The following is a long post and you may want to copy it or put in your Saved Posts.
It was published in a Newsletter (which is now defunct) and written by PMRpro, this time I actually asked if I could post it on here.
The explanation has been written in language that we can all understand,medical jargon has been excluded. The information has been medically checked out.
The HPA axis or the TRIO................................…
Why you should ask to have a Synacthen test done when you have been on long term Prednisolone and have reduced down to 7.5mg and below.
Adrenal insufficiency can be due to a whole range of things and can also range from total through to just a bit slow to react.
The production of cortisol, which is essential for life, by the adrenal glands is the result of a very complex set of interacting factors which work on both positive and negative feedback and involves the hypothalamus, the pituitary and the adrenal glands, what is called the HPA axis. The thyroid and parathyroid glands also play a part in that the whole range of organs and hormones interact with each other in some way.
Prednisolone therapy can cause total failure of the adrenal glands but usually if you reduce the dose of artificial prednisolone slowly enough they will start to function again in the majority of people, although it may take a year or more.
As long as you are taking prednisolone they are not required to do much just as your central heating boiler doesn't do a lot in the summer because it is warm enough. The presence of any corticosteroid substances in the blood leads the body to think it is well supplied and in some ways it is, prednisolone does the job too, the body isn't that fussy whether it is natural or synthetic steroids that are there. But if you were to stop taking that prednisolone suddenly the body wouldn't immediately be able to produce natural cortisol because of the state of hibernation they are in.
There are various causes of adrenal failure and they are classified as primary or secondary. Secondary failure is due to something other than the adrenal glands themselves causing the problem: there is no ACTH from the pituitary gland for example, or there is already plenty of corticosteroid present in the blood as is the case for people needing to take prednisolone.
Primary failure is the total lack of function of the adrenal glands due to their destruction or inability to function at all perhaps due to genetic causes where the genetic code is incorrect, or illness or infection such as TB or surgical removal/damage for various reasons.
However, the most common cause of primary adrenal failure is autoimmune disease which attacks the glands and damages them so badly they don't work.
Autoimmune disease is a strange thing. Sometimes it is very specific-Type 1 diabetes only attacks the pancreas so it is unable to produce insulin. In other cases there may be a lot of different tissues that are attacked by the immune system - cells in the joints, the gut, the muscles, the nerves or the blood vessels-and in turn this can affect various organs such as the lungs, the kidneys and so on.
In the past links were made between specific signs and symptoms and someone gave them a name - but sometimes people have the signs of one disease and some of the symptoms of another which causes some confusion as a mongrel disease is created - like a dog that has lots of features of one breed but the ears of another and a tail that doesn't look anything else's and new names that describe the findings are used instead. Or it is said to be a “non-specific autoimmune disease”.
For some people who have PMR and need to be on prednisolone it is possible that the underlying autoimmune cause may also be attacking the adrenal glands - but no-one really knows there is a problem until they have problems reducing the dose of prednisolone and stopping. Or the adrenal glands may not have been functioning terribly well anyway - they do degenerate with age, like many other things. But it isn't a certainty.
There are probably no accurate figures about how many people with PMR are unable to get off prednisolone altogether for whatever reason - but figures do suggest that about a quarter will be on prednisolone for a long time and some of them will need it for life. Whether they will eventually get off prednisolone depends on a lot of factors and it may be the PMR is taking a long time to go into remission or the adrenals are just sluggish about waking up - or it might be a lack of adrenal or pituitary function that is to blame.
To identify which it might be would be a research project in itself and require a lot of complex testing - and in most cases all you would end up with is the decision “This patient needs a low dose of prednisolone”. But if you do a simple synacthen test you will know whether a given patient should be able to produce enough cortisol to function and remain well once their dose is low or stopped. If that isn’t likely to happen – they stay at a dose that is enough to keep them well, maybe 5mg or 10mg.
The ACTH test (also called the cosyntropin, tetracosactide, or Synacthen test) is a medical test usually ordered and interpreted by endocrinologists to assess the functioning of the adrenal glands stress response by measuring the adrenal response to adrenocorticotropic
hormone (ACTH;corticotropin).
To do the test you usually attend a hospital clinic – it is more convenient for the medical staff and they can keep an eye on you after the injection although there are very rarely any problems. You should not take any prednisolone in the 24 hours before the test – so you simply don’t take your dose that morning until after the test which is done at 9am. They take a sample of blood to get a baseline level of cortisol and then give an injection which should stimulate the adrenal glands to produce more.
Another blood sample shows if that has happened. Then you can take your usual dose of prednisolone as normal. It can be done even though you are still taking rednisolone every day, the test just has to be interpreted differently, but some doctors are unaware of this.
Our thanks to Eileen Harrison Physiology Bsc(Hons) St Andrews, Medical Science Translator.