If you have tapering problems below 5 mg this might explain why.
https://www.nadf.us/secondary-adrenal-insufficiency.html
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The following explains the challenges we need to overcome. I believe this is exactly what happened to me.
"The most difficult issue is that symptoms of adrenal insufficiency will be present during the tapering phase, because low levels of cortisol are the only trigger to the pituitary to stimulate the return of ACTH production and the restoration of normal pituitary-adrenal responsiveness.
The longer high dose steroids were given for a disease like asthma, rheumatoid arthritis, polymyalgia rheumatica or inflammatory bowel disease, the more likely that an individual will suffer from adrenal insufficiency symptoms on withdrawal of the steroids.
In addition, tapering off the steroids may cause a relapse of the disease that had been treated, causing a combination of disease symptoms overlapping with adrenal insufficiency symptoms. That is why it is very common for steroid tapers to be aborted, with a temporary return to therapeutic doses of glucocorticoids, followed by a slow attempt at tapering if the primary disease is in remission. "
Interested in more discussions like this? Go to the Polymyalgia Rheumatica (PMR) Support Group.
I wasn't enrolled in this study but my experience with Actemra mirrors the results of the study. No reason to believe that Kevzara wouldn't work for some people as well but maybe not everyone.
Actemra and Kevzara both inhibit IL-6, so both should help with PMR for some people. I'm starting to understand that IL-6 is an inflammatory substance and also an inflammation controller. If a drug inhibits IL-6, it also inhibits other sources of inflammation that are controlled by IL-6. Inhibiting IL-6 is both good and bad for people with PMR and GCA. It reduces the autoimmune response that is attacking the body's tissues, but it also reduces the body's immune response against infections and vaccines. I've read that people vary as to how much of their inflammation is generated by IL-6 vs other inflammation pathways, so that determines if Actemra or Kevzara will be effective against their disease.
I have stopped thinking about "single inflammation pathways." It seems more like an inflammation network that is tightly regulated by the body. There is a lot of action and reaction happening. My rheumatologist explains it with upstream and downstream regulation of one pro-inflammatory cytokine action and another anti-inflammatory cytokine reaction. Then there are some cytokines with both pro and anti inflammation effects. I will never understand this network but it seems like cortisol is the primary hormone that regulates inflammation.
Artificial intelligence seems to agree:
"That's an excellent way to describe the complexity of the immune system and the challenge of understanding it. Your rheumatologist's explanation captures the current understanding: a sophisticated network of signaling molecules (cytokines) that regulates inflammation, with cortisol acting as a key hormone to keep the system in check."
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In any case, prednisone seems to throw a wrench into the entire inflammation network system and disrupts everything the body does.
I like artificial intelligence because it is generally agreeable but it has no qualms about disagreeing. It expresses itself better than I can.
"Prednisone, a potent corticosteroid, acts broadly to suppress inflammation and the immune system, affecting numerous bodily functions and leading to widespread side effects. By mimicking the natural stress hormone cortisol, it throws a wrench into the body's entire regulatory network, not just the inflammatory response."
🤔
I suppose Actemra and Kevzara can also disrupt the inflammation network and immune system but hopefully not to the extent that Prednisone does. At least my rheumatologist thinks so and neither Actemra or Kevzara suppresses the production of cortisol by the adrenals.
According to artificial intelligence:
"The statement is accurate: Neither Actemra nor Kevzara directly suppresses the production of cortisol by the adrenal glands. Instead, they are interleukin-6 (IL-6) inhibitors that help reduce inflammation, which can allow patients to gradually reduce or stop their use of corticosteroids (like prednisone)."
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I just get a chuckle with some of this stuff. When I was on another PMR forum, a "self proclaimed" PMR expert who was "entitled to know" because of having PMR and taking Prednisone for a long time said "Actemra was dangerous" because of the potential side effects compared to prednisone and "cortisol had nothing to do with it." This person also said my rheumatologist was ignorant and was breaking the rules for prescribing Actemra to me.
It is hard to know what to believe. My rheumatologist was right to say I wouldn't know unless I tried Actemra to see if it works or not.
Has anyone tried Mexicam or hydrochlorot in conjunction with predizone tapering below 5 mg/day to prevent flares?
I do think that Actemra and Kevzara are dangerous. I mentioned recently on this forum that on my patient chart at my rheumatologist, under problems it lists "use of a high risk drug Actemra". You have to assess the risk of Actemra or Kevzara against the benefit to your quality of life of getting off of prednisone. Since I will need to be on a medication for several years to treat my GCA, it makes sense to take Actemra and not take prednisone. But if you're on a relatively low dose of prednisone and hope to be off of it at some point, it might make more sense to not take a biologic drug.
Yes ... it does worry me that my rheumatolgist has no plan to ever stop Actemra. I don't know where the exit ramp for Actemra is either. I have been on Actemra for more than six years. Except for a couple of "interruptions," I haven't been off Actemra.
I know that Actemra can be stopped abruptly because I was off it for 6 months when there was a supply chain problem during Covid. I was actually switched to a different biologic.
Humira was aimed at a flare of uveitis. It was a fiasco of sorts because I wound up on 60 mg of Prednisone again. PMR and everything else flared up all at once while I was on Humira and prednisone until Actemra was restarted. At the time, my rheumatologist said Actemra wasn't likely to add any additional benefit to 60 mg of Prednisone + Humira. There wasn't any Actemra available anyway.
When I tried to taper off Prednisone again I couldn't get past 15 mg. That was when supplies of Actemra improved. It was amazing how I could taper off Prednisone again in about a month after Actemra was restarted. That was in spite of being on more than 15 mg of prednisone for 6 months. My endocrinologist said I had resilient adrenal glands because my cortisol level was still "adequate."
I don't really have much in the way of side effects from Actemra. After I stopped Prednisone again, I was gradually weaned off other medications that were presumably treating prednisone side effects. Now my rheumatologist is adamant about keeping me on Actemra so I don't ever need Prednisone again.
I still have a prescription for 20 mg prednisone tablets. I'm supposed to take 2 tablets daily as needed for any flare of uveitis while traveling. That prescription is to appease my ophthalmologist who was adamant about me staying on Humira.
"But if you're on a relatively low dose of prednisone and hope to be off of it at some point, it might make more sense to not take a biologic drug."
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I just wanted to add that this was exactly what I was told when Actemra was offered to me. The comment was, " If I only needed 3 mg of Prednisone there wouldn't be much concern and Actemra wouldn't have been offered." The context was 12 years on prednisone and still taking 10 mg daily. Even then, I was asked to taper my Prednisone dose as low as I could get before starting Actemra. I could only taper to 7 mg before I went back to 10 mg.
This is very good information.
Thank you