enthesitis/pain in tendons
- Thread starter msf
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I obviously don't have to technical know-how to be able to understand this issue (of immunostaining), but I do understand that it is contentious. I guess people will be swayed one way or the other by the weight of evidence (as they see it), rather than anyone particular piece of evidence (in the absence of techniques that can definitively prove infection). In that context, I though the following statement was interesting:
Reactive arthritis (ReA) is defined as a sterile synovitis developing after a distant infection, usually in the genitourinary or gastrointestinal tract. The detection of microbial components (microbial DNA and RNA) in the joints of patients with ReA has led to the reconsideration of this definition (59). Currently, ReA is better defined as an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body (104, 204).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC387405/
I realise that you might not share this view, but it seems to me that there is increasing evidence in favour of this view (along with increasing evidence against, I am sure). I guess it comes down to whether you think a positive result (i.e. identification of a pathogen) is more significant than a negative result (i.e. failure to identify a pathogen).
I think Simon posted something about how this effects the scientific process, but I think it was written in another language I don't understand, that of statistics.
Reactive arthritis (ReA) is defined as a sterile synovitis developing after a distant infection, usually in the genitourinary or gastrointestinal tract. The detection of microbial components (microbial DNA and RNA) in the joints of patients with ReA has led to the reconsideration of this definition (59). Currently, ReA is better defined as an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body (104, 204).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC387405/
I realise that you might not share this view, but it seems to me that there is increasing evidence in favour of this view (along with increasing evidence against, I am sure). I guess it comes down to whether you think a positive result (i.e. identification of a pathogen) is more significant than a negative result (i.e. failure to identify a pathogen).
I think Simon posted something about how this effects the scientific process, but I think it was written in another language I don't understand, that of statistics.
Finally, here is a study where they found rRNA in the SF of a patient with Y.
pseudotuberculosis http://onlinelibrary.wiley.com/doi/10.1002/1529-0131(199910)42:10<2239::AID-ANR29>3.0.CO;2-L/pdf
This is apparently found in C. trachomatis infection, but not in Yersinia, so it might just be an interesting anomaly. This following review makes a distinction between chronic infectious arthritis (C. trachomatis), and infection triggered aseptic arthritis, in which 'it is likely that these bacteria survive at an extra-articular site, in particular in the mucosal membranes of the digestive system and/or the lymphatic ganglions, and are carried to the joint by monocytes, probably in recurrent fashion'
http://ard.bmj.com/content/61/7/580.full#ref-22
pseudotuberculosis http://onlinelibrary.wiley.com/doi/10.1002/1529-0131(199910)42:10<2239::AID-ANR29>3.0.CO;2-L/pdf
This is apparently found in C. trachomatis infection, but not in Yersinia, so it might just be an interesting anomaly. This following review makes a distinction between chronic infectious arthritis (C. trachomatis), and infection triggered aseptic arthritis, in which 'it is likely that these bacteria survive at an extra-articular site, in particular in the mucosal membranes of the digestive system and/or the lymphatic ganglions, and are carried to the joint by monocytes, probably in recurrent fashion'
http://ard.bmj.com/content/61/7/580.full#ref-22
Jonathan Edwards
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I think it comes down to looking at the evidence without a preconceived idea of what you think the answer will be, to be honest. There are thousands of papers and decades of clinical experience behind the idea that reactive arthritis is a sterile reaction following an infective trigger. There have always been, over the last fifty years, a small number of people who want to stick to the old idea that these diseases are due to persistent infection. Remember that this is not a new idea, but the old one everyone believed in before. There is no 'increasing evidence' except in the sense that if people keep on looking for what they want to be there they will always find more doubtful data to support it. The real increasing evidence is away from persistent infection - with accumulating evidence from biologic therapies. Strangely the same people tend to hark back to the old idea of molecular mimicry, which makes the persistent infection idea redundant because it is an explanation for sterile inflammation. If you look through the review you quote carefully you find that the ideas do not actually add up. And coming back to TNF, they suggest that persistence is due to poor TNF production - yet removing TNF completely turns out to be very effective treatment!
The bottom line, to my way of thinking, about these old ideas that keep raising their heads, is that they are very simple and close to folk explanations. My experience with immunology is that it is much more subtle and that you have to have more subtle explanations to explain all the aspects of the diseases we see.
I appreciate that you have a different viewpoint, but I don't think evidence of rRNA, DNA, antigens, antibodies and culturing of the organism can be wholly put down to people seeing what they want to see. From what I have read, there is conflicting evidence as to whether there is bacterial persistence, but most of the evidence in favour has appeared recently. The same might be the case for the evidence against, but I don't see that evidence of the effectiveness of biologic therapies is proof that there isn't an infection. It seems to me that you might just be treating the symptoms, rather than the infection itself. As for molecular mimicry, maybe I used the wrong term. Perhaps I should have said collateral damage.
I appreciate that some immunological issues are too subtle for non-experts to understand, but just because an argument is simple doesn't make it wrong. I don't see why it's akin to a folk theory when it comes to chronic infection, but not when it comes to acute infection. Again, it all seems to come down to whether you can prove that there is a persistent infection, which comes back to the accumulating evidence on both sides.
