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Re: any hope? momchrisgr 11/12/19 12:40 PM
He is HLB27 negative.

But what difference does it make..? I cannot understand, why all doctors ask to do the test of HLB27, completely useless...
So many people who are HLB27 negative have the disease...
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General Message Board for Ankylosing Spondylitis and Related Diseases Jump to new posts
Re: Enthesitis and COSENTYX momchrisgr 11/12/19 12:32 PM
hi KatherineL16, No, Chris has not started sulpha yet, but rheumatologist has already decided it, we just wait for some results (calprotectine...anyway). What he already has done is 6 weeks of naprosyne (during August and September) but did not work and... prp... in other words: Platelet-rich plasma. Platelet-rich plasma was a waste of money for us. He did it twice, first time at the end of last May and then in the beginning of July. Although he suffers pain without complaining a lot, after this procedure he was in great pain for about a week or so. What a silly decision... such a failure... did nothing at all...
From what I have read, enthesitis is very difficult to cure. First of all, if you inject cortisone in the heel, you can have the Achilles tendon ruptured.
If you have enthesitis in the knee ( Osgood Schlatter) you cannot take cortisone injection.... Dead end...
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Re: Potential "Patch" for AS PainintheAS 11/12/19 06:44 AM
Also, aside from getting your immunoglobulins tested, the other things I mentioned (turmeric/curcumin and berberine) have anti-inflammatory and antibacterial effects. To me, this would represent a safer first choice than FMT's. If you also want to further reduce inflammation, I agree that specific strains (like the L. reuteri yogurt option) could possibly be good. But I would caution anyone from taking high doses of probiotics in an imbalanced state. Generally, the idea is: clear the bad, then heal the damage (manuka honey is good for this if you can handle the carbs at this point in your disease state,) then restore with beneficial flora. You're opting to throw billions of more organisms into the mix with a potentially leaking gut, then you might be asking for trouble. Take the least risky approaches first and the most gradual changes to allow your immune system time to start down-regulating. More organisms rarely would equal downregulated immune system. The only time I would recommend FMT's is if you have a nasty C.diff infection that has not responded to any kind of antibiotics, etc. Then you need to "crowd it out."

Just my $0.02
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Re: Enthesitis and COSENTYX KatherineL16 11/11/19 09:12 PM
Hi @momchrisgr, not silly at all. After the anti-inflammatories failed, I brought up trying methotrexate or sulfasalazine before starting biologics, but my rheumy said they would not be helpful for my case. I just checked to see if I could find literature to back that up, and found this study: https://www.ncbi.nlm.nih.gov/pubmed/16583475. The conclusions echo what she had told me: "Across all patients with AS, SSZ showed some benefit in reducing ESR and easing spinal stiffness, but no evidence of benefit in physical function, pain, spinal mobility, enthesitis, or patient and physician global assessment. Patients at an early stage of disease, with higher level of ESR (or active disease) and peripheral arthritis, might benefit from SSZ."

Every body is different, though. Did SSZ do anything for you?
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Re: Enthesitis and COSENTYX Golanist 11/11/19 09:06 PM
After being on Humira and Enbrell for a few years I changed over to Cosentyx some 9 months ago.
Working pretty well so far for both the enthesitis and arthritis. Upped the dose to 300 mg/month due to waning efficacy at the end and beginning of each month and it's helping.
No magic wand. Still take NSAIDs almost every day but feel better and more functional.
Good luck
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Re: Potential "Patch" for AS PainintheAS 11/11/19 08:25 PM
Originally Posted by achala
I just checked the several blood counts results i had in the past 3 years and usually my eosinophilic count is at the lower limit end. They put me at that time on Montelukast and Budesonide (Budenofalk), that is glucocorticosteroid to no effect, but I was also on COX-2 inhibitor at that time also to no effect much.

