I found an answer to my initial query, which was essentially, how do glucocorticoids both assist in the conversion of T4 to T3 while simultaneously inhibiting the same conversion? To put it another way, we must have cortisol to convert T4 to T3 - but glucocorticoids are administered during a thyroid storm with the intent of inhibiting that exact conversion. This made no sense. My partner has to take steroids so I had to know exactly how this worked. Here is what I've found. I hope it helps illuminate the issue:
Fact: The body has multiple different deiodinase enzymes (the enzymes that change one form of thyroid hormone into another form. Three of the important subtypes of this enzyme are:
D1 -- found throughout much of the body. Converts T4 (inactive thyroid hormone) into T3 (active) but does so in a relatively slow, inefficient manner. This deiodinase enzyme is inhibited by glucocorticoids.
D2 -- found only in the thyroid. Performs the same function as D1, but does so in a much more efficient manner (partially making up for the fact that there is much less D2 than D1). This enzyme is responsible for all the T3 that is released by the thyroid. Not inhibited by glucocorticoids and may actually be stimulated by them.
D3 -- Converts inactive T4 into inactive Reverse T3 (rT3), essentially lowering the amount of T4 that is available to be activated. Stimulated by glucocorticoids.
The situation is more complicated than I anticipated. But, this is how glucocorticoids (such as hydrocortisone) can appear to have contradictory effects.
Conjecture:
Because corticosteroids may have a role in stimulating D2, a deficiency in the body's natural steroid production can reduce the amount of active T3 released by the thyroid. As mentioned above, the peripheral D1 enzyme is inefficient and even though there is a lot of it, it may not be up to the task of cranking out sufficient T3 if the D2 enzyme isn't there to help it out. So in lower than physiologic states, we may become clinically hypothyroid because we have lost the clinically significant portion of T3 that was being produced by D2.
However, in thyroid storm, the thyroid releases vast quantities of T4. The peripheral D1 is no whiz at converting T4 to T3, but when it has so much T4 to play with, it can't fail to be productive. In this context, the amount of T3 that gets generated peripherally is so great that the T3 created by D2 in the thyroid becomes clinically insignificant. When glucocorticoids are administered to someone in thyroid storm, that inhibits the peripheral conversion of T4 to T3 by D1, thereby cutting off the major source of the T3 that causes all the problems in thyroid storm.
Whew! So there you have it. That's my explanation of why glucocorticoids seem to be necessary for generating T3 but can also be used when we have too much T3.
Size of Thyroid and T3 Levels
Differences in hypothalamic type 2 deiodinase ubiquitination explain localized sensitivity to thyroxine
Effect of thyroid hormones on blood glucose
