Ft4 7.6 (12-22) FT3 2.6 (3.1-6.8) With a TSH of only 6.7 ? Is this secondary hypothyroidism?

The range for TSH is (0.27-4.2). If both the free T's are so low why is my pituitary not signalling more? Shouldn't the TSH be much higher? Or does it not work like that?

I know normally in secondary that the TSH VERY low or almost non existent but why isn't mine higher?

I wasn't taking any meds when these bloods were taken by the way. I am now back on my NDT.

I know this is an odd question but maybe someone with a bit more knowledge could help me out!

X

24 Replies

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  • I strongly suspect that some level of compromised pituitary (and/or hypothalamus) function can and does occur. The Wiki page linked below is a start, a very brief summary of one aspect:

    en.wikipedia.org/wiki/Autoi...

    Seems reasonable to me that a compromised pituitary could produce some TSH but not as much as might otherwise be expected.

    Rod

  • Thank you very much for your reply Rod. I shall have a good read.

  • I have had below range free ts, or right at the bottom of ranges, and my TSH has never gone above 3.84. I think maybe I will be reading that article, too.

  • If you have been taking NDT and it made your TSH very low then it will have affected your pituitary leading to low TSH. This happens in treated Graves' patients who have a suppressed TSH for some time. Sometimes the TSH recovers over time but often not fully. The other pituitary hormones are not affected. Was your TSH suppressed while on NDT? What was your thyroid blood results when initially diagnosed?

  • Jmh111 do you have any references for this? I would find them useful for my GP as my TSH is suppressed due to NDT for a long time. Thanks

  • This paper ncbi.nlm.nih.gov/pubmed/?te... is old but shows the TSH still failing after 7 months. Beware that the T3, T4 figures are (I think) for total and not free values, the free assays hadn't developed yet. Also, note that a lot of studies, including this one, used a TRH stimulation test and there is evidence that TRH "wakes up" the pituitary. Papers I have seen which state hormone levels have returned to 'normal' show in fact that the fT3 and fT4 have returned to the bottom of their reference intervals, not what we would regard as normal (i.e. middle of the interval).

    The TSH (and fT3) are less reliable if you are taking T3 containing medications, it's better to look at the fT4 and fT3 around 8 to 12 hours after the last dose.

  • Thanks jmh111 - Whilst I know the TSH & Ft3 is less reliable when using a NDT -the problem I have is in evidencing it to m GP..... Luckily for me Ft4 & TSH are the main tests they have used -the Ft4 is always in range but my GP worries about my TSH being suppressed ( it always is and has been ever since I have had combined therapy). I have to say I don't have secondary hypothyroidism.

  • TSH is often normal with secondary/central hypothyroidism. This is why t4 should always be tested.

    I was reading this paper yesterday for my mum, who I think has central hypothyroidism as a result of radiotherapy for a brain tumour. Apparently 65% of people who have had brain radiotherapy go on to develop central hypothyroidism but they still haven't checked her t4!

    ncbi.nlm.nih.gov/pmc/articl...

    Although it is rare, central hypothyroidism shouldn't be ruled out without proper testing. I firmly believe t4 should always be tested.

    Carolyn x

  • Interesting snippet from that link:

    TSH glycosylation is essential for it to attain normal bioactivity, a process that requires the interaction of TRH with its receptor on the thyrotroph.

    I am well aware that TSH and its glycosylation is important (and there are several possible ways in which sugar molecules can attach to TSH), but had NOT realised that TRH had a direct impact on it. Hardly a surprise, after all, TRH is a very important part of the whole process. But perhaps it explains why the pituitary part of the mechanism cannot simply adjust its own output according to blood thyroid hormone levels? It has often felt as if the pituitary should be able to act autonomously.

    Now, what is the impact of the different glycosylation of TSH... ? :-)

    And, of course, very obviously important where the hypothalamus has suffered any form of damage (howsoever caused).

    Rod

  • Thanks for that. That part hadn't registered when I read it yesterday. 8 hours in A&E has that effect on ones cognitive abilities. Of course, I may not have registered it anyway :)

    The whole process is definitely more involved than doctors appear to understand.

  • This is a scholarly article that might be of interest here;

    Effect of TRH on TSH Glycosylation and Biological Action

    BRUCE D. WEINTRAUB, NEIL GESUNDHEIT, TERRY TAYLOR and PETER W. GYVES

    Article first published online: 19 DEC 2006

    DOI: 10.1111/j.1749-6632.1989.tb54489.x

    Issue

    Annals of the New York Academy of Sciences

    Volume 553, Thyrotropin-Releasing Hormone: Biomedical Significance pages 205–213, March 1989

  • Most interesting. Thank you.

  • Did you find an accessible copy, Carolyn?

  • Not yet, which is very frustrating after reading the first page!

  • if you can't access it I'll ask my colleagues to send it to me, and post it on.

  • Thank you. That would be very helpful.

  • Though I couldn't get the review itself, here are the two papers it was based on:

    The Effects of Anterior Hypothalamic Deafferentation

    on Thyrotropin (TSH) Biosynthesis and Response toTSH-Releasing Hormone*

    TERRY TAYLOR, CHARLES W. SCOUTEN, DAVID M. JACOBOWITZ, AND

    BRUCE D. WEINTRAUB;

    Endocrinology 1986; vol 118/6; pp 2417-2424.

    and

    Thyrotropin (TSH)-Releasing Hormone Regulation of

    TSH Subunit Biosynthesis and Glycosylation in Normal

    and Hypothyroid Rat Pituitaries*

    T. TAYLOR AND B. D. WEINTRAUB

    Endocrinology 1985; vol 116/5

    pp 1968-1976.

  • A few more sources, maybe more accessible;

    1.www.pituitarydisorder.net/central_hypothyroidism.html

    2.Thyroid-Stimulating Hormone and Thyroid-Stimulating Hormone Receptor Structure-Function Relationships

    Mariusz W. Szkudlinski , Valerie Fremont , Catherine Ronin , Bruce D. Weintraub

    Physiological ReviewsPublished 1 April 2002Vol. 82no. 473-502DOI: 10.1152/physrev.00031.2001

    3.Thyroid-Stimulating Hormone

    May 2013 Clinical Laboratory News: Volume 39, Number 5

    Thyroid-Stimulating Hormone

    Why Efforts to Harmonize Testing Are Critical to Patient Care

    By James D. Faix, MD, and Linda M. Thienpont, PhD

  • Thank you for all of these. I shall see what I can learn from these.

    Thanks for taking the time to find these :)

    Carolyn

  • Thank you all so much. I now have some serious reading to do! X

  • All this goes to prove what we have all been saying............ That testing TSH alone does NOT reveal the whole picture! X

  • Your FT4 and FT3 being low suggests that you are not taking a sufficient level of thyroid hormone replacement.

    If you are taking the right levels of T3 and T4 medication, your TSH should be low (mine is typically 0.02), because there is no need to stimulate the thyroid into producing more T4.

  • I wasn't on any meds when these bloods were taken!x

  • Hi mum, I don't know if I've posted any of these videos to you by a functional medicine doctor. There are 22 videos regarding low thyroid. I know there are several that bring out the reason for an unnaturally low TSH. This type of medicine attempts to identify some of the root causes behind thyroid dysfunction. It's a little more practical than the scientific explanations you can research. This type of evidence based medicine is far removed from conventional type which hardly look at symptoms. This is #1 if you care to see how he explains it:

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