This blog post is based on an article from Dr Tania S. Smith, and on discussions between Dr Smith and a thyroid patient on a forum. Please see Dr Smith’s full article at the end of the post.
Atrophic Thyroiditis is defined generally as a thyroid gland volume of 5.0 mL or less. This shrinkage is NOT caused by Hashimoto’s TPO antibody, nor is it caused by ageing.
In Hashimoto’s, the thyroid tissue is destroyed but the gland itself does not shrink. The vast majority of Hashi’s people keep their normal adult thyroid volume their entire adult lives even until old age, even if they got Hashi’s very young as a young teenager.
In Atrophic Thyroiditis, you do not need the TPO antibody to be raised. You can have Atrophic Thyroiditis with or without the presence of Hashimoto’s (detected by elevated TPO or Tg autoantibodies) or Graves’ disease (detected by raised TSAb autoantibody).
Atrophic Thyroiditis is caused by an antibody called the TSH receptor blocking antibody or TBAb. The antibody blocks TSH from stimulating the thyroid gland (instead of overstimulating it as in Graves’). A severe flare of TBAb can block more than 98% of TSH receptors so that TSH cannot reach the gland, no matter how much TSH you have in circulation.
A small percentage (10%) of Hashi’s patients have this antibody at any one time (when researchers have taken a random sampling of patients with elevated TPO levels and clinically diagnosed hypothyroidism).
The raised TBAb antibody can also flare up and then go away again. Therefore, the TBAb antibody need not be constantly present, so it can be extremely difficult to detect.
Atrophic Thyroiditis caused by the TBAb antibody is another type of autoimmune thyroid disease that can occur with or without the presence of Hashimoto’s.
Atrophy can happen before Hashi’s, or during Hashi’s, or in a person who never has Hashi’s (never has had elevated TPO). Most Hashi people do not experience severe thyroid atrophy.
But Atrophic Thyroiditis is not Hashi’s because it is not caused by the TPO antibody.
Gland atrophy does not always happen when the TBAb flares up, and if it happens, it doesn’t always happen at the same rate in all people. Here are the conditions:
- The stimulating antibody TSAb will prevent the death of thyroid cells. Therefore, if you have TSAb (thyroid stimulating antibody), in circulation at the same time as TBAb (which is common), they counteract each other, then atrophy will not occur.
- If you only have TBAb in circulation, your gland is now vulnerable to atrophy.
As mentioned above, there are significant issues with testing for Atrophic Thyroiditis and so it is better to diagnose it in other ways.
Few labs have the ability to test TBAb and the antibody is not always present. You would have to know you’re in the middle of an antibody flare while testing so you can catch it in the act.
TBAb blocking antibodies also disappear in half or more people who have them. They can completely disappear after doing their damage (atrophy), and then they can flare up again years later on therapy and wreak havoc with thyroid levels.
A bad flare of this blocking antibody can steal more T3 conversion from you than DIO1 or DIO2 genetic polymorphisms can, and your FT3 may be low even without any rT3 elevation.
A flare can also cause significantly raised TSH, as the receptors for TSH are blocked and the pituitary attempts to achieve more of a response from the thyroid gland.
The biggest clue of all though is the presence of less than 5.0 mL gland volume. This is very indicative of TBAb action, i.e. Atrophic Thyroiditis.
One very important thing to keep in mind is that during flares of Atrophic Thyroiditis the effect of the antibody can significantly affect the conversion rate of T4 to T3. In a person without Atrophic Thyroiditis, the D2 deiodinase enzyme activity is normally upregulated by TSH i.e. the body makes more D2 enzymes when TSH rises, in order to convert more T4 to T3. So, in a healthy person, the cells will convert more of the T4 to T3, so FT3 levels rise. However, in a person with Atrophic Thyroiditis, the TSH signalling throughout the body can be blocked by high levels of the TBAb antibody. This prevents the T4 to T3 conversion rate from being at the level it should be. In fact, T3 levels can remain far too low for the person, when TBAb levels rise during a flare. So, those on T4 medication may find it very difficult to remain stable. During an Atrophic Thyroiditis flare the T4 (from any remaining thyroid tissue or from T4 medication) will not get converted to as much T4, but when the flare is over the conversion rate will improve and T3 levels rise. It can be a highly unstable situation for the Atrophic Thyroiditis sufferer.
