as part of your journey, did you ever see a rheumatologist or undergo tests for autoimmune issues?

I apologize for posting so many questions in the past several days ....

I've posted before about how I sometimes worry that Lyme and coinfections are a red herring for me, and that maybe I'm one of the people who actually just have an established autoimmune disease that I should be aggressively treating. It's confusing, because I know that several classic autoimmune symptoms (such as the ones I have -- joint pain in fingers as well as in large joints; dry eyes/mouth) can also be caused by Lyme.

So I was wondering how many others here have, at some point or another, been evaluated for autoimmune issues -- either before or after you realized the issue was really Lyme & co.? And what was the outcome of those evaluations?

Also, whatever symptoms led you to be tested for autoimmune issues -- have those improved with Lyme treatment?

Thank you!

I fell sick, kind of like with the flu but worse, and then just didn't get better. I was bedridden and diagnosed with ME/CFS. I had high ANA and RA factor. That suggested autoimmune component, this was before I confirmed I had the infections. In my case I'm pretty much positive it was the infections driving this immune dysregulation (which is often the case, these infections hijack the immune system). I would be willing to bet those biomarkers have resolved to normal as I've effectively treated the infections. My allergies and sinus issues have also cleared up as I've treated the infections.

It's my opinion that a high proportion of autoimmune conditions are caused by underlying chronic infections. That is still a controversial view for most mainstream practitioners I think, but I've talked to a huge amount of lyme patients who were originally diagnosed with fibro, autoimmune condition, ME/CFS, RA where lyme/coinfections were driving the illness. Even with RA, they often use an antibiotic and get good response for patients (I think they assume it is anti-inflammatory component of the medicine, but in my view they are more likely treating underlying infection).

Either way I think looking closely at all angles is a good idea. One trick I always like mentioning is the provocation test. You try some broad-spectrum antimicrobials (can be herbal or pharma) and gauge response. If you get a flare in symptoms (herxheimer) that is a strong indirect evidence of underlying infections. Not everyone who has these infections herxes to effective antimicrobials, but most do to some degree.

My physician felt certain I wold test positive on either thyroid problems or some sort of auto immune. I had all the symptoms of Sjorgens or MS.
Dry eyes, mouth, extreme low body temp 95'. All test came back negative. That's when He tested for Lyme. Dr. Alfred Miller believes most neurological diseases start with a pathogen like lyme.
My theory is to get rid/control of the pathogen and then help the body heal itself.
After my vit D levels were up my body temp went to a steady 98.6 for the first time in 16 yrs.

https://youtu.be/Fr61GV8JCYQ

Yes I was tested for autoimmune - a long list and all came back negative.

The roomy gave me 2 month doxy ...he dx vasculitis and livedo the refered to id doc....i guess im lucky because in iv room they were hurting people with copaxone and steroids ....imho...

For the vasculitis bvt and iv curcumin helped most ....

Crp and ana were high ...every person with msids has a inflammatory problem though.what at the root is the question they never get to....

Ive been tested for autoimmune a bunch, both blood and CSF.
ANA, ESR, rheumatoid factor, c-reactive protein, anti gliadin antibodies. All always comes back normal

LilyPanda said...
Thanks for all the replies. It's so interesting and confusing. I too, have so far tested negative for the specific autoimmune markers that they've checked for (rheumatoid arthritis, Sjogren's Syndrome, scleroderma -- they tested for scleroderma only because of my ANA pattern, not because I was showing symptoms). I do always seem to have a mildly positive ANA.

However, yesterday a dermatologist looked at my cuticles with a handheld microscope and said she saw nailfold capillary changes, which are associated with psoriatic arthritis and scleroderma (among other autoimmune issues). My symptoms seem to line up with psoriatic arthritis (joint pain including in DIP joints, some finger swelling, negative bloodwork), so that makes me worry a little.

I understand that, in some ways, this is an issue of semantics: if Lyme is what is causing these autoimmune-like symptoms, then maybe they'll improve with Lyme treatment whether or not the symptoms themselves are autoimmune. But if I have an Lyme AND an autoimmune issue, then I worry I'm making a mistake not aggressively treating the autoimmune issue. The joint pain/swelling in my fingers has gotten significantly worse recently, and I'm told that permanent joint damage can happen quickly if I don't aggressively try to stop it.

Interesting about the nailfold capillary changes. I have had finger joint pain and stiffness but no swelling.

Yikes - difficult decisions to make - as you don't want the damage to happen...BUT steroids are contraindicated with lyme disease.

bvt and shock wave with hd bart tx has helped my disfigured joints...mycoplasma may play a role in RA one fella just used diet n minocycline.....go for the root cause dont just mask symptoms? .rocephin was a nice anti inflammatory for a while keeping bart from replicating...lf given steroids or any immune suppression, it will allow the pathogens to flourish even more rapidly ....girlie did say contraindicated as a fair warning ...

Post Edited (bluelyme) : 7/27/2018 1:28:09 PM (GMT-6)

LilyPanda,

I totally understand your fears and confusion over the matter. Hopefully you will hear or read something or make a mental/emotional connection that will settle the issue for you or at least ease your worries.

I think I remember responding to one of your older posts that bartonella may be present. The capillaries in the nailbed made me think of bartonella again. Bartonella affects the entire vascular system.

A Dr refused to test lyme for a bullseye decades ago, said I didnt have the symptoms and we dont have it here. She was dead wrong on both accounts, but thats when I was young and believed Drs.

