Predictors of Pain in DAS28 Remission

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RA pain with so-called clinical remission is common

JackolanternWhen I tried to find a new rheumatologist in the spring of 2009, I learned all about clinical remission. The Good Doctors Treat Patients video tells the story of 1 of 3 doctors I saw at the time. Like the nursery rhyme, it was “Same song, second verse, a little bit louder and a little bit worse…” Every one of them took one look at my not-so-swollen fingers on a particular day, quoted my CRP to me, and declared my remission status. None of them inquired regarding pain or disability or physically examined my joints.

If you watch the video, you’ll hear much more about the Smart Doc I now see, so finding a new doc for me is NOT the point of this post.

Then, last February when I published my Swelling Confession, I wasn’t sure what the reaction would be. I wondered how many patients had noticed that external swelling and pain did not always correlate. Were there others like me who hadn’t said it out loud?

There are currently 167 replies to that post. That does not count a couple of hundred comments on Facebook from the 3 or 4 times it was posted there. Or the dozens of emails and private messages I’ve received on the subject of swelling and clinical remission. It’s plain to me now from the responses to the remission series, the swelling post, and several other posts that there’s a discrepancy between the way active Rheumatoid disease is defined by certain doctors and the experience of their patients. Actually, not a day goes by that someone doesn’t tell me this.

My argument with a new study on RA pain and so-called clinical remission

Ok so show us a study, Kelly!

Last week at the American College of Rheumatology Scientific Meeting (ACR), a study was presented that demonstrated that Rheumatoid patients in DAS28 remission still experience pain. The researchers noted that erosions (Sharp scores) and CRP results did not correlate with pain severity. (Please be patient with the link. The study is located in that pdf, number 1050, page S437, but I didn’t find a separate link yet.)

What’s DAS28? It’s one popular measure of clinical remission. This stands for Disease Activity Score with 28 joints considered. Here’s a five year old discussion of DAS28 that’s still relevant.

What’s good for us?

Someone noticed that Rheumatoid patients have pain which is not related to established inflammation markers such as CRP. That’s good. “Physicians often presume that inflammation is the stimulus for pain in rheumatoid arthritis (RA), but many patients have pain despite well-controlled disease.”

What I don’t like

Two things bother me about their conclusion, “These findings suggest that physicians should consider non-inflammatory etiologies of pain, such as a central sensitivity/symptom intensification syndrome, when evaluating pain in RA patients in remission.” First, I’m not sure I agree that based on DAS28, all of those patients are in remission or have “well-controlled disease.” Note that the last day of ACR, there was a session about redefining remission that compared the several major definitions of remission. The session actually included presentations of four studies. We’ll definitely have more discussion about re-defining clinical remission here on the blog soon.

Second, my personal experience (with my own RA and others) does not lend me to believe that a “symptom intensification syndrome” is responsible for Rheumatoid joint pain. Of course with long standing Rheumatoid disease, there’s mechanical pain and osteoarthritis to consider. But with brand new RA, I do not see how a symptom intensification syndrome could be established. To me, it sounds too much like the low pain threshold studies we’ve discussed here at length. When RA strikes the very first time in the middle of the night, with blood curdling pain as it has in so many patients I know, there has been no time to have established any kind of symptom intensification syndrome or pain processing malfunction.

My conclusion

There is physical cause of Rheumatoid pain that has not yet been recognized. The effectiveness of prednisone and NSAIDs would indicate that it may be inflammatory, but our current methods do not measure it successfully.

Recommended reading:

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Kelly Young. All rights reserved.

This entry was posted on Tuesday, November 16th, 2010 at 11:04 am and is filed under RA Research, Resources, and Rheumatology. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.


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