Also, I think there has to be an alternative theory. I would like to hear one for why the antibody response is different in those patients with Yersinia-triggered reactive arthritis from those with uncomplicated infection.
The problem for non-experts, such as myself, is that when you talk to an immunologist they see it as an immune problem, when you talk to infectious disease expert they see it as an infection, etc. So in that sense I think it is very difficult for doctors not to have preconceived ideas, or at least biases towards certain explanations.
As I said before, I would like to know which of the competing theories is true in my case, but since it seems to be a contentious area I will keep my mind open to both possibilities.
I appreciate that some immunological issues are too subtle for non-experts to understand, but just because an argument is simple doesn't make it wrong. I don't see why it's akin to a folk theory when it comes to chronic infection, but not when it comes to acute infection. Again, it all seems to come down to whether you can prove that there is a persistent infection, which comes back to the accumulating evidence on both sides.
Also, I think there has to be an alternative theory. I would like to hear one for why the antibody response is different in those patients with Yersinia-triggered reactive arthritis from those with uncomplicated infection.
The problem for non-experts, such as myself, is that when you talk to an immunologist they see it as an immune problem, when you talk to infectious disease expert they see it as an infection, etc. So in that sense I think it is very difficult for doctors not to have preconceived ideas, or at least biases towards certain explanations.
As I said before, I would like to know which of the competing theories is true in my case, but since it seems to be a contentious area I will keep my mind open to both possibilities.
Jonathan Edwards
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Fair enough. I think the alternative theory for different antibody profiles would be that if T cells in a traffic domain go overboard and start generating cytokines inappropriately that is more or less bound to have a knock on effect on B cells making antibody since the B cell response is dependent on interaction with T cells.
Little Bluestem
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I have been having hip and leg pain for the last month. My chiropractor said it is tendons and seemed a little surprised it is still going on.
@msf Are you taking anything for enthesitis? How are you now?
It has got a bit worse for me, mostly feel it after having got up from resting and it takes about 5 minutes to go after walking around. I'm feeling it more through the whole foot now not just the heel down.
It has got a bit worse for me, mostly feel it after having got up from resting and it takes about 5 minutes to go after walking around. I'm feeling it more through the whole foot now not just the heel down.
Hi Rosie26,
I no longer experience the enthesitis-like pain, except very occasionally. The reason I no longer experience it is the FODMAP diet. I know this because when I don´t stick to it, the enthesitis-like pain returns. I put this down to the fact that Yersinia is known to reside in the ileum, and when inflammation in the gut is increased there is more translocation to other areas of the body, including the entheses. Note that this is not my theory, and fits well with the experience of people with ReA who find that diet relieves some of their symptoms. I am sure Prof. Edwards will have an alternative theory, but whichever explanation is valid does not change the fact that when I stick to the FODMAP diet I do not have the enthesitis-like pain (in fact, all my symptoms are alleviated, which suggests to me that my disease is gut driven).
I have also taken antibiotics for the Yersinia infection, and these may also have had a (less immediately noticeable effect), possibly by suppressing the Yersinia rather than getting rid of it since I still experience the same initial symptoms (mesenteric lymphadenitis, appendicitis-like pain) when I do not stick to the FODMAP diet.
If you try the same diet, I would suggest modifying it to cut out caffeine and as much sugar as possible.
I you do try it, I hope it helps you as much as it helped me.
I no longer experience the enthesitis-like pain, except very occasionally. The reason I no longer experience it is the FODMAP diet. I know this because when I don´t stick to it, the enthesitis-like pain returns. I put this down to the fact that Yersinia is known to reside in the ileum, and when inflammation in the gut is increased there is more translocation to other areas of the body, including the entheses. Note that this is not my theory, and fits well with the experience of people with ReA who find that diet relieves some of their symptoms. I am sure Prof. Edwards will have an alternative theory, but whichever explanation is valid does not change the fact that when I stick to the FODMAP diet I do not have the enthesitis-like pain (in fact, all my symptoms are alleviated, which suggests to me that my disease is gut driven).
I have also taken antibiotics for the Yersinia infection, and these may also have had a (less immediately noticeable effect), possibly by suppressing the Yersinia rather than getting rid of it since I still experience the same initial symptoms (mesenteric lymphadenitis, appendicitis-like pain) when I do not stick to the FODMAP diet.
If you try the same diet, I would suggest modifying it to cut out caffeine and as much sugar as possible.
I you do try it, I hope it helps you as much as it helped me.
@msf I have read up a bit on reactive arthritis and noticed diet can be helpful. I wonder if that diet would help me too even though I don't have major gut problems. My gut is only affected when I am having severe bouts of ME and I think that is caused by neuro-type disturbances not because of changes in gut microbiota. I've never looked at that particular diet but I will take a look and see what it is about.
I can't recall ever having problems with enthesitis until the last few years. Fortunately I don't have it all day long just after resting when I get up to walk I notice it and I walk like I am crippled for about 5 minutes.
Interesting to hear the diet. I will let you know how I get on if I try it.
I can't recall ever having problems with enthesitis until the last few years. Fortunately I don't have it all day long just after resting when I get up to walk I notice it and I walk like I am crippled for about 5 minutes.
Interesting to hear the diet. I will let you know how I get on if I try it.