable results and the entire ME community had clung on buoyantly for the larger phase III trial. Two weeks after my second infusion, I logged on to the Phoenix Rising forums and read the clipped headline “Rituximab Phase III- Negative Result.” The timing of this was particularly cruel for me. If I had found this result out a couple of weeks earlier I wouldn’t have pursued this course of treatment. I felt like I was now waiting for Godot. It was expected the study would be revealed at some point deep into 2018. I still tried to cling to a modicum of hope.


Around 3 weeks after the infusion I started to develop a strange, new type of fatigue that was analogous to crashing despite not having done anything. This occurred seemingly at random around 2 days a week and resulted in me having to lie in bed unable to talk or move any great deal. I would toss my Adelaide Crows scarf outside my door as a sign to my family to not disturb me. Fatigue is a noted side effect of Rituximab, something I’m all too used to. The goalposts had now shifted. I had gone from yearning for an ME improvement from the Rituximab to now wishing that it didn’t make my ME worse. The new, extra type of fatigue lasted intermittently until 4 months after the infusion. At this time it stopped and it hasn’t re-emerged since.


Four months after the infusion I began to experience a spate of neurological symptoms. I developed a tremor in my hands and legs that is omnipresent. I also acquired another type of tremor; perhaps known as a postural tremor. If I raise my legs, bend my knees, raise my head and even smile then the muscle I am using begins to shake; in the case of my legs, quite violently. The symptom of mouth quivering every time I smile seems almost emblematic of my entire Rituximab experience.


I have also developed vision problems- a sensitivity to certain types of light. I’ve been plagued by hypnic jerks: sudden bodily shakes that occur when I’m falling asleep. I have begun to feel slightly wobbly on my feet- not severe enough for others around me to notice but a definitive symptom all the same. Whilst lying in bed, I’ve also experienced regular burning hands and red palms in tandem with a strong pulse. The former symptom is perhaps erythromelalgia whilst the later symptom occurs on different parts of my body. As a collective, most of my new symptoms seem to wax and wane in intensity. For a fortnight I might not notice them as much and for the next month they may return with a vengeance.


It would be foolish to definitively link this new glut of symptoms to the Rituximab. I had a brain MRI performed which was normal and fortunately for me ruled out MS and PML  a rare disease that is sometimes caused by Rituximab. I was fast-tracked to see a neurologist and bypassed the long waiting list to see one within 2 days which in itself was slightly alarming. The neurologist seemed uncertain as to what was causing my symptoms. My specialist physician is on the same page as me regarding the most likely root cause of the plethora of my new neurological symptoms. He thinks the Rituximab either directly caused my symptoms or set off some other process in my body that has resulted in the aforementioned neurological signs. The timing seems to fit. Rituximab isn’t renowned for causing neurological signs such as tremor, some 4 months after treatment  on occasions it causes them directly after infusion yet there doesn’t seem to be a better explanation at the moment  although I am exploring an enterovirus reactivation hypothesis. I am reluctant to paint the new symptoms as ME- for starters I have only developed a couple of new ME symptoms in the past decade.


Overall, as I write this 9 months after my infusions, I can tolerate the new symptoms yet in a week’s time they may again increase in intensity. The Rituximab saga certainly caused some turbulence in my life and it had prevented me from trying other treatments. I have just started to dabble in some more treatments for my ME. There were certain moments across this Rituximab journey that are etched in my mind as pivotal points. For me the greatest lesson has been to not necessarily treat events as intrinsically good or bad. The ripples cast from each event spread in unlikely, unforeseen ways. In some ironic sense, learning this lesson has been the one good ripple from my Rituximab experience


According to a trial of ritumixab for CFS, it was not succesful Rituximab Phase III - Negative result however, it was a small sample size and perhaps the patients chosen weren't with an autoimmune CFS subtype


Taken from User lrn "My doctor, who was an AIDS doctor for 30 years before treating ME/CFS patients, tests for and treats all infections before putting patients on Rituximab. The risk with wiping out B cells which are antibodies, without killing off infections first, is that infections can potentially run amok without antibodies to fight them. He also has patients on intravenous immunoglobulins from donor antibodies for several months to help battle any infections before starting Rituximab.


User Xana said:

Could plasmapheresis be effective?

In the short term, yes. It can wipe out "bad" antibodies temporarily, until they grow back, giving you an idea if Rituximab might be a better long-term solution. It is rarely done in the United States, But possible, and seems to be slightly more available in Europe. I am not sure about other countries, But I would assume most would have it at least somewhere.


User jaybee00 said:

Rituximab doesn’t work for MECFS— I don’t know who is recommending this treatment for you (or why it’s being recommended).


The problem with this study is it was on a random group of ME/CFS patients, with a variety of conditions. Some may have been appropriately chosen and benefited while others likely did not have the appropriate characteristics to be prescribed Rituximab. As @Judee says, everyone is different.


