Few unclear things in AP – could you help me understand?

[Maciej P.]

Hi,

Short background:
I am 31 y.o. male from Poland (Europe). I have been diagnosed with RA 3 years ago (when I was 28). I actually started as palindromic rheumatism. My blood test are:
– HIGLY POSITIVE: aCCP/ACPA, ANA
– NEGATIVE: RF, CRP, Chlamydia, Lyme

My treatment was as follows (in that order):
1. NSAIDs – no improvemnt
2. sulfasalazine – no improvement
3. chloroquine – in improvement
4. methotrexate (injections) – IMPROVEMENT!!

After 2 years on MTX (starting with 10mg, then 15, 20, 15, 10, 7.5 and finally 5 and quit) after 4 monthos without MTX, the RA suddenly got back, few times wors that it was 2 years ago.

I have started to read a lot about RA cause and treatment, and AP (antibiotic protocol) seems very resonable, however I have few doubts. Could you kindly explain?

1. if mycoplasmas are the cause of RA – why it is not present in all people that were stuided for mycoplasma presence in RA? Several studies shown that mycoplasmas were found only in 30%-50% of examined cases of RA.

2. which antibiotic should I really try? there is a lot about tetracycline, doxycycline and minocycline, and I think the best in minocycline – however it is not clearly stated.

3. there is a lot about dosage, e.g. 2x100mg of minocycline on Monday, Wenesday and Friday or every day, or once a week, or … etc. … so again, it is not clearly stated what dosage should be at the beginning? how fast/often to increase it? how and when starting decrease dosage?

4. can I combine Methylprednisolone (4mg daily) with those antibiotics?

5. can I combine methotrexate with those antibiotics? there is only information about “methotrexate + doxycycline” but nothing about “methotrexate + minocycline”

kind regards,
Maciej

March 2016:
31 y.o. male, Poland, Europe.
Diagnosed with RA (started as palindromic rheumatism) at age 28 (SED negative, RF negative, CRP negative, Lyme negative, Chlamydia negative, ANA highly positive, aCCP/ACPA higly positive.
Treated with sulfasalazine - no success. Chloroquine - no success. NSAID - no success.
Treated with MTX injections (10mg->15mg->20mg->15mg->12,5mg->10mg->5mg) for 2years. Almost total remission. 3 months after MTX quit - got RA again with trippled strength.

[lynnie_sydney]

Hi Maciej and welcome
The weekends are usually a little quiet on the forum, so you may receive additional answers/perspectives in the coming week.

The FAQs section of the site should help answer most of your queries: https://www.roadback.org/faqs/. I have referenced some key ones in answers to your 5 questions below:

1. Many infections, in addition to mycoplasmas, have been studied as triggers for rheumatic diseases. Dr. Brown’s area of interest was specifically mycoplasmas but his book also spoke about Lyme, strep and brucellosis. Other researchers since his time have claimed other infectious agents such as bartonella, chlamydias and many others to be triggers or cause in rheumatic disease.
2. FAQ #10 addresses this question
3. FAQ #13 and #15 address this question
4 & 5. The answers to both are yes. There is a very good article which addresses this in our Resources section written by a renowned M.D. at Harvard Medical School (recently retired) who both researched minocycline in R.A. and treated patients with it. It is worth reading the whole article. Here is an excerpt, with a link to the article on the site below it:

Clearly minocycline can provide adjunctive therapy for RA. In other words, minocycline can be combined with any other available agent. There are no exceptions! Examples include Plaquenil, methotrexate, Arava, anti-TNF compounds like Enbrel & Humira and the new intravenous drug, abetacept (Orencia). Decreased doses of one or both agents may help to avoid gastrointestinal side effects. This regimen usually reflects a desire to obtain additional improvement or to gradually convert to the safer drug, minocycline. Examples include 1. Not having to increase the dose of methotrexate and 2. By increasing the dose of minocycline additional improvement and /or stability may be gained. Perhaps use of two oral drugs might preclude the necessity for an injectable and more expensive drug. Obviously judging the net effect of either drug is difficult or impossible. The same impasse may arise if a clinical or laboratory side effect occurs

https://www.roadback.org/resources/journal-articles/antibiotic-therapy-for-rheumatic-disease/

It is worth you taking a look at the whole FAQs and Resources sections of the site. There is a lot of valuable information there.

