Can sed rate and c reactive results be normal while taking Prednisone?

PMR for 12 years. Was put on prednisone by ER doc prior to diagnosis. (He said I had sciatica and the shoulder pain was coincidental!) I’ve never been below 5mg. Never had ESR or CRP tests before I started pred. Never tested outside normal range for either test- always low range of normal.

In a way ... I was always "fortunate" in regards to my inflammation markers. My diagnosis was largely based on a high ESR and CRP.

After PMR was diagnosed ... my prednisone dose was largely titrated based on my inflammation markers AND how I reported my level of pain. The way I reported my pain wasn't too fancy. I simply reported "more pain" or "less pain" or the "same amount of pain" from one week to the next. When my pain stayed the same ... I reported "no change" and my rheumatologist understood that I didn't mean "no pain."

My rheumatologist didn't have to be told that I had pain because she would document things like "antalgic gait" and "facial grimace" and other descriptions in her own words. Many times she quoted my exact words in her notes for how I described my pain. Most of the time, my "body language" expressed pain so I didn't have to say anything.

I never sensed that my pain level was ever doubted by my rheumatologist. Sometimes I was told that I should be experiencing more pain than I reported based on my higher than normal inflammation markers which were trending higher many times.

@ceedub If you have an AI tool, you might ask it the question about reliability while on prednisone and GCA symptoms. I believe that both doctors could be correct because one is looking solely at potential eye damage and the other is looking much more holistically at overall symptoms returning. Just because doctors don't agree does not make one right and the other view point wrong.
I have had totally asymptomatic GCA for several years that went undiagnosed and has done vascular damage, not eye damage because I have never had a cranial symptom. Plus my eye doctor examined me annually and looked for signs of GCA. It was silently doing damage elsewhere.
I am telling you this mainly so you realize that there are patients outside the fat area of the bell curve and from time to time it could be you. Doctors look mainly at the fat area because that's where most of us are most of the time.

@jabrown0407 Appreciate your insight and your taking time to reply! I did as you suggested and found what appears to be fairly reliable information regarding inflammatory markers while on Tocilizumab .
I was unfamiliar with droracle.ai but believe site may be quite trustworthy. Below are a couple of links, including one that was a footnote to original. To summarize the latter: "Conclusions: CRP levels may not correctly reflect the severity of infectious diseases during tocilizumab treatment. Increased awareness of the masking effect of tocilizumab on the APR during infection is needed in order to avoid a delay in the diagnosis."
https://www.droracle.ai/articles/918233/can-tocilizumab-actemra-suppress-creactive-protein-resulting-in-a
https://pubmed.ncbi.nlm.nih.gov/33804790/

@ceedub Interesting. Please keep in mind that PMR and GCA are not infectious diseases. CRP and Sed Rate measure inflammation in your system. They do not distinguish between sources of the inflammation.
Based on my understanding, simple things like exercise can contribute to inflammation. As can a cat scratch or any other simple injury as well as infections and autoimmune problems.

@jabrown0407

ESR and CRP are “indirect” measures of inflammation as compared to being able to directly quantify the actual amount of inflammation. This why ESR and CRP are never very reliable but are useful when a doctor expects excessive amounts of inflammation.

Suppression of inflammation in cases of an infection isn’t a good idea because it delays treatment with antibiotics. This isn’t why inflammation is suppressed in the context of PMR.

@dadcue They are considered indirect measurements because they do not actually quantify the inflammation in your system. They quantify a normal consequence of inflammation and thus the interpretation that if you have that much of what ever is being measured then your inflammation is high, low, normal.
Other indirect measurement tests that we see routinely are sodium, potassium, creatine, several thyroid tests and liver tests. In reality many blood tests fit the definition of indirect measurement. Even glucose is indirect.
The catch with inflammation is there are so many different types of inflammation, all the IL's, MMP's, TNF's, Th's, Treg. Each of these super types have sub types. More than I care to learn about. That's my doctor's job!

My Sed Rate and C Reactive were always normal. While my primary doc put me on Prednisone , the second so-called specialist gave me an aggressive reduction rate which I could not do so I resisted, went at my own pace and did what gave me less pain. His sense was that I didn’t have PMR, it was a mistake I was on it and he wanted me off Pred fast. He decided it was something else but he didn’t know what ! I KNEW it was PMR based on everything I read on this Mayo Connect site. He finally admitted that it was PMR. But still berated me for getting information from the internet! He knew best!! Turns out he did not. That said, 17 Months later I was fine and out of pain. And off Pred.

@janetilley

It is worse when doctors equate pain levels to how high or low our inflammation markers are. There isn’t any way to verify the amount of pain we should experience solely based on inflammation markers.

Pain is purely subjective and can’t be objectively measured. That rate your pain from 1 to 10 is the most ridiculous thing that was ever devised. It is better than nothing though.

Chronic pain is different than acute pain. I told my rheumatologist that PMR was my “normal pain” and was tolerable.

A flare of PMR was an abrupt uptick of severe pain that had to be stopped and it wasn’t tolerable. I didn’t care what my inflammation markers were when PMR was suddenly worse.