Could Atrophic Thyroiditis Be Your Problem? It is Not Always About Hashimoto’s Thyroiditis

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:

Best wishes,


Paul Robinson

Paul Robinson is a British author and thyroid patient advocate. The focus of his books and work is on helping patients recover from hypothyroidism. Paul has accumulated a wealth of knowledge on thyroid and adrenal dysfunction and their treatment. His three books cover all of this.

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  1. Linda Sanday on 19th June 2020 at 11:48 am

    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

    • Paul Robinson on 19th June 2020 at 4:14 pm

      I’m glad it helped Linda. It also has implications for treatment described in the article.
      Good luck!

  2. CJ Hinke on 14th July 2020 at 7:44 am

    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.

    • Paul Robinson on 14th July 2020 at 9:41 am

      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,

  3. Bente Seljestokken on 20th November 2020 at 11:28 pm

    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 🙂

    • Paul Robinson on 21st November 2020 at 10:10 am

      Good luck Bente!
      Best wishes, Paul

  4. Helen on 30th December 2020 at 2:05 pm

    Thank you for this clear and concise summary, Paul. Most helpful.

    • Paul Robinson on 30th December 2020 at 4:53 pm

      Thanks for the feedback Helen!

      • C J Edwards on 6th July 2021 at 10:07 pm

        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!

        • Paul Robinson on 7th July 2021 at 10:49 am

          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

  5. Christiane Beland on 25th April 2021 at 7:30 pm

    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

    • Paul Robinson on 26th April 2021 at 9:47 am

      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

  6. Emily Scopes on 8th June 2021 at 7:20 am

    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?

    • Paul Robinson on 8th June 2021 at 5:49 pm

      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

  7. Sandy Epley on 23rd July 2021 at 5:59 pm

    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?

    • Paul Robinson on 23rd July 2021 at 7:10 pm

      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

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