Incidentally, Palindromic Rheumatism is a common way that Lyme Disease initially presents. You mention that you have tested negative. However, a lot depends on the lab used for the testing. In your part of the world Infectolab in Germany is considered one of the best and most reliable to use.

I am sure you will receive other helpful and informative responses. But hope this helps to start with.

Be well! Lynnie

Palindromic RA 30 yrs (Chronic Lyme?)
Mino 2003-2008 100mg MWF - can no longer tolerate any tetracyclines
rotating abx protocol now. From Sep 2018 MWF - a.m. Augmentin Duo 440mg + 150mg Biaxsig (roxithromycin). p.m. Cefaclor (375mg) + Klacid 125mg + LDN 3mg + Annual Clindy IV's
Diet: no gluten, dairy, sulphites, low salicylates
Supps: 600mg N-AC BID, 1000mg Vit C, P5P 40mg, zinc picolinate 60mg, Lithium orotate 20mg, Magnesium Oil, Bio-identical hormones (DHEA + Prog + Estrog)

[Maciej P.]

Many thanks Lynnie for your answer!

Let me discuss bit more (let me number them for easier reference).
So far I have found that there are few possible causes of RA:

C1: mycoplasma
C2: amoeba
C3: L-form bacteria
C4: any other microorganism not clearly found yet (but in the internet the most info is about C1 and C2)

Possible treatments are:
T1: Antibiotic Protocol – low-does antibiotics for many months (6-24mo or even more) – works for causes C1, C3 and C4(?)
T2: Allopurinol for 1 week + Metronidazole for 6 weeks (according to Roger Wyburn-Mason anti-amoeba treatment)
T3: healthy diet (omega3, turmeric)
T4: boron suplementation
T5: classical modern medicine approach (DMARDs and NSAIDs)

I am really confused, since everyone claims to be right about “how to cure RA”, and in the same moment, nothing (except T5) is proven in scientific manner (yet, it is possible that farmaceutical comanies funds these researches… and you know 😉 )
It is also possible that all C1, C2, C3, C4 causes RA (assumption: RA is final form of many starting diseases) – so this could explain why not common and single reason for RA has been found yet.

I have already tried T3 and T4 simultaneously (1 month, no improvement – but the diet was not strict; my symptomes got worse, so I started steroids; don’t know if the worsening was HERX, or just RA attacked harder).

Honestly… what I want to try now (btw: I am fine with my lungs, liver and kidneys) is:
T2 (anti-amoeba) + doxycycline (Mino is barely avaible in Poland) + Methylprednisolone
(I am trying to quit Methylprednisolone if possible, but pain is too big quite often)

Of course everyting will be under supervision of my RA doctor.

I am just afraid if T2 (anti-amoeba) + doxycycline + Methylprednisolone would not get me any severe side effects and not help for RA at all? … too many questions… just don’t know if all of this make any sense or I am fooling myself.

What do you think about T2 (anti-amoeba) + doxycycline + Methylprednisolone?

many regagrds,
Maciej

P.S.
Is there anyone actually cured (e.g. remission for 10 years od more) by AP?

March 2016:
31 y.o. male, Poland, Europe.
Diagnosed with RA (started as palindromic rheumatism) at age 28 (SED negative, RF negative, CRP negative, Lyme negative, Chlamydia negative, ANA highly positive, aCCP/ACPA higly positive.
Treated with sulfasalazine - no success. Chloroquine - no success. NSAID - no success.
Treated with MTX injections (10mg->15mg->20mg->15mg->12,5mg->10mg->5mg) for 2years. Almost total remission. 3 months after MTX quit - got RA again with trippled strength.