Only after switching to Sulfasalazine for 8 months AAU & Achilles enthesitis subsided. But I cannot use it at this moment due to some other plans so I am back fighting AAU with Predonisone. IKB kinase inhibitor would be a good path to explore.
By the way I understood SSZ doesn't work for Axial but not sure why....


If it doesn't work for axial, it could be that my theory is correct and that tolerance to self is lost. You're just attacking the lymph fluids draining from your intestines, which the first place they exit is the lymph network that surrounds the lower spine and sacroiliac region. This would be a different form of attack than say, the homodimers formed by HLA-B27 causing peptides to bind at various sites around the body, including in the eyes.


Originally Posted by Caturday
So, what would you recommend for hla-b27 negative and positive patients in terms of supplements they can easily acquire to stem the affects of inflammation? What would be your foundation that leads to a protocol? You've done so much research I think you should condense this info and create something like a protocol for people to follow I think this would be easier. I understand everyone is different but this anti-biotic stuff and the research you've shown on this thread has opened my eyes more.

I still think however, ultimately fecal matter transplant is the ultimate way to heal a leaky gut and reverse inflammation permanently in our biome. But, the donors have to be in perfect health and that is hard to find.


I was trying to say that going to an immunologist should be your first course, as you need to know what you're reacting to. I don't think fecal matter transplant is the right option for everyone because each person has different genetics and thus will respond to different bacteria differently. We need to normalize the system first, then it will be able to handle the influx of different bacteria more appropriately. If you are not HLA-B27+, then please find out what your body is reacting to by going to an immunologist and checking what IgA and IgG levels are, perhaps do an entire immunoglobulin panel. We cannot say that everyone arrives at the same place via the same route. It is just a common "response" to various assaults on the immune system, which I believe are related to pathogens. I would use EXTREME caution when considering fecal matter transplants...if your immune system is over-reactive, then using even healthy bacteria (but different drastically from what you have currently) then you could be promoting a HUGE influx of new pathogens into your bloodstream, etc. This could then cause even more upregulation of your immune system if done incorrectly or at the wrong time (the immune system is not functioning properly and will misbehave.)
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Re: Potential "Patch" for AS achala 11/11/19 07:58 PM
I just checked the several blood counts results i had in the past 3 years and usually my eosinophilic count is at the lower limit end. They put me at that time on Montelukast and Budesonide (Budenofalk), that is glucocorticosteroid to no effect, but I was also on COX-2 inhibitor at that time also to no effect much.

Only after switching to Sulfasalazine for 8 months AAU & Achilles enthesitis subsided. But I cannot use it at this moment due to some other plans so I am back fighting AAU with Predonisone. IKB kinase inhibitor would be a good path to explore.
By the way I understood SSZ doesn't work for Axial but not sure why....
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General Message Board for Ankylosing Spondylitis and Related Diseases Jump to new posts
Re: Potential "Patch" for AS Caturday 11/11/19 07:08 PM
So, what would you recommend for hla-b27 negative and positive patients in terms of supplements they can easily acquire to stem the affects of inflammation? What would be your foundation that leads to a protocol? You've done so much research I think you should condense this info and create something like a protocol for people to follow I think this would be easier. I understand everyone is different but this anti-biotic stuff and the research you've shown on this thread has opened my eyes more.

I still think however, ultimately fecal matter transplant is the ultimate way to heal a leaky gut and reverse inflammation permanently in our biome. But, the donors have to be in perfect health and that is hard to find.
70 4,727 Read More
General Message Board for Ankylosing Spondylitis and Related Diseases Jump to new posts
Re: Enthesitis and COSENTYX bizzylizzy 11/11/19 05:54 PM
@KatherineL16--I think that would be great to stay in touch and compare notes as we try to figure this out! I'm going to try to get into a teaching hospital rheumatologist so I can be around folks that are getting the first info on new treatments.

@momchrisgr-I tried sulphas years ago-it was a no-go. Zero effect after 6 months. Interestingly I had to request it. I ALWAYS have to request my med changes. It's frustrating.