My doctor carefully selects patients for this treatment. I also went to a large medical research center to get a second opinion from another doctor who was an expert on both immunodeficiency and autoimmunity. We discussed the potential use of stem cells, Bortezimub and Rituximab, and he thought Rituximab was my best, least risky choice, and it just might work. He recommended the exact protocol my ME/CFS specialist had, which I went ahead with and benefited from.


User lt "In my opinion, if IVIG (removes infections) makes things better, Rituximab (reduces the immune system) will make things worse."


It may be your opinion, but IVIG provides antibodies. While they may help with infections, most of us are also given some sort of anti-infective, like an antiviral like Valtrex or Valcyte, antibiotics appropriate for the bacterial infection, an antifungal or a drug appropriate to kill a parasite. IVIG can also, over time, help with autoimmunity.


While Rituximab was originally approved for certain cancers, it is now approved for multiple types of autoimmunity. It kills off CD20 cells which create the autoimmune antibodies. If one has symptoms caused by "bad" antibodies, removing them can be helpful. The treatment is given multiple times, as the B cells mature and more are made, until they are all killed off. If you don't have this problem but you do have live infections, it could definitely be a problem, but that's why you check for and kill off Infections first. If the infections are gone and one has one or multiple types of bad antibodies, it can provide a great deal of relief.


Instead, try IVIG + Valtrex + Equilibrant for 4 months

If you have a problem that these will solve. I tried Valtex, which didn't do too much, but was more successful with Valcyte and antibiotics for the combination of infections I had.


As for Equilibrant, I found 2 sets of ingredients on the web:


1) astragalus root extract, shrubby sophora root extract, olive leaf extract, licorice root extract, and shittake mushroom extract.


2) active ingredients, plus Dextrose, Cellulose, Silicon Dioxide, Cellulose Gum, Magnesium Stearate (Vegetable Source), titanium Dioxide, Glycerine, Stearic Acid (Vegetable Source), Yellow #5, Blue #2 and Carnuba Wax


I'm not sure which is correct or if both are, but as someone with hyper POTS, licorice root could raise blood pressure alarmingly which could be a stroke risk, and dextrose is typically a corn derived sugar, and many of us are allergic to corn, which could lead to anaphylaxis.


It is always good to work with a doctor to identify ones exact issues and treat accordingly rather than just following someone's advice which could prove dangerous for someone else


User Xana said:

At my local hospital I made positive beta 1 and 2 and alpha antibodies, achr positive antibodies, positive ANA antibodies and positive non-organic antibodies as well. I have low c3 and c4 add-ons.


Having a number of problematic antibodies may create a very good case for trying Rituximab. You would want to ensure you do not have any infections first, and if so, treat with IVIG or plasmapharesis, and then Rituximab if one or both are helpful. One would assume you are under the care of doctors who are well versed in the use of these tools, and it would be wise for a parent, partner, friend or caregiver to accompany you to do for appointments to understand the treatment and the potential for risks and benefits


Rituximab can be risky if you contract COVID while on it, because you lose your antibodies. I stopped it one infusion short of the original treatment plan because COVID broke out that month. I waited for over a year for my CD20 cells to grow back and start making antibodies.


User Xana said:

I really do meet all the M.E. criteria.

Sounds like you do, but you are lucky to have found some other, treatable diagnoses, and a doctor willing to treat you.

User lt: You need to fix these as soon as possible. Normally doctors would give a course of Prednisolone first, and only if that didn't work, Rituximab.


No, doctors would not normally prescribe prednisolone first. Each patient is unique and a lot is not normal about these situations.


It would be wise to find all antibodies you'll want to find first, before embarking in these treatments, as IVIG gives you don't antibodies, which makes testing your own antibodies useless and Rituximab wipes out antibody making nh B cells, and therefore, antibodies.


IVIG can be given along with treatments to fight infections. It is extremely prudent to identify all infections before Riruxumab. As doctors typically look for antibodies to infections, You would need to complete this set of tasks prior to starting IVIG. If it doesn't get done in time, then the ways you would look for any remaining infections are through PCR tests or culture.


User heapsreal said:

Being prone to herpes and viral infections personally would scare me if going on rituximab. I have heard of several cfsers who have had issues with herpes infections get severe breakouts and deterioration in their overall wellbeing


This is why looking for and treating all herpesviruses and other infections with antivirals etc. BEFORE wiping out all your antibodies with Rituximab is an important step. It is also wise to support the body and immune processes with nutrients like antioxidants, methylation nutrients, amino acids, zinc, etc.


User heapsreal said:

All i have written is out of my depth but stuff id ask a dr about.

That seems very true.


It is very wise to read all you can in any treatment, understand the ingredients, mechanism of action, type of patient it can be helped by, whether you fit this profile and discuss with those close to you and your doctor. Many treatments are reversible - some are not, so before doing them you must be assured of why you are doing them and what to expect. And if you don't understand them, that you find someone you trust who can help you understand what


Did they check d-dimer, thrombin/antithrombin, or any other clott




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