Ten years after that another Dr tests my thyroid, and I was well into autoimmune hashimoto by that time. Finally I thought, now ill get better with thyroid med....nope, not much. I had a feeling something else was lurking. That was 20 years ago.

Stopped treating Lyme a couple years ago, hashimoto did not go away. One antibody normalized and diet helped that too. The other thyroid antibody stayed elevated and continues to destruct my thyroid gland.

There used to be a handful of people here with hashimoto. I also have high ANA sometimes and my immune system lymphocytes are low (B and T cell). Nat killer cells are good though. I think i'm the only one here to do this testing, more should in my opinion if your cd57 is low (thats a grouping of lymphocytes).

I feel better but the above issues show I may never be optimal again.

"............we historically suck at finding the actual infectious causes but as more research comes out that is becoming a more and more accepted reality."

yep

I just want to post a visual that I think helps because I see a lot of people getting confused on this topic. Top one is ganglioside which is expressed in nerve cells and helps mediate cell-cell recognition between neighboring neurons by binding corresponding lectin receptors. Bottom one is outer surface structure (endotoxin/lipopolysaccharide) of the bacteria C. jejuni. In a pathogen like Borrelia a similar dynamic is likely to occur as a means of binding the lectin receptor or slowing down adaptive immune response. Often times a pathogen needs to bind its target cell as a means from being swept away by fluid dynamics or even brownian motion. It is also a first step to invasion of a particular cell line. This use of similar molecules is called "molecular mimicry" and once thought to be a rare chance occurrence is now being shown to be a widespread behavior of various pathogens as it allows them to interact with host cells and slip by the immune system

However, see how the Lipid A domain and ceramide are different? This is what ultimately distinguishes the two. When the pathogen dies or sheds it's cell wall the Lipid A domain becomes accessible to immune cells and activates TLR4 which stimulates an immune response because it is recognized as definitely not human. The problem is however, the antibodies attacking the oligosaccharide portion (which are identical on the nerve cell and bacteria) end up being able to bind and attack both cells. When the pathogen is gone Lipid A is gone and the immune system dials back it's response. We rarely see this because we rarely treat autoimmune diseases with antimicrobials. But there are cases of acute autoimmune diseases where the body naturally clears the infection and the autoimmune disease disappears with it. Except in cases where people are at risk of permanent organ damage, the use of immunosuppressants is highly irresponsible given the current state of science on the issue. I would not recommend approaching this as an "autoimmune" disease unless all other modalities of treatment fail. "Autoimmunity" is not a mistake. It is a "calculated" response to infection where the body sacrifices tissue under pressure to avoid a potentially fatal infectious disease.

http://iai.asm.org/content/74/12/6517/F2.large.jpg

Post Edited (Psilociraptor) : 7/28/2018 11:47:28 AM (GMT-6)

The leaky gut hypothesis is an extension of this, not a different theory. A lot of people have focused on intestinal permeability to proteins and have not put nearly as much emphasis on the intestinal absorption of endotoxin and viable microorganisms. Many of these microorganisms are "pathobionts" which means they are normally harmless except in conditions that allow them to cause disease. Such as translocating from the lumen of the gut to systemic circulation. There ARE other mechanisms of autoimmunity besides molecular mimicry but it all comes back to the basics. Without activation of TLR, CLR, Nod-like receptors from pathogen associated molecules (PAMP) like Lipid A or flagellin it is very unlikely that you sustain a chronic inflammatory response. There are so many redundant mechanisms for preventing this.

To be honest I don't know why people keep thinking that. One problem that is rampant is the inability to differentiate "absence of evidence" from "evidence of absence." Many assume if they haven't found a pathogen it's not there. But advancements in microbial ecology have shown a small glimpse of how limited out detection methods are. Another problem is that our culture has a habit of treating the body as a fragile and often faulty system. The immune system is "over reacting", insulin resistance is "pathological", your cholesterol is "too" high, beta amyloids are "misfolded". See what I'm saying? Very few stop and ask "what is the functional purpose of this, what do these states actually indicate" which is usually a responsive behavior to infection or stressors of various types.

And yeah. I finished my bachelors in biochemistry last year, have been studying these darned diseases since I got sick 4 years ago, and am applying to medical school right now. Don't be hard on yourself. It's confusing stuff. Not because the concepts are hard but because of the politics surrounding it obscuring the truth. I feel like I'm constantly trying to untangle myself from it.

As for the drugs. Like I said, these drugs can prevent irreparable damage. I absolutely recommend them when they are warranted. My criticism is that they are not used as indicated. Which is as an adjunct to treating the actual cause and not a permanent solution. If you are experiencing progressive joint damage that you are worried about being permanent it's worth talking to a doctor about trying it and seeing how it goes. I'm just saying, if you have a chance to actually treat underlying causes and get off that crap you owe it to yourself. It's not always easy though and in those cases it's good to have immunosuppresives as an option. If it's a virus it can be tough. Even bacteria can be tough due to drug resistance/tolerance. I was lucky in that my disease responded very strongly to antibacterials and I've been able to reverse all my "autoimmune symptoms". But others are not as lucky. It's all about balancing quality of life with optimal health and there is no right or wrong way to go so long as you know what you're up again and are making the decision that feels most right to you

Post Edited (Psilociraptor) : 7/28/2018 8:03:17 PM (GMT-6)