Thanks you guys!
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Re: Potential "Patch" for AS PainintheAS 11/11/19 05:42 PM
Originally Posted by Caturday
Originally Posted by PainintheAS
Originally Posted by achala
Here, in continental Europe Rifaximin is prescribed for Crohne D.

I think what you are describing here is an inflammation of mesenteric lymph nodes where T cell–dependent IgA class switching takes place. However, in case of for example mine (during the first onsets of AAU and AS in general I performed Colonoscopy that indicated Eosinophilic Ileitis), it is more likely thateosinophils contribute to T cell–independent IgA class switching, which mainly occurs in the small intestinal lamina propria, where abundant numbers of eosinophils reside.
Notably the up regulation comes with caloric intake, that would explain the fact that in some instance prolonged fasting can bring benefits, at least for the poeple with similar to mine expressions (but how often we know what really is there, my colonoscopy was purely coincidental)

Eosinophilic link

What activates dendritic cells, and the mechanism could be explained above (interesting article).
Now I am thinking, due to different roots, paths AS was triggered, people fail biologics that answer to specific circumstances... bringing us back to the HLA B27 + predisposition as secondary phenomena in this vicious circle.

just food for thought not a challenge of any kind..., we are all in this wink


While this is interesting, it seems that this theory doesn't fit the bill of IL-23/IL-17 activation. From reading your article, this exists in an IL-5/IL-13 axis. Not to mention, in AS, it is noted that EPC (eosinophilic progenitor cells) are depleted in AS patients (Link.) The drugs that would mitigate the effect you are talking about would be anti-eosinophilic in nature, as mentioned in the conclusion of your article (many drugs similar sounding to that of those that are prescribed for AS, however, they work on different interleukins.) The drug reslizumab is also listed to affect the same interleukin, and is indicated for asthma. I did have asthma growing up, so that is of some interest for me to ponder the lung association.

I think the loss of tolerance to self is causing inflammation that is degrading/depleting specific areas of the intestine of eosinophils, which is why they are found to be depleted in AS patients per the article above. Leaky gut is known to be associated with those that have joint/tendon and soft-tissue disorders. The inflammatory pathways activated by bacteria and other pathogens created by dietary carbs are the kind that can flag the immune system to produce TNF-alpha, which activates NF-kB signaling, which then promotes the IL-23/IL-17 axis. This is the axis described as being both a) correlated with changes in affected individuals through GWAS (genome-wide association studies) and b) the target of the other drugs people are taking (inhibiting their joint/tendon and bone. Rifaximin also works on NF-kB signaling, so the fact that it is beneficial for me and a few others reinforces that it is working on the same pathways as these other drugs, albeit a more targeted inhibition.

I have also been reading on how to stop HLA-B27's propensity to form homodimers, as those are the substances that are binding strange peptides and antigens. The HLA-B27 molecule folds slowly, which is what allows for the creation of homodimers. This activates the UPR (unfolded protein response,) in the cell, which upregulates both NF-kB and, subsequently, cytokine expression (the NF-kB upregulates TNFα, IL-1, IL-6, and IL-23. IL-23 is required for the survival of Th-17 cells.) It has also been shown that certain pathogens take advantage of this pathway, such as Salmonella. That particular pathogen utilizes the UPR to infect cells, and, in HLA-B27+ individuals, the bacterial load to the cell is quadrupled compared to controls! One approach is to reduce the formation of homodimers by using Sulfasalazine. I read into Sulfasalazine and the literature states that it is its IKB kinase inhibitory activity that reduces homodimer formation. These homodimers recognize natural killer cells (KIR3DL2) and these are present on the surface of Th17 cells, which release IL-17 when activated, who have been granted increased survival from the IL-23 via the upregulated UPR. (Link.)

So, I did some more digging on natural IKB kinase (both alpha and beta inhibitors.) Turns out, I was onto something with Baicalein, from skullcap. I mentioned I took it alongside Rifaximin with really great results. Turns out that Baicalein not only stimulates ~20 tight-junction proteins to help seal the leaky intestines, it's also an IKB kinase inhibitor (Link!)

