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@wilmingtonemperor

Good morning. I just had my 2d injection of Kevzara this morning, Nov 7. Administered by my lovely wife. the next one in 2 weeks I will self-inject. I was diagnosed in January of this year and put on 20mg of prednisone that we all have a love/hate relationship with. I tapered to 0 for 5 weeks and then had a brutal 5 day flare which put me back on prednisone. Doc told me when I was diagnosed about Kevzara in trials for PMR. Approved for RA since 2017 and approved for PMR in February of 23. Had labs on Oct 30 and Sed and CRP all back in normal range. But too early to say if Kevzara is the reason. Kevzara can take up to 3 months to achieve full effectiveness. Next week I drop to 10mg of prednisone and the plan is to continue to reduce the prednisone until I am off it entirely while on Kevzara. If a self injections every two weeks gets me of prednisone for good, no problem. I think it is worth a try for you.
Good luck

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Replies to "Good morning. I just had my 2d injection of Kevzara this morning, Nov 7. Administered by..."

I remember when I first started taking Actemra about 4 years ago. My ESR and CRP were always somewhat elevated while I was taking prednisone. I just assumed being slightly elevated was normal for me.

After Actemra was started, my ESR and CRP were so low that I got concerned. I asked my rheumatologist if my inflammation markers were too low. My bubble burst when I learned that these labs aren't reliable anymore when you are treated with an IL-6 blocker.

My inflammation markers remain low on Actemra. I think in conjunction with having no PMR symptoms then PMR might be in remission and my chronic inflammation is controlled. However, CRP levels may not accurately reflect the severity of infectious disease in patients who are being treated with Actemra. The same is probably true for Kevzara.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8003879/
If you have symptoms of an infection, don't let someone tell you you don't because your inflammation markers are normal.

"CRP levels may not accurately reflect the severity of infectious disease in patients who are being treated with TCZ. Although this fact may be known to rheumatologists, it should be disseminated among physicians attending patients at the ED. Prompt recognition and special attention is needed when evaluating these patients for probable infectious disease while on TCZ treatment. Interestingly, in our study, despite the impressive effect of TCZ on acute phase response, symptoms were not masked by the treatment and no significant delay in the diagnosis was made, leading in a prompt initiation of antibiotics and resolution of symptoms."