Once the thyroid gland is destroyed, the variation in the effect of TSH, due to flares in TBAb (which can continue even once the gland has atrophied), can still continue to affect the conversion rate of T4 to T3 in those patients on T4 based thyroid medication. Hence some thyroid patients who suffer from this condition may find that they do better on T3 medication once most of their thyroid gland has been destroyed by Atrophic Thyroiditis. This is because T3 is already biologically active and is not affected in the same way as T4 by the TBAb antibody.
Note: this last point is made worse by the fact that the loss of the thyroid gland itself will already have significantly worsened the individual’s T4 to T3 conversion ability, as the thyroid gland is the most important converter of T4 to T3 in the body (with usually at least a 25% contribution of the body’s ability to convert T4).
Here is Dr Smith’s original article on the spectrum of autoimmunity conditions. There is a detailed section in the article on Atrophic Thyroiditis:
https://thyroidpatients.ca/2020/04/12/the-spectrum-of-thyroid-autoimmunity/
Best wishes,
Paul
Thank you Paul.
My own thyroid volume has been described after ultrasound as very small. It has, in light of Dr Smiths Writings on this subject, occurred to me that this is a possibility for me, but wrapped up in a pituitary apoplexy. Thank you
I’m glad it helped Linda. It also has implications for treatment described in the article.
Good luck!
Paul
Thank you, Paul. I had read Thania S. Smith’s original article at Thyroid Patient Canada. But you’ve explained this phenomenon clearly & concisely for the not-so-scientific among us. It should be noted that Dr. Smith is not a physician but a PhD.
Thank you for your comment. I try my best to write things in the simplest way possible. I do not always achieve this but it is an important goal for me in all my written work including my books.
Best wishes,
Paul
Thank you so much 😀 In Norway its not easy to have this condition. According to the doctors, there is nothing but Hashimoto and everyone will be happy on T4. I’m happy I found a doctor who gives me T3. I will have an ultrasound of my thyroid gland ASAP 🙂
Good luck Bente!
Best wishes, Paul
Thank you for this clear and concise summary, Paul. Most helpful.
Thanks for the feedback Helen!
My thyroid is completely atrophied according to ultrasound, and I do well on NDT. The atrophy preceded my switch from levothyroxine, when according to my levels I was having difficulty converting T4 to T3, hence the switch to NDT.
Thank you for this excellent explanation as to why!
Hi CJ, Many people with this type of thyroid condition do better with T3 Only therapy. I would keep that in mind.
Best wishes to you, Paul
Un endocrinologue m a déjà dit en touchant à ma glande thyroide qu il en restait peu. Est ce à dire que je dois prendre un ajustement de t4 et de t3.
le 16 fevrier 2021 mes prises de sang:
ths 1.2 (0.5-5.4)
t4 11.8 (11-22)
t3 1.2 (1.3-3.1)
Je prends 50 de synthroid et 20 cytomel depuis décembre 2020. J’ai une tendinite au biceps gauche depuis 4 mois. je suis droitiere je ne comprend pas comment je peux avoir attraper une telle douleur. merci
I translated this using Google:
An endocrinologist once told me when touching my thyroid gland that there is little left. Does this mean that I have to take an adjustment of t4 and t3.
on February 16, 2021 my blood tests:
ths 1.2 (0.5-5.4)
t4 11.8 (11-22)
t3 1.2 (1.3-3.1)
I have been taking 50 synthroid and 20 cytomel since December 2020. I have had tendonitis in my left biceps for 4 months. i am right handed i don’t understand how i can get such pain. thank you
My answer: Your FT3 level is far too low and really could do with being well above 2. This can be achieved by increasing the thyroid medication.
So, yes, you do need an adjustment of thyroid medication now. The TSH level should not prevent the medication from being raised, even if it gets very low indeed. Tendonitis takes many months to improve because blood flow in the tendons is poor. The thyroid situation won’t be helping this heal either.
