Rheumatoid Arthritis Support Group
Rheumatoid arthritis is a chronic, inflammatory, multisystem, autoimmune disorder. It is a disabling and painful condition which can lead to substantial loss of mobility due to pain and joint destruction. The disease is also systemic in that it often also affects many extra-articular tissues throughout the body including the skin, blood vessels, heart, lungs, and...
So, RA is supposed to be "mostly" caused by over production of either IL-6, TNF, or T-Cell activity...and I'm sure research will uncover additional types of cytokines that affect RA, especially since the drugs that target these still leave people with full blown RA.
What happens if one of these works well but then you can't take it? For example, I had a liver enzyme elevation on Enbrel twice. It's no longer an option. Does that mean all anti-TNFs are out or should be out? And since it worked so well, does that mean my RA is only suppressed via anti-TNF? Is it even worth it to consider biologicals outside the anti-TNFs? Can our RA have just as strong an IL-6 contribution as TNF?
I'd love to hear your input.
What happens if one of these works well but then you can't take it? For example, I had a liver enzyme elevation on Enbrel twice. It's no longer an option. Does that mean all anti-TNFs are out or should be out? And since it worked so well, does that mean my RA is only suppressed via anti-TNF? Is it even worth it to consider biologicals outside the anti-TNFs? Can our RA have just as strong an IL-6 contribution as TNF?
I'd love to hear your input.
Minocin inhibits Il-6. Since it put my mother's aggressive advanced-stage RA into full remission, it can be interpreted as her primary inflammatory cytokine was indeed Il-6
Since minocin was reasonably effective - but did not put me in full remission - it can be interpreted that part of my inflammation is caused by Il-6 but the rest is another cytokine that produced in response to certain foods. (Since strictly following diet of avoiding positives on food allergy tests - does put me in remission)
Each case is different, and I'm sure a percentage of us have multiple cytokines causing our misery.
I was just going to say what 2scicrazed did, that there are probably several different inflammatory agents going after us. There are people here who have done well on anti-TNFs and then on a different one later. The anti-TNFs are all a little different, and you may do fine on another. I've read that the upcoming biosimilars (what would be a generic in another type of drug) will be a bit different than the name brand. There's hope that this will give us more options. Biosimilar Enbrel may not irritate your liver at all.
I know you said your unhappy liver is quite rare- does your rheumy have any answers on this?
We realized she could eat watered down canned food - and then had open heart surgery. She can eat now, does it slow and steady.
I haven't discussed the liver with my rheum yet. We did before he called in the liver doctor. My rheumatologist sticks to just his area...but he's good at coordinating efforts with other specialists.
I'll see him July 13. Before I see him, I'll see liver doc. I suspect my liver reaction to Enbrel is the "drug induced autoimmune hepatitis". It might just be standard elevation though.
I was on the higher dose by IV and at month 8 developed serious infection. So it worked TOO well. I can't recommend the 8mg/kg dose but I do think the 4mg/kg dose is worth a shot. If you choose SubCu stick with the 2 week interval as the weekly interval is the same as the higher IV dose (risky).
So Initial TNF inhibitor worker for me and IL-6 worked, T-cell did not.
I was seronegative on diagnosis however later tested positive. Recent anit-ccp was a "weak" positive. I have severe RA in stage 2 moving onto stage 3 and I am currently wheelchair bound. Off biologic therapy due to complications but getting back Actemra soon.
Giving it one more try at a much more conservative dose and interval and two week blood monitoring. If my CRP drops below 3 we will backoff a bit.