I just reread your question.

Simple answer ... yes my inflammation markers (CRP and ESR) were checked routinely. I don't recall any time when these biomarkers were not elevated. Prednisone decreased my biomarkers but rarely were they within the normal range. Actemra normalized my CRP and ESR. I was so surprised that I asked by rheumatologist if my CRP and ESR were "too low." These labs aren't reliable when a person is taking Actemra but my symptoms were also nil.

I still recall the day when I was on 30 mg of Prednisone. My rheumatologist was surprised when my CRP and ESR were STILL elevated and said I should take 35 mg. On 35 mg, my ESR and CRP were "mildly elevated." Multiple NSAIDs and DMARDs in addition to prednisone were tried but mildly elevated was the best I could ever achieve unless my prednisone dose was very high.

My biomarkers were used in conjunction with my symptoms. I would tell my rheumatologist when I experienced more pain when I tried to taper Prednisone lower. I think she believed me but she would check my inflammation markers just to see if my inflammation markers correlated with my symptoms. My CRP and ESR always correlated with my symptoms so my rheumatologist would say increasing my prednisone dose was warranted.

Actemra was approved on the basis that nothing else worked well. The other criteria was that I was "unable to taper off prednisone." All other alternatives including methotrexated had failed to normalized my inflammation markers but also for other reasons like infections and/or side effects.

Sometimes the failure of a medication was because of my intolerance for the medication. For example, methotrexate was working to control my PMR symptoms. I took methotrexate for more than a year. However, methotrextate over time increased my liver enzymes and was making me sick.

Does that answer your question any better?