Using Google translate, My answer is:
Ma réponse: votre niveau de FT3 est beaucoup trop bas et pourrait vraiment être bien au-dessus de 2. Ceci peut être réalisé en augmentant la médication thyroïdienne.
Donc, oui, vous avez besoin d’un ajustement de la médication thyroïdienne maintenant. Le niveau de TSH ne doit pas empêcher l’augmentation du médicament, même s’il devient vraiment très bas. La tendinite met plusieurs mois à s’améliorer car la circulation sanguine dans les tendons est faible. La situation thyroïdienne n’aidera pas non plus cette guérison.
Best wishes, Paul
I have been on Synthroid or levothyroxine since 1990. I’ve been up and down over that time from 100-200 mcg. I’ve had great changes in my body and wellbeing throughout that time. I was diagnosed with Hashimoto’s in 1990 after years of denial that I had a problem at all, but a goiter led to a radioactive uptake scan showing an enlargement that was then reduced w thyroid (non canerous), so we went on from there. About 5 years ago, I was having a lot of difficulties and was given a sonogram that showed I had NO thyroid. I was stunned, and I asked my very good Endocrinologist what caused this, and she said it had simply atrophies, not to worry. Well – I DO worry. I have not been able to determine from the small body of literature what the CLINICAL issues may be. I have weight gain (slowly losing due to fasting), brain fog, etc. but ave not had any changes in meds. No one is dealing with the finding that I have no gland at all, just tiny pinpoints of tissue, I am on 125 mcg of levothyroxine, but I have no idea what my next steps should be. Reading the literature, I learned this is NOT Hashimoto’s but a separate condition all on its own. Help! Where do I go and what do I do, and what is the prognosis?
Well if the gland is completely atrophied it is likely that you did have atrophic thyroiditis.
The thyroid gland won’t come back – it is just gone now. With losing the thyroid you will have lost a significant amount of your ability to convert T4 medication to the active hormone T3. Some people lose 25% of the total ability to convert and others lose a lot more than that. My The Thyroid Patient’s Manual book is a worthwhile investment for you as it will give you the understanding that you likely need right now in order to get a solution that will work for you.
Levothyroxine (T4) medication is likely not going to be as effective for you as it would be for someone with a thyroid. However, you have said very little about your symptoms so I don’t want to assume too much. If you are quite symptomatic it is likely that you’d do better with a mixture of T3 and less T4. Atrophic thyroiditis patients often need a lot more T3 and less T4 (see the blog again for the explanations).
The prognosis is very good as long as you are on the right mixture of medication for you – this is likely to include T3 and probably less T4 than now. So, you’d need a doctor to work with who was open to that. I would read my book though – it will be a real help to you in arguing your case.
Best wishes, Paul
Paul, I was diagnosed hypothyroid in 1996. Was on Synthroid only until 2015. My TSH always fluctuated sometimes going as low as .50 and in 2014 as high as 3.1 all the while being on the same dose of 125 mcg. In 2015 I started having all kinds of allergic type reactions (not knowing to what) and felt as though I was literally going to die. I was referred to an Endo because my PCP wasn’t knowledgeable enough to do much for me. The Endo increased my dose of Synthroid to 137 mcg. Didn’t do much for me. Then late in 2015 she added to my 137 mcg Synthroid 10 mcg T3 ( 5 two times daily). Ok on my labs 3 months later (Spring 2016) my FT3 had went to 3.9 (top of range) FT4 was 1.67 ( at top of range) and TSH .011. I felt like a million bucks and I can safely say I had not felt like that in all the years since my diagnosis. It was, however, short lived. In the late Summer of 2016 I started having all the hypo symptoms come back ten fold and the next lab I had in October 2016 showed FT4 1.95 (way over range) and my RT3 60.2 (normal top of range is like 25). After a month I took