Lesson 1: TSH, and especially TSH only, is inadequate for testing and monitoring.
rendering TSH a misleading disease progression indicator
Lesson 2: FT4 and FT3 can be adequate for testing and monitoring.
with monitoring based solely on free thyroid hormone levels.
Obviously this is unusual and difficult case. But you cannot assume that any individual case isn't just as unusual, just as difficult, by sticking to TSH only and ignoring symptoms and other evidence.
Graves' Disease in Hypopituitarism Due to Pituitary Apoplexy
In Press, (this is not the final "Version of Record"). Available online 11 July, 2024
Author(s): Chiara Mura*, Rebecca Sonnino, Laura Crispino, Carlo Antonio Rota and Alfredo Pontecorvi
Published on: 11 July, 2024
DOI: 10.2174/0118715303322830240528051609
Background: Central hypothyroidism and autoimmune hyperthyroidism are contrasting pathologies requiring careful hormone monitoring for restoring euthyroidism. Their coexistence is rare and challenging for clinicians [1, 2].
Case Report: We have, herein, presented the case of a 41-year-old female patient with an unremarkable clinical history except for chronic autoimmune thyroiditis in euthyroidism. At the 21st week of gestation, she experienced a spontaneous abortion. The patient underwent an assessment of the uterine cavity, which was complicated by bleeding and hypotensive shock. In the postoperative course, the patient presented worsening headache, and after an MRI, the diagnosis of pituitary apoplexy due to an ischemic-hemorrhagic base was made. Laboratory tests showed anterior panhypopituitarism. Multiaxial replacement therapy was initiated with hydrocortisone, levothyroxine (LT4), and subsequently estrogen-progestin and GH. After two years of good recovery with stable LT4 dosage, the patient experienced palpitations and fine tremors; blood tests showed hyperthyroidism with suppressed Thyroid-stimulating Hormone (TSH) levels and elevated free thyroid fractions and anti-TSH receptor antibodies. Diagnosis of Graves’ disease was made, and therapy with methimazole was initiated. During antithyroid therapy, TSH remained persistently suppressed, consistent with the underlying central hypothyroidism. This condition required close follow-up, with monitoring based solely on free thyroid hormone levels. After six months of antithyroid therapy, disease remission was achieved, with negative antibodies and mild hypothyroxinemia. Therefore, methimazole was discontinued and replacement therapy gradually resumed until optimal hormone levels were reached.
Conclusion: This case is unique demonstrating autoimmune hyperthyroidism to coexist with central hypothyroidism, rendering TSH a misleading disease progression indicator. Consequently, managing Graves' disease has become more complex and challenging.
This is good stuff and I'm.going to invest a bit of time in trying to understand it .thanks Helvella. My initial.thought ,( I'm dyslexic which is like a reading stutter ) is to wonder if it has anything to do with the late and great Diogenese' wisdom on downregulation/ supression of tsh following a bad bout of autoimmune thyroiditis / Graves.???
I have this so my tsh is supressed, so that even if my t4 and 3 levels are very low the pituatory wont raise the tsh .
in this instance, if i'm understanding it correctly , the low TSH ( and all the other pituitary hormones) were caused by the sudden blood loss at birth , (sheehans syndrome) this causes the pituitary to chuck a dicky-fit and not produce enough of any of the hormones it produces,( including TSH) hence the need for hydrocortisone , growth hormone etc
getting grave's 2yrs later was just coincidental ( edit ~ the low TSH was presumably already there as a result of the damaged pituitary , and not as a result of the high T4/T3 of graves)
although by the sound of it there was already evidence of some sort of thyroid issue before the pregnancy / miscarriage depending on what exactly they mean by this :
"the case of a 41-year-old female patient with an unremarkable clinical history except for chronic autoimmune thyroiditis in euthyroidism. "
(i suspect it may mean she was subclinical hypo with positive TPOab ? and going into pregnancy age 41 with over range TSH ? thus making the miscarriage more likely ? )
edit ... or since they say 'euthyroid' , perhaps it just means TSH/T4 in range but with positive TPOab ?
Yesterday i talked to Psych about Sheehan's syndrome(GP wont accept that TSH is ever ever unreliable but Psych more enlightened) ....Anyway he say that ,as far as he understands Sheeshas , it damages the Pituitary which controls lots and lots of body hormones ,so if had Sheehan's there would be more than just thyroid issues . with downreg /suppressed tsh following a bad Graves/Hyper episode this would only affect Thyroid ,so he thinks that is probably what I've got which is why TSH,for me< is no good as an indicator of Thyroid output .
In the postoperative course, the patient presented worsening headache, and after an MRI, the diagnosis of pituitary apoplexy due to an ischemic-hemorrhagic base was made. Laboratory tests showed anterior panhypopituitarism
Having hypopituitary, at least any form that results in low TSH being produced/released, would result in hypothyroidism. That would be called Central Hypothyroidism (rather than Primary) or - as the precise cause is known - Secondary Hypothyroidism.
(Tertiary Hypothyroidism is when the hypothalamus is not creating and releasing sufficient TRH. Central Hypothyroidism covers Secondary and Tertiary, especially when it is not know where the cause lies or if both issues are present.)
It could be, but mostly it isn't to do with pituitary. However low pituitary could be caused by low thyroid thyroid hormones as it requires a good amount of them to work, produce acth and therefore stimulate adrenal glands. Also hypopit could cause low thyroid hormones if something is wrong with the gland (primary hypopit). Also if there is an adenoma on pituitary that could cause high cortisol, low tsh etc etc.
If someone had autoimmune thyroid disease Hashi or Graves , could this result in Hypopit..... y ?Nb I stand to be corrected but I believe that autoimmune..can start in a Graves / hypo form ( the thyroid reacts by going hyper in the preliminary stage , .and then ,as the disease progresses to secondary stage when gland runs out of" steam" / becomes very damaged , it then goes UNDER I.e hypo .?????
AND the big point is that the Hyper/ preliminary stage has impact on Pituatory which responds to very fery high hyper via feedback system ( hypothalamuscetc).by almost completely shuting off the tsh output , BUT what can happen is that the Hyper was so high that the tsh is PERMANENTLY supressed so that, even though t4/3 is very low ,the tsh is so downregulated that it fails to go up again even when the thyroid is very hypo ....
When this happens it is not true central hypothyroidism but known as downregulation of tsh ( down reg meaning always low , a bit like a lorry speedlimiter keeps it at 60mp max speed .
The problem.with this illness is that it hasn't made its way into the NHS Rulebook , so gps and consultants refuse medication as the tsh rule is " L.ow = Hyper and High = hypo" ONLY.
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Second attempt at Monitor my Health results in hope to link with high HR
Hashimotos & FT3. Advice needed - Rock bottom - About to try Thybon (poor FT4- FT3 conversion).
