A rheumatologist has put me on a steroid pack, Medrol, a couple of times to relieve the symptoms of gout. I’m not asking for medical advice, just the reasoning behind the dosage which I find puzzling.
For the record, the pack starts you off with 6 the 1st day, then reduces by one each day; 5 on the 2nd, 4 on the 3rd, etc.
First, if we want to restrict a person’s intake of steroids to only what’s necessary, why do you have to go all the way through the multi-day dosage instead of quitting as soon as the symptoms are removed? It specifically says to keep taking them once you start the program. I could understand this with antibiotics but it surprises me for steroids.
Do the strengths contained in each day’s dosage vary? Are the pills in the day 1 row any different from that of day 6?
Why is there a day/consumption component instead of just a staggered release one. It says on day 1 to take them all even if you start late. This I find to contrast with other meds that might direct only a more evenly scheduled program.
Short strokes: Suddenly cutting off a high dose of steroids can cause serious problems, including temporary psychosis. Therefore, a “steroid taper” is standard at the end of any therapeutic course
There are lots of docs and pharmacists on the board so I’m sure one of them will give a technical explanation. I took Prednisone once and was on a similar schedule. I think if you take the same dosage for several days and then just stop you have kind of a crash effect. You need to wean off of it slowly, though I’m not sure exactly why.
You can’t compare steriods to antibiotics, or any other medication really. They work completely differently, are are for different kinds of problems.
First toxicity might be managed better by scaled dosages, or dosing all at once, rather than over a period of time. That ‘6 up front’ approach says to me that managing toxicity is important. Spread over time, they might be more toxic, believe it or not.
Second, your adrenal glands make chemicals that might likely be supressed temporarliy by using the drug, therefore it is normal to scale down the dose to allow your adrenal glands to up their output. Additional effort might be made by issuing packs that do an even better job of scaling down the meds, allowing your body to kick up output, lest you stop the drugs cold and have a lag time between when your own adrenal glands are up to speed.
Yes, as noted, there is a theoretical concern that, having taken “exogenous” steroids for a while, your own adrenal glands may have been turned off. In theory, it may take a while to get them restarted. Actually, there is no risk of this whatsoever unless you take more than two weeks of steroids.
Interesting - I didn’t realize you had to be on them that long before the risk really kicked in.
That said: I think standard practice among most doctors indicates that you do a taper (e.g. the Medrol dosepak) rather than stopping suddenly because a) they’ve always done it that way, b) it’s unlikely to be harmful, and c) reduces even that theoretical concern, so why not… Certainly every time I’ve taken them in the last 20+ years, it’s been a taper. I guess doctors aren’t in a rush to adapt to newer info.
I wonder also if (depending on the reason for steroids) part of the thinking is: taper down, then you’ll know if the underlying condition is still there before it has a chance to come back full force.
Another concern is that if you’ve been on steroids for a while, and stopped/tapered them as expected - if you get sick/injured within a few months, your body might still have its own endogenous production somewhat impaired, and might need a little extra steroid help during the illness. KarlGauss, do you know more about the current thinking there? I get the impression they’re less worried about this than they used to be.
You are 100% correct - if someone has been using steroids “chronically” and then has them stopped (with a proper taper), it is still possible for some time thereafter that their own adrenal glands will not be able to respond appropriately to stress situations.
As background, let’s note that with a major physical stress such as major surgery or severe trauma, one’s adrenal glands increase their production of steroids (i.e. cortisol) by up to 1000% - a ten-fold increase over baseline.
So, after someone’s been on long-term steroids and then tapered and stopped, their adrenal glands may still not be capable of mounting a proper stress response (a ten-fold increase) even though they’re OK producing basal amounts. Presumably, this is simply a reflection of more subtle atrophy or suppression of the endogenous “hypothalamus-piutitary-adrenal axis” (the atrophy or suppression can occur at any or all of those sites/levels).
One problem in all this is determining what a “major” stress is. Further, it is not as straightforward as it seems to measure steroids (cortisol) in the blood of sick people. In particular, there are various substances that bind cortisol in the bloodstream (and thence render it inactive). The levels of these substances fluctuate in critically ill, “stressed” people.
Since there is some risk in overzealous replacement of steroids (cortisol or equivalent) in “stressed” individuals (e.g. high blood sugar, yeast infection, delirium), and since most people do NOT have the 1000% increase of cortisol levels (or, if they do, only for a short period), there has indeed been a tendency to lighten up a bit in the amount of cortisol (or equivalent) given to “stressed” individuals who have a history of having been on exogenous steroids in the last six months to one year, and thus who are at risk of not being able to endogenously respond as expected.
All that being said, the “standard of practice” (for medicolegal purposes, at least) is probably still to give the equivalent of a ten-fold increase of cortisol (or equivalent) to at-risk individuals who are under major physical stress, or who are critically ill, for at least one or two days.
I thought I would use this opportunity to add that it is quite possible to determine if someone who had been taking steroids chronically, but has stopped within the last six months or so, will be able to ‘rev up’ their own steroid (cortisol) production during a time of major physical stress. The problem is that for many people, the major physical stress is unexpected, eg. trauma from a car accident, emergency surgery, etc., so there’s no opportunity to check.
IF there is time in advance for a patient at risk of hypothalamus/pituitary/adrenal gland suppression (i.e. who used steroids, say, for one year, until 6 months ago), you can check things as follows:
Measure the cortisol level in the blood - if it is low, you don’t have to go any further, you know they would be unable to increase their cortisol level during stress since they can’t even get it to normal when healthy and unstressed.
Give them an injection of the hormone that normally stimulates a person’s adrenal glands to make cortisol (i.e. ACTH). If their adrenals don’t respond well to the ACTH, you know they would also be unable to respond during a period of stress (i.e. it’s the same ACTH that would be produced during and in response to stress, in an effort to stimulate their own adrenal glands. If they don’t respond during a test situation, you sure can’t expect them to respond during stress).
If the first two tests have been “passed” or if you just want to test everything at once, you would then perform an insulin hypoglycemia test. As a background, note that hypoglycemia is a very potent stimulus for the body to make cortisol. During hypoglycemia, the brain (as a “whole”) signals the hypothalamus (a specific part of the brain involved in the stress response and many other vital functions) which in turn signals the pituitary gland which in turn signals the adrenal glands to make cortisol. If the patient passes this test (which, by the way, is a very reasonable approximation and mimic of a “major stress”), then you know everything needed to make cortisol, and to increase cortisol production during stress, is intact.
In truth, it’s far easier (and probably safer) just to assume that an at-risk person will be unable to mount an adequate cortisol (steroid) response in the face of major stress and therefore simply “cover” them with steroids (cortisol or equivalent) prophylactically.
Finally, and in passing, there is some evidence that in some cases, the long-term use of topical or even inhaled steroids (eg. for asthma) may lead to suppression of the adrenal glands in the same way that taking steroids by mouth may.