Does prednisone help Fibro?

I’m confused. I have fibromyalgia. Every blood test I’ve had comes back negative for inflammation or autoimmune disorders. A year ago I had an MRI of my brain which came back normal. For over two years, I have between having 1 and 4 flares a week. Periodically my psychiatrist will give me a medrol dose pack ( prednisone) . It helps a lot. Why? I only have Fibro. That’s it. Supposedly Fibro does not cause inflammation. Because of the side effects of prednisone, I can only take it every 3 months. I don’t use it that often. I use it if I have an invasive procedure or need to be “ pain free” for a few days, like when I visit my mom. Then bam! The pain comes back. Does anyone take prednisone for fibromyalgia???

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Great question, @Freedom! My thinking is that some or a lot of us have a sort of inflammation which reacts to the prednisone, but isn’t measurable yet. When I feel feverish, fluey-achey I often think there’s some sort of inflammation, something autoimmune going on. My cold showering feels counter-inflammatory too, that’s what my rehab-doc (who understands fibro & me) thinks too.
But also the question: how many blood tests have you had? In my case, it was a centre for rare diseases, who took 12 test-tubes of blood and cost a lot of money, and not the rheums, endocrinologist or nephrologist, who found it looks like a preform of Sjögren’s and also found Hashimoto, which the endocrinologist didn’t, 6 months before. Still got to talk to a rheum. about this, but I’ll probably be looking for a 3rd one here…
Good on you for keeping the use of the prednisone down! Sounds very dangerous… :roll_eyes:

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Thanks JayCS! I’m not sure if we have a center for rare diseases in the US. I’ve had tubes and tubes of blood taken. It’s weird because you want the test to come back positive so you have a valid explanation as to why you feel so bad. But then you DON’T want the test to come back positive because you don’t want anything serious wrong with you. Did I understand you correctly that you have fibromyalgia, Sojourns and Hashimotos? Yikes!

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I do think there are centers for rare diseases (inspired by House MD, I think) in the US and the UK, when I look I don’t have problems finding some.
I’ve also had lots of tubes of blood taken, but not 12 in one go, they even had to change the vein for the last one. The results are 5 pages long, full and in small type, impressive. I think endocronologist & nephrologist were 1.5-2 pages each…
Well I’m sure the fibro diagnosis is correct. The centre for rare diseases were suggesting that Sjögren’s is behind it, that I haven’t really got fibro (very similar symptoms). But other docs & fibromites have said that you can have both at the same time. And my symptoms show in both directions, but more clearly to fibro. 4 months later that diagnosis is still not really confirmed, altho there is quite a bit of indication of it. The result of the lip biopsy showed a stadium 2, not 3 or 4, so I’m thinking it’s a preform, not fully fledged (yet?). Hashimotos is something I have, but also not fully fledged, just need to check regularly.

I have had this same experience. I’m taking prednisone right now for an ear problem, and since I’ve been taking it I’ve hardly had to take any advil or tylenol. I only have one day left on it and I’m kind of sad, I’m afraid I’m going to lose energy and get all the pain back right away. I’ve had this happen once before too with prednisone. I have had every test imaginable and everything else is fine; I also have a history of fibromyalgia in the family so the diagnosis is probably right. It doesn’t make sense that it helps but for whatever reason, it does.

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I think its because the inflammation is at the cellular level, not in the blood…that was some research one of my pts said…its a bad drug for your bones tho

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Thanks for the impulse, Lmd! I’ve now looked at PubMed-studies to see if I can validate it. Turns out that saying it is on a “cellular” level is probably just that it’s not sure yet, praps because of the possible role of mast cells.

#1 2018 thinks inflammation is more neurogenic:
There is increasing evidence of neurogenically derived inflammatory mechanisms occurring in the peripheral tissues, spinal cord and brain in fibromyalgia. These involve a variety of neuropeptides, chemokines and cytokines with activation of both the innate and adaptive immune systems.

#2 from 2019 thinks that it’s partly mast cells increasing neuroinflammation
Mast Cells, Neuroinflammation and Pain in Fibromyalgia Syndrome: We hypothesize that
thalamic mast cells contribute to inflammation and pain, by releasing neuro-sensitizing molecules that include histamine, IL-1β, IL-6 and TNF, as well as calcitonin-gene related peptide (CGRP), HK-1 and SP.

#3 from 2020 says inflammatory cytokines and MC products play a role in FM
Impact of mast cells in fibromyalgia and low-grade chronic inflammation: Can IL-37 play a role?
The goal of this article is to demonstrate that inflammatory cytokines and MC products play a role in FM and that inflammation may be inhibited by IL-37.