[Lynne G.SD]

Hi Maciej;
I have been on AP for 17.5 years and full remission for 15.It takes a long time to see things improve but it’s worth the wait.
Lynne

[jasregadoo]

Hi Maciej,

I agree with Lynne G. Sometimes improvement takes awhile. I know for many people, it can take a couple of years. I have been on Minocycline for my RA for just over a year now. I am SO MUCH better, though I would not claim remission by any means. I’d say I’m 70% to 80% better. The worst of my pain is gone, but I still have inflammation, can’t wear rings on my fingers, etc. It took me about 3 months before I started to see real improvement, and I have stalled a few times since then. My doctor is not an AP doc per se, and is willing to put me on this treatment because I did not want to try the methotrexate, which was what she wanted to try (after plaquenil and sulfasalazine did not give me results). I am still on the sulfasalazine, as well as the minocycline.

There have been studies in the US that show Minocycline improves many people with RA. They are not big studies, because as you say, the money isn’t there. I know that some people do have to stay on Minocycline or other medications for life, if the disease is not to return. Some people do not have to do this, and are able to maintain remission. Because so many people relapse, I would hesitate to call any of these treatments a CURE, but instead a treatment.

Some people find a lot of benefit from further diet modifications, such as gluten and sugar free, etc. I tried that for a short time (3 weeks) but did not stick with it. I did have some tests run for food allergies, which all came back negative. I know the tests are not always conclusive. I am hopeful that I can get to full remission without such changes. When I read ‘The New Arthritis Breakthrough’, the emphasis is on the Minocycline, not diet changes. Many people though have had very good results from diet changes. Just something to consider.

I don’t know enough about the drugs you mention to speak to the combination. I can say that many patients use Prednisone to get them through the first few months of AP therapy, as reducing inflammation can help the antibiotics to get in and do their thing, as well as reducing the suffering of the patient.

Best on your journey!

[Maciej P.]

Lynne G.SD wrote:

Hi Maciej;
I have been on AP for 17.5 years and full remission for 15.It takes a long time to see things improve but it’s worth the wait.
Lynne

Thanks Lynne,
Please notice, that official medicine claims that Mino has anti-inflamatory activity (besides bacteria killing) and this anti-inflamatory is supposed to be reason why it helps some people having RA. Having into account, that you are taking it for 17.5years it could mean that it works very well for your inflamation, but not the cause of the inflamation itself? If it works in “killing bacteria” manner, you could stop it after the bacteria is killed (mycoplasma or whatever else) and be cured once forever? Am I right? Or am I missunderstanding something?

Thanks Jasregaddo for your answer as well. My MTX treatment also took a while (like 3-6 months) but I had like 98% of remission (just rare, gentle, 48hours flares were left). Some people (from what I have heard) also having long remissions after MTX (same like on Mino) – but that was not my case, so I wonder if either try T1, T2 or T5 from my first post in this topic.

I am just trying to investigate if Mino targets reason, not symptomps??? It is hard to say now.

The drugs I’ve mention also targets some ‘microorganisms’ – not the mycoplsmas, but kind of amoebas. I think I’ll give it a try… 6 weeks on Metronidazole shouldn’t be very long.

March 2016:
31 y.o. male, Poland, Europe.
Diagnosed with RA (started as palindromic rheumatism) at age 28 (SED negative, RF negative, CRP negative, Lyme negative, Chlamydia negative, ANA highly positive, aCCP/ACPA higly positive.
Treated with sulfasalazine - no success. Chloroquine - no success. NSAID - no success.
Treated with MTX injections (10mg->15mg->20mg->15mg->12,5mg->10mg->5mg) for 2years. Almost total remission. 3 months after MTX quit - got RA again with trippled strength.

[jasregadoo]

Maciej P. wrote:

I am just trying to investigate if Mino targets reason, not symptomps??? It is hard to say now.

That’s a question that many people have. I certainly don’t know the answer. I agree, it seems like if it were an infection, that you could be on the antibiotics for awhile and then stop. But I’m not a doctor, nor a scientist, so I can’t say for sure. For me, what is important is that it works. I’m willing to let the rest of it go. Some with perhaps a more curious mind than mine will want to figure out the answer. It did bug me for awhile, but when I kept reading different theories, by well qualified doctors and scientist, I decided not to spend any more of my time on it.

Good luck with your treatment, and I hope you find relief soon!

