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 aging.
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 TPOs 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. 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. This means the body is trying to create a higher level of T3 in the body. However, TSH signaling throughout the body can be blocked by high levels of the TBAb antibody. This prevents the T4 to T3 conversion rate being at the level it should be. In fact, T3 levels can remain far too low for the person, when TBAb levels rise. So, those on T4 medication may find it very difficult to remain stable.
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.
Here is Dr. Smith’s original article on the spectrum of autoimmunity conditions. There is a detailed section in the article on Atrophic Thyroiditis: