Letter From Leading British Endo - Graves' Disease and Thyroid Discussion - Living with Graves Disease

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Letter From Leading British Endo

TSH FT3 Osteo Afib RAI

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#1 Allies

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Posted 15 December 2017 - 04:19 AM

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Hi all

 

I thought i would share the following with you. It is a letter written by a leading British endocrinologist and published in the December 2017 issue of the Journal of the Royal College of Physicians of Edinburgh.

 

Thyroid hormone replacement a counterblast to guidelines
AD Toft

 

J R Coll Physicians Edinb 2017; 47: 3079 | doi: 10.4997/JRCPE.2017.401

 

(it's a downloadable pdf)

 

http://www.rcpe.ac.u...e_47_4_toft.pdf

 

"In the meantime, I am so concerned about the state of advice on the management of primary hypothyroidism that I am increasingly reluctant to suggest ablative therapy with iodine-131 or surgery in patients with Graves disease, irrespective of age or number of recurrences of hyperthyroidism. 
Treatment with a thionamide, in which the hypothalamic-pituitary-thyroid axis remains intact, making interpretation of thyroid status simpler, is currently a more attractive proposition"

 

While the letter is mostly concerned with the inadequate treatment of patients with hypOthroid conditions (iatrogenic or otherwise), Dr Toft does seem to be suggesting that afib and osteo are highly unlikely to be caused by a low TSH but rather are more likely to be a result of high levels of FT3. Many of us have been treated by doctors who place too much weight on TSH results and have struggled to get our meds adjusted appropriately, hopefully this counterblast heralds the beginnings of a paradigm shift in the treatment of autoimmune thyroid conditions :)

 

Cheers
Allies
:D




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#2 FourT6and2

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Posted 15 December 2017 - 07:18 AM

Now if we can just get researchers to look into the root cause of the autoimmune response in the first place, rather than merely treating the symptoms.



#3 Mudra

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Posted 15 December 2017 - 12:20 PM

"exogenous subclinical hyperthyroidism was a different entity from endogenous subclinical hyperthyroidism, even although serum TSH was suppressed in both conditions. In other words, a low serum TSH concentration in patients taking LT4 did not necessarily indicate overtreatment."

 

I basically blew my brain power because of studying too much at uni (ha, ha), but I think that this is the crux of the argument, although I don't quite understand it. If any of you can explain this is layman's terms, I'd be grateful.

 

Cheers!



#4 FourT6and2

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Posted 15 December 2017 - 12:53 PM

"exogenous subclinical hyperthyroidism was a different entity from endogenous subclinical hyperthyroidism, even although serum TSH was suppressed in both conditions. In other words, a low serum TSH concentration in patients taking LT4 did not necessarily indicate overtreatment."

 

I basically blew my brain power because of studying too much at uni (ha, ha), but I think that this is the crux of the argument, although I don't quite understand it. If any of you can explain this is layman's terms, I'd be grateful.

 

Cheers!

 

This is just a guess. I'm not a doctor nor a researcher or anything. But exogenous subclinical hyperthyroidism = hyperthyroidism caused by external factors (environment, for example) in which the patient does NOT show severe symptoms. Endogenous subclinical hyperthyroidism = hyperthyroidism caused by INTERNAL factors (autoimmunity, genetics, etc.) in which the patient does NOT show severe symptoms.

 

Even though both patients in each circumstance have low TSH levels in blood tests, those patients taking LT4 (thyroid hormone replacement) weren't necessarily being over-treated, because the cause of their symptoms are different than the other group. So you can't really treat one group like the other. They each have their own unique circumstances. That's really all it means. It's nothing revolutionary.

 

I should point out that LT4 is a thyroid hormone replacement. And if someone were taking it, it would mean they are either on a block/replace treatment or are hypOthyroid. So basically, if a doctor is merely looking at TSH levels with a patient who is on LT4, it might lead to an incorrect interpretation of the patient's current state. But it might not necessarily mean they are being over-medicated. It just depends on the specific situation. So it's important to look at the T3/4 levels too.



#5 Allies

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Posted 15 December 2017 - 07:31 PM

What is potentially revolutionary is an endocrinologist with 40 years experience treating thyroid disorders, a man who played a part in the development of the hypothyroid treatment guidelines expressing concern over how the said guidelines are being applied.

 

As a Grave's patient, who like many, have been put under a fair bit of pressure to have my thyroid either removed or ablated with RAI, the part that stood out to me was the veiled admission that once the thryroid has been destroyed the treatment provided by many doctors is likely to be insufficient at best. If i wasn't already determined to keep my thyroid this admission would make me think twice.

 

The letter doesn't go into why treating Grave's disease according to TSH is such a bad idea. The situation for us is a little different, as often our TSH levels are totally suppressed (by TSH receptor antibodies) and not just low. The studies he seems to be referring to were carried out on patients receiving thyroid hormone replacement therapy (T4 monotherapy) and these showed that a low (but not suppressed) TSH was not a risk factor in either osteoporosis or atrial fibrillation. He also points out that these studies were flawed as they did not take into consideration other likely confounding factors, like thyroid hormone levels, T3 in particular.

 

He doesn't go into the effects that antibodies may have on our bones or our hearts, which to my mind is as significant or even more so than lack of TSH. A number of papers have been published recently that call for further studies into the role that antibodies play in osteoporosis. One of these even went so far as to say that osteoporosis is possibly an autoimmune disorder itself because of the various antobodies that interact with bones

 

Is osteoporosis an autoimmune mediated disorder?

 

Rosebella A. Iseme, Mark Mcevoy, [...], and John Attia

 

https://www.ncbi.nlm...87/#!po=34.2593

 

I second the call for more research into the whole area of autoimmunity!

 

Cheers
Allies
:D



#6 mmztcass

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Posted 16 December 2017 - 12:55 PM

Allies:

 

Wonderful article!   :)  I really appreciate the Endo saying that the AFib and Osteo connections are from the high T3 levels. 

 

I will be going for my labs soon later this month as a self pay (no insurance involved) and the only two tests I ordered are the FT3 and the FT4.  I never put much stock into the TSH.  This is the first time I am doing this as a self pay.  My doctor insisted on testing thyroid once per year because he felt all of my other labs were just perfect.  However if I am still on a wee amounts of MMI, I want to test twice a year just the same to make sure the Free Ts are where I'd like for them to be at.

 

{{{hugs}}}    



#7 Allies

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Posted 16 December 2017 - 10:19 PM

The part that stood out to me was the veiled admission that once the thryroid has been destroyed the treatment provided by many doctors is likely to be insufficient at best. If i wasn't already determined to keep my thyroid this admission would definitely make me think twice.



#8 Mudra

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Posted 17 December 2017 - 11:38 AM

You are so right, Allies!

 

And...I would hereby like to thank you, Mmztcass, for giving me advice in the decision-making process about whether or not to have my thyroid removed. I'm glad I still have my thyroid. Thank you!

 

Cheers!







Also tagged with one or more of these keywords: TSH, FT3, Osteo, Afib, RAI


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