I was talking to a guy who is hypothyroid, and he says his doctor gave him a prescription for 12.5mcg a day of T3 (notice i said T3, not T4, which is usually given). He says he feels better, he also said that 25mcg is the normal replacement dose which i figure means is what you take if you have 0 thyroid functioning.
However, wouldn’t taking 12.5 just shut your own thyroid production down via a negative feedback system, putting you in the same position you were in before? Like lets say you aren’t making enough, if you take a small amount like that why isn’t his thyroid shut down and now totally dependent on that 12.5mcg, making him still hypothyroid because 12.5mcg is only 1/2 what a normal person makes? He says he feels better now, i don’t get it.
I dont know alot about biochem or the physiology of the endocrine system, but can glands only undergo ‘partial suppression’ or ‘no suppression’ when external hormones (that would activate the negative feedback system) are present or does the gland just shut down 100%?
If his body is producing only 12.5 ug/d, then giving him an additional 12.5 would simply get him to where he should be.
The supplemental 12.5 wouldn’t turn off the production of his own 12.5 ug/d, since his thyroid gland would continue to be stimulated to make more thyroid hormone if less than the equivalent of 25 ug/d was present in the bloodstream.
The way this works is via the pituitary gland (well, actually the hypothalamus too). If they sense too little thyroid hormone, the pituitary gland makes something called TSH which stimulates the thyroid gland to make more thyroid hormone. When the level of thyroid hormone satisfies the hypothalamus and pitutary, TSH secretion is turned down.
So hypothyroidism is due to a thyroid that cannot handle the demands placed on it by the body and TSH and has nothing to do with a bad negative feedback system (which incorrectly tells the thyroid to produce too little)?
Yes, that is the case in 99% of cases of hypothyroidism, i.e. the thyroid gland itself doesn’t respond to TSH stimulation. This is most often due to autoimmune destruction of the thyroid gland.
Very rarely, the problem is that the pituitary produces too little TSH. This is called scondary hypothyroidism and is most often due to pituitary tumors.
Nice site, Karl. At first I thought you must have built it. One of your colleagues, I assume?
BTW, see many cases of secondary hyperthyroidism? I had a guy a few months ago with the TSH and the free T3 and T4 thru the roof. Sent him for a head scan, but he transferred to another prison before I got the results. Our endocrine guy says he’s never seen a case of secondary hyperthyroidism before.
Yes, indeed. The site is a colleague’s labor (self-taught HTML years ago).
Secondary hypothyroidism is probably underdiagnosed since we’ve become so dependent on elevated TSH’s to establish the diagnosis of hypothyroidism.
Before I de-differentiated back into GIM, I saw a lot, but they were always part of a bigger picture of pituitary disease. I can’t recall a pure, isolated TSH deficiency except from my training days (when the ice had just started to recede!) I do recall a tertiary hypothyroidism (hypothalamic deficiency of TRH) in a colleague’s patient, though.
One case will interest you. A patient post-hypophysectomy with panhypopit. Put on T4 replacement. Unfortunately, patient’s ongoing physician depended on TSH to titrate the dose. Lowered, and eventually stopped, the T4 since the TSH was “suppressed”!
Now that’s whacky case management! I’d be pretty damned embarrassed to get caught doing that. Not that I haven’t made equally stupid oversights in my career.
But I meant secondary hyperthyroidism. TSH of 800, free T4 of in the low double digits. He had some sort of TSH producing lesion not subject to feedback loops!
Yes, I’ve seen that. It’s important to try to distinguish pituitary resistance to T4 (leading to clinical hyperthyroidism with high TSH) from generalized resistance to T4 (with high TSH and high T4 and clinical euthyroidism) from TSH-secreting pituitary adenoma. We had many more rounds about that these illnesses than patients with them!
Sattua: An interesting question. The answer, unlike with, say, prednisone and the adrenal gland, is no. Administration of thyroid hormone does not seem to lead to prolonged or persistent “atrophy” of either the thyroid or the TSH cells in the pituitary. Conversely, if you take prednisone, your adrenal glands (and ACTH cells in the pituitary) atrophy.
It may be that the prolonged half life of thyroid hormone, unlike with prednisone and cortisol for the adrenal, allows time for the thyroid to recover before there’s a problem.
Yes, I’ve seen that. It’s important to try to distinguish pituitary resistance to T4 (leading to clinical hyperthyroidism with high TSH) from generalized resistance to T4 (with high TSH and high T4 and clinical euthyroidism or even clinical hypothyroidism) from TSH-secreting pituitary adenoma. We had many more rounds about that these illnesses than patients with them!
Of course, our consulting endocrinologist seemed to be amazed that a prison doc had recognized apparent secondary hyperthyroidism in the first place! LOL!
Thanks for the info. If I ever find out what he had, I’ll let you know!
This is so weird, i just had a class on the thyroid last thursday. I didn’t get ,uch info, though, so I’m actually glad I came across this thread. I have a test a week from wednesday and I can help use it to study!