ME/CFS or lyme
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Marky90
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I think you were thinking of antibiotics, not steroids. From the latest Ritux study:
Two patients had several upper airways infections. In one major responder (S4 Fig panel C) three repeated antibiotic courses were given for sinusitis. She was then given normal human immunoglobulins (20 g) twice, after which the symptoms resolved and she received in total five rituximab infusions. One non-responder (S6 Fig panel W) had several courses of oral antibiotics due to respiratory tract infections, also seemingly with therapeutic benefit from two infusions of normal human immunoglobulins (20 g). This patient, however, also had a tendency for repeated upper respiratory tract infections before entering the study. One patient had an uncomplicated episode of upper urinary tract infection.
Two patients had several upper airways infections. In one major responder (S4 Fig panel C) three repeated antibiotic courses were given for sinusitis. She was then given normal human immunoglobulins (20 g) twice, after which the symptoms resolved and she received in total five rituximab infusions. One non-responder (S6 Fig panel W) had several courses of oral antibiotics due to respiratory tract infections, also seemingly with therapeutic benefit from two infusions of normal human immunoglobulins (20 g). This patient, however, also had a tendency for repeated upper respiratory tract infections before entering the study. One patient had an uncomplicated episode of upper urinary tract infection.
Marky90
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but im not 100 % sure infections was the main problem, so its wrong to speculate here i think.. I will ask him next time
heapsreal
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Theres a couple of studies on cfs patients improving with ivig but didnt have cvid.
heapsreal
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Steroids may help if neutropenic as it helps increase neutrophil counts which can come down due to infections . I would probably still want to be on a broad spectrum antibiotic .
Marky90
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Yep! A theory is that IVIG-antibodies compete with self-antibodies for receptors which prolong their half-life (fc receptor)
Jonathan Edwards
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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 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?
Jonathan Edwards
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Not very many. Immune cytopenias might also apply - as someone mentioned - especially an autoimmune neutropenia.
BurnA
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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 ?
Jonathan Edwards
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It is an area where it is difficult to pin down precise facts. Steroids certainly lower B cell levels and it is likely that most that die would have died anyway, but maybe not all.
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.
Haha, I meant a bet with nothing at stake, except for the chance to say ´I told you so.´
Briefly, I think the autoimmunity may be either molecular mimicry, or autoimmunity to some substrate that is produced as a result of the infection (like the autoimmunity to nitrosative and oxidative epitopes that Maes has reported), or both.
I think this will partially explain why there are more severe cases of ME on average in Scandinavia (if indeed there are), but that this will also be a result of the climate and latitude of Scandinavia, as both factors reduce the amount of sunlight being absorbed by these patients, and thereby the amount of serotonin, Vitamin D and other important substances being produced.
Briefly, I think the autoimmunity may be either molecular mimicry, or autoimmunity to some substrate that is produced as a result of the infection (like the autoimmunity to nitrosative and oxidative epitopes that Maes has reported), or both.
I think this will partially explain why there are more severe cases of ME on average in Scandinavia (if indeed there are), but that this will also be a result of the climate and latitude of Scandinavia, as both factors reduce the amount of sunlight being absorbed by these patients, and thereby the amount of serotonin, Vitamin D and other important substances being produced.