it upon myself to remove the Synthroid and start adding T3 only until I could clear the RT3. Once that was accomplished I did try to add Synthroid back in while reducing the T3. My RT3 ended up back over range although not to the degree it had. So went T3 only for about 18 months. Had to see an new Endo and she would not hear of T3 only even with all the background, past labs and medical history I provided. So fine, I slowly added T4 (Tirosint) and slowly backed off the T3. I always had RT3 taken at labs so as to see where things were headed. I got as high as 75 mcg T4 and 25 mcg T3 and decided not to change anything further. Since that Endo was fixated on TSH (& feedback loop) and not how I was actually feeling we ended up parting ways. I had an ultrasound taken in 1999 at that time my thyroid measured 4.1 x 2.0 x 2.0 cm and 4.3 x 1.7 x 2.5 and in 2021 it now measures 2.8 x 0.9 x 1.0 and 3.2 x 0.9 x 1.1 although 2019 showed 2.7 x 1.1 x 1.2 cm and 2.6 x 0.6 x 1.2 cm. I do have a nodule. I’m sure it is just the difference in the different facilities that did the ultrasound. In any event, my thyroid is considered atrophied on these docs. I do have TPO antibodies although I have gotten them down to 12 according to last lab. I am wondering if when I had that severe increase in TSH of 3.77 I was having some sort of flare? No other thyroid labs were taken at that time. I’m just now learning of Atrophic thyroid disease and am wondering if this is what I have in combination with Hashimotos. I have all my labs and ultrasounds since being diagnosed but up until some few short years ago no doc ever tested more than TSH. You say thyroid doesn’t shrink on it’s own so I am thinking this is what I have, your thoughts?
Hi Sandra, I only deal with complex problems via 1-1 coaching. I reply to simple comments here but not ones where I would need to ask a lot of questions.
A flare wouldn’t be a TSH of 3.77 by the way – it would be far higher.
However, the shrinking of the thyroid suggests that it could be Atrophic Thyroiditis and in which case more T3 and less T4 would be a better option.
You also can’t clear rT3 by using T3 and then expect to go back on Synthroid. RT3 just comes back.
I would read The Thyroid Patient’s Manual book – it covers most things that people need.
If you’ve lost thyroid tissue and cannot keep FT3 up in the range without lowish rT3 then T4 meds mostly aren’t working for you.
I can only do more detailed work in 1-1 coaching and I don’t do many of these at all. Recently, I was thinking of retiring from doing them but haven’t decided yet.
Best wishes, Paul
I am interested in coaching with you for my son, who is 38 yrs old and has been ill/unable to work/housebound since 2009 (possibly longer) I have records of thyroid testing since 2003, and now wondering if he has thyroid issues that are difficult to diagnose, such as atrophic thyroiditis. He only ever had antibody testing included in 2015 bloods and the results said he was “borderline positive” with a level of <0.30 IU/L (0.81 – 3.00) for TSH receptor antibodies (TRAb).
THYROIDSTIMULATING HORMONE 2.55 mIU/L 0.27 – 4.2
FREE THYROXINE 18.3 pmol/l 12.0 – 22.0
Thyroglobulin Antibody
15.9 IU/mL (0-115)
Method used for Anti-Tg: Roche Modular
IMMUNOLOGY
Thyroid peroxidase ab's 7.4 IU/mL (0- 34)
Method used for Anti-TPO: Roche Modular
SPECIAL PATHOLOGY
TSH receptor antibodies (TRAb) <0.30 IU/L (0.81 – 3.00) Borderline
Can you please help ? Many thanks.
Clare Johnston
Clare,
If you wanted to assess for Atrophic Thyroiditis then he would need an appropriate thyroid scan to see how much thyroid volume remains. That is the definitive test. If the thyroid is still there but fibrotic then it has been Hashimotos not AT. If the volume is very low (see the blog post) then it was AT. Definitely worth getting an endo to get the scan done to assess for AT if that is your concern. However, if that FT4 is based on no thyroid meds then it seems very unlikely.
He would definitely need a proper test of thyroid labs including TSH, FT4, FT3, reverse T3 – definitely not just TSH and FT4 – only FT3 is a genuine thyroid hormone that actually does work at the cell nuclei.
