That seems to be the part that many doctors leave out. After my ACTH stim test looked OK, the endocrinologist decided he was done, and I was simply exaggerating symptoms and looking for attention.
Yeaaaah. I had a pretty good endo for the ACTH stim test. She was able to say that the numbers didn't "look right" even if they were in range. Also, my response to increased cortisol is a big bucket of awful.
The tech administering the test could not believe I was exaggerating because she was the one who spotted it first. "What just happened? Don't move." Still, she was sure it was because she was drawing blood at first. When she fed me juice and I still looked like... whatever I'd looked like to concern her, she called up to endocrinology. No one picked up the phone. She called again five minutes later, after piling me with blankets -- I was shaking very hard at this point. I felt almost as bad for her -- here was a patient going through something she'd never seen before, she wasn't equipped to handle it, and no one would help her. She eventually carted me off to the ER. By then I was having trouble breathing.
While cortisol is a very good idea for some PWME, as Twisk mentioned in
his latest article, PWME/CFS often have exaggerated reactions to glucocorticoids, and adverse reactions to corticoid therapy.
At HIGH doses, cortisol is an immunosuppressant. For people who have multiple infections and are primed to over-respond to glucocorticoids, exogenous corticoid administration -- or cortisol stimulation -- is an extraordinarily bad idea. Nevertheless, I had a second ACTH-stim test several months later, because they were really hoping to catch something. This time, they elevated my feet up, gave me buckets of water to drink, and piled blankets on me before I started. I still felt horrible, but it was much better this time. Finally, after the ITT test, even further down the line, a physician gave me a cortisol pill (f-cort) to try out. The same result, x 10. Then I was sure it was the cortisol itself that was the issue, rather than, say, the typical carrier used for ACTH injection or something.
I feel obliged to add that, while other PWME have had this or similar reactions, there are lots of people here who do quite well on cortisol replacement therapy. Which just goes to show that there are a lot of primum mobiles in this illness, and I think that depending on what 'gets you' here to ME, you can have wildly differing reactions to different meds.
From the Twisk article:
....HPA dysfunction in ME/CFS can manifest itself in reduced levels of stress hormones,
e.g., cortisol, at specific moments of the day[
199,
200] and aberrant diurnal production of specific hormones,
e.g., cortisol, cortisone and adrenocorticotropic hormone (ACTH)[
201,
202]; a blunted response to provocation,
e.g., by insulin[
203], ACTH[
204] or CRH[
78]; a (long-lasting) deviant response to psychological[
205] or physical stress[
205,
206], and
an enhanced sensitivity of the cellular immune system to glucocorticoids[
207,
208] and
increased negative feedback of glucocorticoids to the HPA axis[
209,
210]. HPA axis dysfunction is not likely to be the primary cause of the illness, since HPA axis hypofunction,
e.g., hypocortisolism, is only present in a subgroup of patients[
200,
211], HPA axis abnormalities manifest themselves at a later stage of the illness[
212-
214] and
hydrocortisone/fludrocortisone seem to have limited[215] or adverse[216] effects.
Emphases mine. Though I do wonder. Like I said before, there are plenty of people who do quite well on corticoid replacement. I wonder if they have primary adrenal insufficiency rather than secondary, or if that matters at all...
-J