[Lynne G.SD]

Hi Maciej;
The reason AP works so well for people with SD is that it breaks down fibrosis.Zithromax does the same thing.Here are a few links you might like to read.
http://aac.asm.org/content/40/4/934.full.pdf

http://diabetes.diabetesjournals.org/content/54/5/1559.full

http://jid.oxfordjournals.org/content/199/9/1379.full

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3307860/

https://marshallprotocol.com/forum39/14650.html

http://www.ncbi.nlm.nih.gov/pubmed/23274564

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0060817

http://www.nature.com/cddis/journal/v4/n3/full/cddis201354a.html

http://www.ncbi.nlm.nih.gov/pubmed/23470532

http://www.emedexpert.com/facts/minocycline-facts.shtml

http://web.stanford.edu/group/hopes/cgi-bin/hopes_test/minocycline/

https://clinicaltrials.gov/ct2/show/NCT00203697

http://www.ncbi.nlm.nih.gov/pubmed/16443056

And this one that I can’t put into a link

Scholarly articles for minocycline and IL-6
Minocycline attenuates mechanical allodynia and … – ‎Ledeboer – Cited by 505
Minocycline prevents IL-6 increase after acute ischemic … – ‎Switzer – Cited by 10
… cytokines (IL-1α, IL-6, TNFα) by minocycline – ‎Celerier – Cited by 17
Search Results

PLOS ONE: Minocycline Suppresses Interleukine-6, Its …
journals.plos.org/plosone/article?id=10.1371/journal.pone.0060817

Apr 8, 2013 – Here, we investigated the effects of minocycline on IL-6 and its signaling pathways in ovarian cancer. In vitro, minocycline was found to …
Minocycline suppresses interleukine-6, its receptor system …
http://www.ncbi.nlm.nih.gov/pubmed/23593315
by P Ataie-Kachoie – ‎2013 – ‎Cited by 13 – ‎Related articles
Apr 8, 2013 – Here, we investigated the effects of minocycline on IL-6 and its signaling pathways in ovarian cancer. In vitro, minocycline was found to …
Minocycline prevents IL-6 increase after acute ischemic stroke.
http://www.ncbi.nlm.nih.gov/pubmed/23105953
by JA Switzer – ‎2012 – ‎Cited by 10 – ‎Related articles
Mar 15, 2012 – Higher levels of the inflammatory biomarker interleukin-6 (IL-6) correlate with poor clinical outcome in acute ischemic stroke (AIS). Minocycline …
Abstract 5603: Minocycline abrogates IL-6 signaling and …
cancerres.aacrjournals.org/content/73/8_Supplement/5603.short
by P Ataie-Kachoie – ‎2013
Apr 15, 2013 – Methods: Expression of IL-6 in control and minocycline-treated ovarian cancer cell lines (OVCAR-3, SKOV-3 and CAOV-3) was determined by …
The Tetracycline Derivative Minocycline Differentially Affects …
aac.asm.org/content/40/4/934.full.pdf
by M Kloppenburg – ‎1996 – ‎Cited by 114 – ‎Related articles
Minocycline is a tetracycline derivative that has beneficial effects in noninfectious … cells, whereas the production of interleukin 6 (IL-6) remained unaffected.
Cell Death and Disease – Minocycline selectively inhibits M1 …
http://www.nature.com › Journal home › Archive › March 07 2013
by K Kobayashi – ‎2013 – ‎Cited by 72 – ‎Related articles
Mar 7, 2013 – Figure 6 – Unfortunately we are unable to provide accessible … Primary cultured microglia were treated with LPS, IL-4, minocycline, or a …
Suppression of interleukin-6 by minocycline in a rat model of …
http://www.researchgate.net/…/7094398_Suppression_of_interleukin-6_by_mino…
In this regard an important role is assigned to interleukin-6. The present study, evaluated the effect of pretreatment with minocycline, on pain behavior …
Minocycline is an excellent Anti-inflammatory – Prof. Marshall’s …
https://www.marshallprotocol.com/forum39/14650.html
Feb 16, 2012 – 20 posts – ‎4 authors
Minocycline protects SH-SY5Y cells from 6-hydroxydopamine by …. by reduced mRNA levels of Interleukin (IL)-1β, IL-6, and indoleamine 2, …
A pilot open-label trial of minocycline in patients with autism …
http://www.jneurodevdisorders.com/content/5/1/9
by CA Pardo – ‎2013 – ‎Cited by 10 – ‎Related articles
Apr 8, 2013 – Minocycline is a tetracycline derivative that readily crosses the blood … The cytokines TNFα, IFN-γ, IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, …
Minocycline Reduces Proinflammatory Cytokine Expression …
diabetes.diabetesjournals.org/content/54/5/1559.full

by JK Krady – ‎2005 – ‎Cited by 294 – ‎Related articles
Minocycline represses diabetes-induced inflammatory cytokine production, … (3) documented local production of interleukin (IL)-6 in the vitreous humor of …