I would read my ‘The Thyroid Patient’s Manual’ book before doing anything else as it also covers all the other relevant testing. I would need a lot more test results than you mention above. In particular, cortisol, B12, folate, iron, ferritin, and vitamin D. B12 can only be tested if off ALL B12 supplements for 4-6 months. Most of the others can be tested if off the supplement for a week.
For information on coaching please contact me via the Contact section on my website homepage. I won’t discuss that here, as this is an open page.
Best wishes, Paul
I got an ultrasound on my thyroid yesterday. It says AT. I have been on levothyroxine for over 30 years. I have always felt tired sluggish out of sorts foggy achy. I finally put my foot down saying SOMETHING IS WRONG! My doctor ordered an ultrasound of thyroid. I’ve told doctors my thyroid is achy. But whatever. Anyway they just say I’m depressed and I’ve been in and out of therapy and the longest list of antidepressants I’ve tried you’ve ever seen.. Wouldn’t it be something if it’s due to AT. And a simple change in medication could help me.
Hi Tina,
I’m surprised you can feel anything in the thyroid now if it has shrunk that much.
Hopefully, they will prescribe T3 but a lot of doctors don’t understand things that well.
I hope they are amenable.
Best wishes, Paul
Could it be that all of these years I’ve been having these symptoms it could have been thyroid. Even when I was taking levothyroxine? Would AT cause me problems like that. And being shaky too and very irritable? Also thank you for your reply.
It is possible yes. I can’t say it has been that.
Levothyroxine often doesn’t work well and frequently leaves people with too little FT3.
AT causes fluctuations in conversion rate as you can read in the blog post.
Best wishes, Paul
I got a phone call from my doctor office today that is very confusing. The nurse told me that the doctor looked at my ultrasound and he said that I am just fine that I have a small thyroid but that everything is fine and there’s nothing to worry about. I was confused because the statement on my condition according to the ultrasound said atrophic thyroiditis and so I just feel very confused. Everything I look up says it’s a lot more than just a small thyroid I never even saw anything that said it’s a small thyroid. What should I do I just literally don’t know where to turn. I have a lot of symptoms of extreme fatigue dizziness out of sorts foggy shaky irritable etc. Please help me.
The scan report should state what the thyroid volume is.
Your doctor may not know much about Atrophic Thyroiditis. So, you should get the report and compare the thyroid volume to that mentioned in the article. If it is AT then you’d need to be treated accordingly – see the blog post. There isn’t a lot more I can say about it. He may be right but equally, he may be wrong – without knowing thyroid volume it is hard to say.
You should also have some other things tested like cortisol – see my The Thyroid Patient’s Manual book for details on basic testing. Low cortisol can also cause dizziness and low BP.
Best wishes, Paul
Can an Atrophic Thyroid happen within a few months time. I have had hypo for 40 yrs since birth of first child. A CT scan I had for lungs 6 mths ago states normal unremarkable thyroid. A CT scan I had recently showed Atrophic Thyroid. I asked my doctor if this is something that just happened recently and she said likely they just didn’t add it to your scans before and it’s common with people with hypo. Just recently my routine thyroid tests have gone from 1.2 to 2.5. She said I will just need more meds that’s all. A little frustrating.
Yes, it can occur like that. Note from the blog post that people with AT do much better on T3 meds and not on T4 ones due to the fluctuations and the loss of T3 due to losing the thyroid gland.
Best wishes, Paul
After a recent CT scan for a different purpose, the comment on the CT report read “Thyroid gland diminutive in size or surgically absent.” This was news to me, as I have never had thyroid surgery (though I have had Hashimoto’s for 25+ years). I have been stable on the same dose of levothyroxine for a long time, only now I am hyperthyroid. I am positive for the peroxidase antibody but negative for the thyroglobulin antibody. I am hoping I can find someone to manage this and get levels back into an acceptable range. Thank you for the very useful information.
