Today, my Roo is six years old. Saturday, I went shopping with Mary Khris to buy supplies to create a little Thomas the Tank Engine party. Since I can’t draw characters with icing any more, we look for ways things can be used creatively. I found some lightweight rubber train engines (actually bath toys!) that we can use on top of the cake. Wish us luck – we’ll be doing that this afternoon. (I’ll try to post a photo later.)
Does inflammation cause the usage principle?
Saturday morning I was typing at home, thankful my fingers were doing better. It seemed perfectly reasonable to get up and go on this short errand. As I got out of the car, I thought let’s do this quickly.
You can probably guess what came next. I dragged myself as far as I could, but within a few minutes, I sat on the floor because I couldn’t find anything to sit on. My knees and hips would not hold me up another second.
The next two hours passed that way with me sitting at the grocery store to rest, too. At least they have chairs!
My hips, knees, and feet were screaming when we got home. I looked down at slightly puffy legs and felt like I had a revelation. Inflammation.
Screaming is what our joints feel when we talk about the usage principle. But inflammation is probably what’s actually behind it. That’s why NSAIDs work. Or prednisone.
Many patients like me have been told that we have no inflammation because our inflammation markers are not severely elevated (CRP and sed rate). That’s why many have fibromyalgia attached to their diagnosis. There has to be an explanation for joint pain, fatigue, and fever with “normal” markers – and that one makes sense to some doctors.
Citrullination as a signpost of inflammation
Over the last week, I’ve been reading a detailed new article on anti-CCP – read abstract here. My eyes sometimes glaze over during science lectures, so I read this thing five times. Determined to get it.
Here’s one thing I grasped:
“During inflammation, when many cells die by apoptosis or necrosis, it is possible to detect citrullinated proteins at the site of inflammation, both in animal models of inflammation and in the inflamed synovial tissues of patients with or without RA.” So, citrullination occurs at the site of inflammation.
Anti-CCP tests measure anti-citrullinated protein antibodies (ACPA). My anti-CCP has stayed very high (over 250) while I had “no inflammation.” Why did Dr. Dip tell us “Anti-CCP is always that high in RA patients, but it doesn’t reflect inflammation”? By the way, if you’re in the minority of RA patients who fail the anti-CCP test, the article indicates future research should lead to tests for ACPA-negative RA subgroups who have a non-citrulline-dependent immune response.
Mary Khris put ice packs on my feet and it helped. She didn’t read the article; she just knew. My hip was the worst and I did not want ice there. I dragged that leg all day Sunday. It sounds so simple, but it just sunk in for me. This is real. I really do have this inflammatory disease, despite my low-CRP genes and Doc Space Heater’s insisting: “You have no inflammation.”
- Click here to read the description for the illustration of current theory of the RA inflammation cycle – it’s a good summary of the article if you don’t have access to the full pdf.
- Link to view diagrams in the inflammation and anti-CCP article called Anti-CCP antibodies: the past, the present and the future.
- Evidence of inflammation in bone and synovial tissue of patients doctors thought were in remission
- Inflammation contradictions & genes influence CRP test up to 232%
- Which Biologic Treatment Should RA Patients Try Next?
- Rheumatoid Arthritis Fevers