The table provided in this study suggests that there are many natural substances that are IKB kinase inhibitors. Since baicalein is working well for me, I am willing to try a few other of these natural compounds to test their effects. The next goal would be to see how to regain dendritic cells in the intestines and to regain tolerance to self. This would effectively be a double-whammy. You'd reduce the UPR-induced stress as well as reduce the inflammation being upregulated in the intestinal cells.

P.S. I've also found this link between dendritic cells and HLA-B27. It seems that just like in so many of us who have had an "event," and then began to experience symptoms, the dendritic cells are activated after maturation. This starts a transient production of homodimers. These homodimers would then cause the associated binding of peptides and antigens, which then causes more stress. I believe this is why the disease takes time to build because these transient cycles occur over and over until the system is finally degraded enough from the constant barrage of inflammation due to these dendritic cells being activated (Link.)


What about with people who are negative for hla-b27 gene? Since, you talk about leaky gut often why not take certain probiotics to help your microbiome go into a less inflammatory state? Have you considered fecal matter transplant or even helminthic therapy? They are running clinical trails for FMTs in denmark and finland for psoriatic arthritis at the moment. The helminths are interesting as they do upregulate IL-10 and other anti-inflammatory properties but I don't know which ones specifically off the top of my head.

So, the article you linked mentioned some chinese herbs that would help assist in IKB kinase inhibitors. And, yet again I can't find a doctor willing to give me Rifaximin sadly.


Yea, I've mentioned HLA-B27 negative people earlier in the thread. I was saying it would be a good idea to go to an immunologist to see what IgA and other immunoglobulins you might be producing. Usually, IgA/IgG to specific pathogens will be elevated. Probiotics are a great idea, but you have to consider if your gut is leaking...you need to be careful what you put in it. The Chinese herbs can help with the sealing of the guts, allowing you to be "safer" when putting probiotics in your system.

For Rifaximin, you'd need to approach it from the "I have IBS" route. Rifaximin is approved for that indication, including SIBO. Look for some studies related to Rifaximin having VERY few side-effects (since it's not absorbed by the body) and also dealing with SIBO/IBS. Present these to a GI, then see if you can get him to prescribe you a trial run (usually 2 weeks.)
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General Message Board for Ankylosing Spondylitis and Related Diseases Jump to new posts
Re: Potential "Patch" for AS Caturday 11/11/19 04:23 PM
Originally Posted by PainintheAS
Originally Posted by achala
Here, in continental Europe Rifaximin is prescribed for Crohne D.

I think what you are describing here is an inflammation of mesenteric lymph nodes where T cell–dependent IgA class switching takes place. However, in case of for example mine (during the first onsets of AAU and AS in general I performed Colonoscopy that indicated Eosinophilic Ileitis), it is more likely thateosinophils contribute to T cell–independent IgA class switching, which mainly occurs in the small intestinal lamina propria, where abundant numbers of eosinophils reside.
Notably the up regulation comes with caloric intake, that would explain the fact that in some instance prolonged fasting can bring benefits, at least for the poeple with similar to mine expressions (but how often we know what really is there, my colonoscopy was purely coincidental)

Eosinophilic link

What activates dendritic cells, and the mechanism could be explained above (interesting article).
Now I am thinking, due to different roots, paths AS was triggered, people fail biologics that answer to specific circumstances... bringing us back to the HLA B27 + predisposition as secondary phenomena in this vicious circle.

just food for thought not a challenge of any kind..., we are all in this wink


While this is interesting, it seems that this theory doesn't fit the bill of IL-23/IL-17 activation. From reading your article, this exists in an IL-5/IL-13 axis. Not to mention, in AS, it is noted that EPC (eosinophilic progenitor cells) are depleted in AS patients (Link.) The drugs that would mitigate the effect you are talking about would be anti-eosinophilic in nature, as mentioned in the conclusion of your article (many drugs similar sounding to that of those that are prescribed for AS, however, they work on different interleukins.) The drug reslizumab is also listed to affect the same interleukin, and is indicated for asthma. I did have asthma growing up, so that is of some interest for me to ponder the lung association.