Hi Ann, the loss of the thyroid gland due to Atrophic thyroiditis (which it sounds like it is) usually responds better to T3 treatment and not Levothyroxine. You may have hyperthyroid symptoms but this could easily be due to low cortisol at this stage due to the loss of some FT3. Losing the thyroid means a loss of a lot of conversion ability from T4 to T3. This cannot be recovered and T3 treatment is very often the only way to manage it when Atrophic thyroiditis is suspected.
The blog post you have commented on explains most of this.
Best wishes, Paul
Thank you very much.
Dear Paul,
I found this post very helpful. Thank you. I was diagnosed with Hashimoto’s back in 1997 and have been taking various doses of Synthroid ever since. My levels always seemed to bounce around a lot, for no obvious reason — and I’ve generally had most of the hypothyroid symptoms despite being treated. I recently went back to an endocrinologist who said my labs suggested I was not converting T4 to T3 well; she added in a small amount of T3 (5mcg). I just had a thyroid U/S which worried me in showing I have AT (right + left lobe volume = 0.6 cc)
I’m going to go ahead and order your books. I’m sure hoping there are treatment options for someone in my situation that will help prevent worsening myxedema. It sounds like you believe there are? (And do you still offer 1:1 coaching, btw?)
Hi Kathy, for sure there are treatment options. But you’d need to get FT3 well up the range without high rT3.
That isn’t going to occur through the addition of only 5 mcg of T3.
There are several relevant blog posts apart from the AT one you’ve read. Here are some links:
https://paulrobinsonthyroid.com/research-shows-free-t4-and-free-t3-ranges-for-individual-thyroid-patients-are-less-than-half-as-wide-as-the-wide-population-laboratory-ranges/
https://paulrobinsonthyroid.com/only-free-t3-ft3-tracks-changes-in-symptoms-during-thyroid-treatment-research/
and
https://paulrobinsonthyroid.com/more-t4-t3-thyroid-medication-might-not-always-raise-patients-ft3-levels-in-thyroid-hormone-treatment/
The bottom line, is that people often need to add quite a lot of T3 and lower the T4 meds substantially. In the case of AT, often the only treatment that works well is T3-Only.
Yes, I still do some 1-1 coaching. There is a Contact Us button on the front page of this site which you can use to reach me if you need more information on that.
Best wishes, Paul
I was diagnosed hypothyroid abroad from UK in “92 and after a trial of T4 which I didn’t get on with, was told I had “thyroid resistance” and put on T3. All went well till I returned to UK and in 2006/7 told I had Hashimoto’s with positive TPO and TbAb. UK endo kept small amount of T3 but put me on combination T3/4 and eventually just T4. 2011 changed Endo’s who adjusted dose but then suggested NDT but I could not get on with it so settled back on combination T4/3. Also discover I have DIO2 gene. Biggest issues have been my deficient TSH and trying to convince Endos not to reduce dose despite them doing so and my FT4 going as low as 3 and as high as 24 (12-24 ref range) with no change in TSH.
Since pandemic I have been monitoring myself due to waiting to see Endo’s. My dose has remained 100mcgs of liquid T4 (just could not get on with tablets or capsules) and 40mcgs of T3. Last year I decided to get a thyroid scan and the report said “Thyroid gland appears small, isthmus measures 1.2mm” which he told me was Atrophic. I have symptoms of both under and over medication – two hours after morning meds I get very sweaty and any exertion causes extreme sweating but I also get palpitations at times which I get when Im under as well as dry skin and bad sleep. Last Labs were FT4 14.3 FT3 5.3 TSH 0.01
My questions are why is my TSH not budging and is this because of the autoimmune AT? What sort of dose change do you think I might benefit from?
Lynn, if it is atrophic thyroiditis (AT) then people usually respond better to T3-Only. T3 only ensures that any variation in conversion due to AT is eliminated.
TSH should never be used in the way it has been with you. The FT4 and FT3 are the main measures with FT3 being the most important one. See this blog post: https://paulrobinsonthyroid.com/is-it-safe-for-tsh-to-be-low-or-suppressed-on-thyroid-treatment-research/
You also haven’t had rT3 tested so you don’t know how much of your FT4 is going into high rT3 – which it may well be. This can be tested privately.
Best wishes, Paul