#4 from 2017 thinks it’s systemic inflammation as well as neuroinflammation
Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients, as assessed by a multiplex protein panel applied to the cerebrospinal fluid and to plasma

#6 from 2019 is a study which looks at recent other studes about inflammation
Role of inflammation in the pathogenesis and treatment of fibromyalgia
"Recent evidence on this highly studied topic indicates that fibromyalgia has an immunological background. Cytokines/chemokines, lipid mediators, oxidative stress and several plasma-derived factors underlie the inflammatory state in fibromyalgia. There are potential new therapeutic options targeting inflammatory pathways in fibromyalgia patients. In conclusion, there is evidence to support the inflammation-driven pathways in the pathogenesis of fibromyalgia. However, further research is required to fully understand the network of inflammation and its possible role in diagnosis and/or treatment of fibromyalgia. "

What I love about the abstract of study #1 is the first sentence:
“Fibromyalgia is a high impact chronic pain disorder with a well-defined and robust clinical phenotype.” - in case anyone still says it is a rubbish bin diagnosis. NO, it isn’t, it is “well-defined”!

Interesting is that proteins that in several studies, proteins called cytokines and chemokines are mentioned, which gives the claim of EpicGenetics to be able to diagnose FMS with a blood test a little bit of a basis. Just that this is not at all definite yet. We talked about this last here:

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WAY TO GO JayCS!!! High five to you!!! :raised_hand_with_fingers_splayed::clap: You did an AWESOME job of getting this information! I have two days left of prednisone. I feel pretty good. I took it so I could make it through an outpatient procedure without beyond incredible pain. It’s a great drug. But it’s not very good to take frequently. It has major long term side effects. Sometime I’m going to research the role of mitochondria and fibromyalgia. I’ve heard little things here and there. I’m just glad someone is trying to figure it out instead of pushing it aside and saying it doesn’t exist.

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Yes, the cells engine is underperforming…i take corvalen m to help with that…it reduces the fatigue

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Yep, I keep having a look at D-Ribose, the substance in Corvalen m, which is part of ATP, in the mitochondria, but I’ve been afraid of the adverse effects on the gut, which my IBSD always gets from everything. I’ve also tried Q10, but side effects there too. But my ozone-autohemotherapy is also targeting the ATP and mitochondria, so it’s not that I’m ignoring it. Far from that, there’s a doc here who claims his supplement regime targets both, which he sees as a central part of fibro. Problem is, it’s only one theory, and the studies there he bases his multiple theories on are scant. I had my ATP tested before and after fatigue, but as there are no real numbers/tests for that, it didn’t help much to find it is reduced from fairly normal, after running up and down 4 storeys 5 times with every bit of energy I had, staggering (and getting strange looks and laughs :rofl: - when I went back in the lab panting, they asked: everything OK? Yup, this is all part of the plan…). I showed the results to other docs and they just shrugged, and said - we don’t know enough yet.
I tried his regime for a few months all the same, spending 300€ on it, and it did absolutely zero for me. First the moderate version, then including Vitamin B12 5mg-injections, which made my B12 rocket to 1700 (700 is the normal max.). All of my minerals & vitamins were OK anyway. I think it may be OK for some, but as I keep saying (as does my rehab-doc): fibro is probably too varied that one regime fits everyone, it will probably turn out to be a set of various types.
I agree with you @Freedom - looking at these recent studies gives hope that docs are taking us seriously. Maybe COVID-research will help there too, as some people suggest, but I think the overlap is too little as well. But take your time before looking into mitochondria-research, maybe then they’ll have something new. Last time I looked (2 months ago) I cdn’t find much. And of course any research there either shows that above inflammation-research is wrong, or only a small part of the puzzle.
@Lmd As I gather it, the ATP does have at least a little to do with inflammation. Looking now, I think the ones going in that direction most are these two, however they seem to have to do with autoimmune diseases, and the link of those to fibromyalgia is up to now more co-morbidity (like my ?Sjögren’s-pre-form), and at least are very much basic/fundamental research as yet. It might be that ATP in the mitochondria is something that can regulate/cope with inflammation.

Mitochondria are able to perceive signals of inflammation initiating danger by activating and managing the innate immune system. This review provides the information on the relationship of the immune signaling receptors (Toll-like receptors (TLR); RIG-1-like receptors (RLR); NOD-like receptors (NLR)) with mitochondrial functions and describes the role of mitochondria in the initiation and development of inflammation.

Finally, by regulating the energetic state of immunological synapse between dendritic cells and lymphocytes, mitochondria regulate the inflammation fate toward immunotolerance or immunogenicity. As dysregulations of these processes have been recently involved in various diseases, the identification of the underlying mechanisms might open new avenues to modulate inflammation.