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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Hi marky.
Which clinic is doing the treatment?
All the very best with it. Wish you well.
Are you sure about that? I think IVIG would be a much more normal thing to give them.
Ah, you were talking about someone outside the trials? Still, I would be wary of someone who gives steroids for an infection.
Its because most infections can be treated with steroid or IVIG. I think many with ME/CFS actually have undiagnosed CVID
This is a very experienced oncologist, he knows what he`s doing. Im pretty sure he said it was steroids..
Theres a couple of studies on cfs patients improving with ivig but didnt have cvid.
I knew Prof. Edwards would have something interesting to add to this. I guess if you have the antibiotics and they are doing their job, you can probably take almost anything with them, and still get rid of the infection. The lupus thing is interesting - I wonder if there are any other cases like this?
Steroids are not normally a good idea in the presence of infection but there are paradoxical situations. Steroids in lupus may help to restore immunity to infection through a roundabout route. Steroids can reduce damaging effects of infections like TB as long as they are given with antibiotics. Steroids are given with rituximab largely to reduce risk of hypersensitivity but they also deplete B cells so probably add to the effect of rituximab. It all depends on the dosage and context of usage so it is hard to draw generalisations.
I think you mentioned before that the B cells that die due to steroids are the ones that were going to die off anyway, therefore would such b cell depletion considerably weaken the immune system ? ( i am talking under normal circumstances, not with rtx ) I know Dr Chia has associated steroids taken at the wrong time during an infection, with ME/CFS onset - do you have any opinion on this ?
Well if the prevalence of autoimmune disease is higher in scandanavia then in theory yes.
But I would add ....
Is the prevalence of me/cfs higher in scandanavia ?
If yes this would indicate me/cfs is at least in some cases autoimmune.
Even if me/cfs and or autoimmune diseases were 10% higher in scandanavia then the rtx response rate should only be higher by the same % at most. So it shouldnt impact results too much.
Going back to this idea, I was just reading an article on Yersinia and found this:
The incidence of reactive arthritis following Y. enterocolitica infection is very high among adults in Scandinavia, where it is estimated to be 10 to 30% (20). The incidence is much lower in most other countries, including the United States. The most commonly affected joints are the knees and ankles; but other joints, such as the toe, finger, and wrist joints, can be involved. In most cases, two to four joints become involved sequentially and asymmetrically over a period of a few days to 2 weeks. Monoarticular arthritis occurs less commonly. In two-thirds of cases, the acute arthritis persists for 1 to 4 months. Chronic joint disease or ankylosing spondylitis occurs rarely. Subsequent complications of Y. enterocolitica infections that occur less often include reactive uveitis, iritis, conjunctivitis, glomerulonephritis, and urethritis. Reiter's syndrome (arthritis, conjunctivitis, and urethritis) is seen in only 5 to 10% of patients with yersinia-induced arthritis (4).
So Scandinavia leads in ReA too! From what I understand of what Prof. Edwards has told me, ReA is a MALT-associated T-cell disease, governed by HLA-B27 subtypes. It seems slightly surprising to me then that it the incidence is higher in Scandinavia, as are other, unrelated autoimmune diseases. Of course, this could just be bad luck on the Scandinavians part, but I wonder if the genetic contributions for these different types of autoimmune disease overlap?
That brings me on to my second idea. From what I´ve read (and contrary to Prof. Edward´s opinion), I believe that ReA is caused by the persistence of the triggering organism, and that it is also possible to have an chronic Yersinia infection without ReA (this is what I think I´ve got). So it seems to me that ME (ICC) is caused by a chronic infection, plus the autoimmune/immunological problems caused by this infection. If that is the case, I would expect Scandinavia to have more ME cases with a large autoimmune component, and that these cases would on average be sicker than the cases with a small autoimmune component (I have heard reports that Scandinavia has a lot of severe ME cases, although this could also be due to differences in climate, latitude, etc). Finally, as was suggested above, I would expect Rituximab to be more effective in Scandinavia.
Nope.Yup, wanna bet?