Scholarly articles for minocycline and IL-4
IL‐4 attenuates the neuroinflammation induced by … – ‎Lyons – Cited by 79
… to the M2 promoting effects of IL-4 are impaired in … – ‎Fenn – Cited by 47
Minocycline as a neuroprotective agent – ‎Stirling – Cited by 193
Search Results

Cell Death and Disease – Minocycline selectively inhibits M1 …
http://www.nature.com › Journal home › Archive › March 07 2013
by K Kobayashi – ‎2013 – ‎Cited by 72 – ‎Related articles
Mar 7, 2013 – On the other hand, IL-4 did not induce upregulation of NF-κB. This study indicates that minocycline selectively inhibits the microglia polarization …
Minocycline blocks asthma-associated inflammation in part …
http://www.ncbi.nlm.nih.gov/pubmed/23184953

by AS Naura – ‎2013 – ‎Cited by 7 – ‎Related articles
Nov 26, 2012 – Minocycline blocks asthma-associated inflammation in part by interfering with the T cell receptor-nuclear factor κB-GATA-3-IL-4 axis without a …
Minocycline Blocks Asthma-associated Inflammation in Part …
http://www.jbc.org/content/288/3/1458.full.pdf
by AS Naura – ‎2013 – ‎Cited by 7 – ‎Related articles
Sep 13, 2012 – Background: Minocycline protects against asthma independently of its antibiotic … Restoration of IL-4, ex vivo, rescued IgE production by.
Substance P (subP) and Minocycline Suppress Induction of …
https://aaaai.confex.com/aaaai/2015/webprogram/Paper19487.html
by C Kim – ‎2015
Feb 21, 2015 – Rationale: We reported that CD4+ and CD8+CD60+ T cells and 6 cytokines, including IL-4, were required for ragweed specific (RS) memory …
MINOCYCLINE BLOCKS ALLERGEN-INDUCED …
http://www.fasebj.org/cgi/content/meeting_abstract/27/1…/254.2
by AS Naura – ‎2013
Minocycline protects against asthma independently of its antibiotic function. … Such IL-4 production blockade was linked to a preferential inhibition of the NF- …
Asthma: New Insights for the Healthcare Professional: 2013 …
https://books.google.ca/books?isbn=1481657046
2013 – ‎Medical
University of New Orleans: Minocycline Blocks Asthma-associated Inflammation … and Th2 cytokine production (IL-4/IL-5/IL-12(p70)/IL-13/GM-CSF) and a partial …
A pilot open-label trial of minocycline in patients with autism …
http://www.jneurodevdisorders.com/content/5/1/9
by CA Pardo – ‎2013 – ‎Cited by 10 – ‎Related articles
Apr 8, 2013 – Minocycline is a tetracycline derivative that readily crosses the blood … The cytokines TNFα, IFN-γ, IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, …
IL4 attenuates the neuroinflammation induced by amyloidin …
onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2006.04370.x/pdf
by A Lyons – ‎2007 – ‎Cited by 79 – ‎Related articles
cycline, we assessed the ability of both IL-4 and minocycline to modulate the … Following treatment with Ab, IL-4 or minocycline, rats were assessed for their …
PLOS ONE: Minocycline Suppresses Interleukine-6, Its …
journals.plos.org/plosone/article?id=10.1371/journal.pone.0060817
Apr 8, 2013 – In vitro, minocycline was found to significantly suppress both constitutive and IL-1β or 4-hydroxyestradiol (4-OH-E2)-stimulated IL-6 expression …
Stem Cell Research & Therapy | Full text | Effective …
stemcellres.com/content/4/4/77

by Y Hou – ‎2013 – ‎Cited by 8 – ‎Related articles
Jul 5, 2013 – Minocycline is a semisynthetic tetracycline analogue suitable for ….. of IL-4 production in the hBM-MSCs or minocycline treatment groups …

1 2 3 4 5 6 7 8 9 10 Next

[Maciej P.]