I think the loss of tolerance to self is causing inflammation that is degrading/depleting specific areas of the intestine of eosinophils, which is why they are found to be depleted in AS patients per the article above. Leaky gut is known to be associated with those that have joint/tendon and soft-tissue disorders. The inflammatory pathways activated by bacteria and other pathogens created by dietary carbs are the kind that can flag the immune system to produce TNF-alpha, which activates NF-kB signaling, which then promotes the IL-23/IL-17 axis. This is the axis described as being both a) correlated with changes in affected individuals through GWAS (genome-wide association studies) and b) the target of the other drugs people are taking (inhibiting their joint/tendon and bone. Rifaximin also works on NF-kB signaling, so the fact that it is beneficial for me and a few others reinforces that it is working on the same pathways as these other drugs, albeit a more targeted inhibition.

I have also been reading on how to stop HLA-B27's propensity to form homodimers, as those are the substances that are binding strange peptides and antigens. The HLA-B27 molecule folds slowly, which is what allows for the creation of homodimers. This activates the UPR (unfolded protein response,) in the cell, which upregulates both NF-kB and, subsequently, cytokine expression (the NF-kB upregulates TNFα, IL-1, IL-6, and IL-23. IL-23 is required for the survival of Th-17 cells.) It has also been shown that certain pathogens take advantage of this pathway, such as Salmonella. That particular pathogen utilizes the UPR to infect cells, and, in HLA-B27+ individuals, the bacterial load to the cell is quadrupled compared to controls! One approach is to reduce the formation of homodimers by using Sulfasalazine. I read into Sulfasalazine and the literature states that it is its IKB kinase inhibitory activity that reduces homodimer formation. These homodimers recognize natural killer cells (KIR3DL2) and these are present on the surface of Th17 cells, which release IL-17 when activated, who have been granted increased survival from the IL-23 via the upregulated UPR. (Link.)

So, I did some more digging on natural IKB kinase (both alpha and beta inhibitors.) Turns out, I was onto something with Baicalein, from skullcap. I mentioned I took it alongside Rifaximin with really great results. Turns out that Baicalein not only stimulates ~20 tight-junction proteins to help seal the leaky intestines, it's also an IKB kinase inhibitor (Link!)

The table provided in this study suggests that there are many natural substances that are IKB kinase inhibitors. Since baicalein is working well for me, I am willing to try a few other of these natural compounds to test their effects. The next goal would be to see how to regain dendritic cells in the intestines and to regain tolerance to self. This would effectively be a double-whammy. You'd reduce the UPR-induced stress as well as reduce the inflammation being upregulated in the intestinal cells.

P.S. I've also found this link between dendritic cells and HLA-B27. It seems that just like in so many of us who have had an "event," and then began to experience symptoms, the dendritic cells are activated after maturation. This starts a transient production of homodimers. These homodimers would then cause the associated binding of peptides and antigens, which then causes more stress. I believe this is why the disease takes time to build because these transient cycles occur over and over until the system is finally degraded enough from the constant barrage of inflammation due to these dendritic cells being activated (Link.)


What about with people who are negative for hla-b27 gene? Since, you talk about leaky gut often why not take certain probiotics to help your microbiome go into a less inflammatory state? Have you considered fecal matter transplant or even helminthic therapy? They are running clinical trails for FMTs in denmark and finland for psoriatic arthritis at the moment. The helminths are interesting as they do upregulate IL-10 and other anti-inflammatory properties but I don't know which ones specifically off the top of my head.

So, the article you linked mentioned some chinese herbs that would help assist in IKB kinase inhibitors. And, yet again I can't find a doctor willing to give me Rifaximin sadly.
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