So this all proves that Mino just suppress inflamation (similar to other DMARDs), rather than targeting root cause of our disease(s)… 🙁

March 2016:
31 y.o. male, Poland, Europe.
Diagnosed with RA (started as palindromic rheumatism) at age 28 (SED negative, RF negative, CRP negative, Lyme negative, Chlamydia negative, ANA highly positive, aCCP/ACPA higly positive.
Treated with sulfasalazine - no success. Chloroquine - no success. NSAID - no success.
Treated with MTX injections (10mg->15mg->20mg->15mg->12,5mg->10mg->5mg) for 2years. Almost total remission. 3 months after MTX quit - got RA again with trippled strength.

[lemons]

Maciej P. wrote:

So this all proves that Mino just suppress inflamation (similar to other DMARDs), rather than targeting root cause of our disease(s)… <noscript></noscript>

Hello Maciej
In my opinion , nothing is proven or disproven with regards to these diseases. Doctors , scientists , rheumatologists , experts and the like, are still no closer to finding the root cause.
I have a friend who was diagnosed with Lyme disease over twenty years ago. As you will know , this is, and has been proven to be caused by bacteria transmitted from ticks. She has in the past been treated long term with many different antibiotics, including Minocin. She is no better , she has not regained her health , she is very sick. As she used to work in the medical profession , she tests and assesses herself and has found spirochetes still detectable in her blood. She believes this is because antibiotics were not prescribed at the onset of the disease, it was several years until she was prescribed doxycycline.
I was diagnosed with sudden onset sero negative rheumatoid arthritis in 2013. I declined the standard treatment to treat the disease prescribed by my rheumatologist, consisting of weekly doses of 12mg methotrexate , 5mg of folic acid and found a doctor who agreed to treat me with 300mg of Minocin per week, for a year. I began treatment with AP within weeks of diagnosis.
In 2014 , a year into treatment I reached remission, blood work all back to normal range. I stopped taking Minocin at this point, on the advice of my doctor. He said that in approximately 65% of patients the antibiotic will stop the disease in its tracks and for me , he is proven correct. I have sustained remission for two drug free years, I have not even found the need to take the occasional non steroid anti inflammatory drug such as Ibuprofen.
I believe that for people treated late into the disease , the AP supresses the formation or growth of bacteria involved , but if administered early, there is a good chance that it can be eradicated. This assumption is also shared with the doctor who treated me.
Conclusion, for me , Minocin was the key to remission.

[Maciej P.]

hi Lemons,

are you Male or Female?

Nice to hear about your remission. It is also good thing to notice, that maybe only early started AP can gain “permanent remission”.

Have you been tested for: RF, CRP, ANA, aCCP/ACPA (aCCP is other name of ACPA). what was your results and what they are now?

March 2016:
31 y.o. male, Poland, Europe.
Diagnosed with RA (started as palindromic rheumatism) at age 28 (SED negative, RF negative, CRP negative, Lyme negative, Chlamydia negative, ANA highly positive, aCCP/ACPA higly positive.
Treated with sulfasalazine - no success. Chloroquine - no success. NSAID - no success.
Treated with MTX injections (10mg->15mg->20mg->15mg->12,5mg->10mg->5mg) for 2years. Almost total remission. 3 months after MTX quit - got RA again with trippled strength.

[lemons]

Morning Maciej ( Im in the UK),
I was initially tested with high SED rate of 27 , CRP of 32 , Rheumatoid Factor was negative, ANA negative. CCP was not performed due to negative RA factor.
My most recent test results were all well within normal range.
Nancy.

[Maciej P.]

lemons wrote:

I was initially tested with high SED rate of 27 , CRP of 32 , Rheumatoid Factor was negative, ANA negative. CCP was not performed due to negative RA factor.

thanks Nancy… so you had very different blood tests than mines – however it is valuable piece of info – many thanks!

btw: I had also RF negative but aCCP very positive (over 130, norm is under 4 in my lab). Seems like RF and aCCP are not related.

so my first conclusion is:
Mino worked extremely fine, for Female, started early, with SED and CRP positive and RF and ANA negative (aCCP unknown).

March 2016:
31 y.o. male, Poland, Europe.
Diagnosed with RA (started as palindromic rheumatism) at age 28 (SED negative, RF negative, CRP negative, Lyme negative, Chlamydia negative, ANA highly positive, aCCP/ACPA higly positive.
Treated with sulfasalazine - no success. Chloroquine - no success. NSAID - no success.
Treated with MTX injections (10mg->15mg->20mg->15mg->12,5mg->10mg->5mg) for 2years. Almost total remission. 3 months after MTX quit - got RA again with trippled strength.

[lemons]

I was diagnosed through the NHS, which is currently struggling to cope with a dramatic increase in the general population. The hospital I was allocated, is notoriously strapped for cash and will not perform diagnostic tests that it deems unnecessary.
My diagnosis of RA was based on clinical and physical symptoms. Many have suggested that there is no correlation between an RA factor and the CCP test , but I have read elsewhere that some disagree. Never the less , I am in remission and that is exactly the outcome I like everyone else, hoped to achieve.
The more I read and the more I speak to others with these diseases, strikes me how differently our symptoms present themselves, no one is the same. This leads me to believe that unlike other diseases, where patients share the exact predictability of disease course, auto immunity is the result of different strains of bacteria.
.

[Maz]

Maciej P. wrote:

thanks Nancy… so you had very different blood tests than mines – however it is valuable piece of info – many thanks!

btw: I had also RF negative but aCCP very positive (over 130, norm is under 4 in my lab). Seems like RF and aCCP are not related.

so my first conclusion is:
Mino worked extremely fine, for Female, started early, with SED and CRP positive and RF and ANA negative (aCCP unknown).

Hi Maciej,

You might find this study interesting, correlating anti-CCP to p. gingivalis:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748386/

I have been both highly positive for RF, anti-CCP, and CRP (SED is variable). I did very well on a combination of low dose minocycline and azithromycin, but the antibiotic that brought my anti-CCP down (by 40 points a month) was a long-acting penicillin (called Moxatag here in the US).

My RA was triggered by Lyme disease, but I have a history of bacterial meningitis as a baby, a very heavy vaccination schedule as a teen for travel abroad, constantly ill when young with tropical GI infections, lots of dental work, strep, childhood illnesses as an adult (Fifth’s and chicken pox), and then Lyme disease in my 40s and later discovering I was also dealing lead and mercury poisoning and a toxic multinodular goiter (thyroidectomy last summer). I think there is much in a person’s health history that can lead to the one last apple that tips the apple cart to an already overburdened immune system – a perfect storm of events. The book by Harold Clark, “Why Arthritis?” discussed how this can happen.

Many infections remain with us in latent state for life and others become reactivated when immune function is compromised. It’s like animals in a zoo who are happy while being well-fed, but when an earthquake hits, the zoo cages break open and the animals in the zoo escape to cause havoc.

You might also find this article interesting regarding mycoplasma:

http://www.rain-tree.com/myco.htm#.VumtHPD3arU

I think it would also be worth your while to read The New Arthritis Breakthrough, by Henry Scammell, because it should answer many questions. E.g. in terms of mycoplasma, these bugs are ubiquitous in nature…they are everywhere and the most common contaminant in a lab setting. It’s not that a good percentage of the world’s population isn’t infected – they are – the thing is that in folks with rheumatic disease, these bacteria release endotoxins that create a kind of allergic reaction, leading to tissue hypersensitivity and an inflammatory response.

There is a lot more info that can be supplied, but this might be a useful start. The goal with this treatment is to re-train the immune system to stop over-reacting to the toxic substances the bugs release, while lowering the pathogen load. Getting to this early, as Lemons has described beautifully, is the ideal, but in longer standing, more severe disease, the journey can take much longer and require treatment for life with maintenance dosing to prevent relapses.

[Author]

Posts