The THIRD type of autoimmune thyroid disease: Atrophic Thyroiditis

Do you know about the THIRD type of autoimmune thyroid disease?

Atrophic Thyroiditis causes hypothyroidism, but it’s NOT Hashimoto’s.

atrophic thyroiditis

Myths and lack of knowledge

Most doctors and patients have never heard about Atrophic Thyroiditis (AT). That’s because it’s not taught in med school, and an ultrasound is not usually ordered unless a thyroid gland is enlarged or has nodules.

An atrophied thyroid is NOT “end-stage” Hashimoto’s — that’s a common myth.

Thyroid glands do NOT normally shrink with age — that’s also a common myth.

The surprising facts

Believe it or not, AT is actually a HYPOthyroid form of Graves’ disease.

There’s even an article that calls atrophic thyroiditis “Hypothyroid Graves’ disease” (Starrenburg-Razenberg et al 2010)

The normal form of Graves’ HYPERthyroidism is caused by TSH-Receptor *stimulating* antibodies that overstimulate the thyroid gland to produce hormone, even in the absence of TSH.

But Atrophic Thyroiditis is the mirror image of Graves’ disease. It is caused by TSH-Receptor *blocking* antibodies that prevent TSH, even extremely high levels of TSH, from stimulating the thyroid gland. This form of thyroid disease may also present with Hashimoto’s antibodies.

According to Frohlich 2016, “Thyroid Autoimmunity,” blocking anti-TSH-Receptor antibodies occur in 25–75% of Graves’ Disease patients.

Jara, 2009 explains that Atrophic Thyroiditis patients usually have a Graves’ disease genetic profile, which is distinct from Hashimoto’s.

You can flip between hypo and hyper status

According to Takasu et al, 2012, Graves’ disease patients can flip between hypothyroid, hyperthyroid and euthyroid status over many years, depending on whether the blocking antibody predominates over the stimulating antibody, or whether the two antibodies are in balance with each other. TSHR antibody levels can fluctuate wildly and can also completely disappear or resurface over time.

A real example — one of us

One of our team members in the Canadian Thyroid Patients Campaign has atrophic thyroiditis.

A normal female gland is about 12-15 mL volume. Her gland is 0.5 mL, a size that is found in less than 2% of autoimmune thyroid patients, according to Carle et al, 2009.

She was without hypothyroid symptoms until her late 20s. In her early 30s she presented with a TSH over 150. Throughout her 13 years on Synthroid, she continued to have a high and variable TSH level despite T4 in the upper part of normal reference range.

Common signs and diagnosis

A very high TSH (over 50) at diagnosis and a variable TSH over time are common findings in studies of Atrophic Thyroiditis. TSH can be so variable and biased by antibodies that TSH becomes a distraction, not a useful measure of hypothyroidism, so Free T4 and Free T3 testing is necessary.

Atrophic Thyroiditis can be diagnosed by ultrasound measurements and a TBII test, (Thyrotropin-Binding Inhibitory Immunoglobulin) (Khoo et al, 1999).

TBII tests measure both stimulating and blocking TSHR antibodies and add them together to yield a single number, which is very high in AT when blocking antibodies are active.


Carlé, A., Pedersen, I. B., Knudsen, N., Perrild, H., Ovesen, L., Jørgensen, T., & Laurberg, P. (2009). Thyroid Volume in Hypothyroidism due to Autoimmune Disease Follows a Unimodal Distribution: Evidence against Primary Thyroid Atrophy and Autoimmune Thyroiditis Being Distinct Diseases. The Journal of Clinical Endocrinology & Metabolism, 94(3), 833–839.
Fröhlich, E., & Wahl, R. (2017). Thyroid Autoimmunity: Role of Anti-thyroid Antibodies in Thyroid and Extra-Thyroidal Diseases. Frontiers in Immunology, 8.
Jara, L. J., Vera-Lastra, O., & Medina, G. (2008). Atrophic Thyroiditis. In Diagnostic Criteria in Autoimmune Diseases (pp. 221–225). Humana Press.
Khoo, D. H. C., Eng, P. H. K., Ho, S. C., & Fok, A. C. K. (1999). Differences in the levels of TSH‐binding inhibitor immunoglobulins in goitrous and agoitrous autoimmune thyroiditis after twelve months of l‐thyroxine therapy. Clinical Endocrinology, 51(1), 73–79.
McLachlan, S. M., & Rapoport, B. (2013). Thyrotropin-Blocking Autoantibodies and Thyroid-Stimulating Autoantibodies: Potential Mechanisms Involved in the Pendulum Swinging from Hypothyroidism to Hyperthyroidism or Vice Versa. Thyroid, 23(1), 14–24.
Starrenburg-Razenberg, A. J., Castro Cabezas, M., Gan, I. M., Njo, T. L., Rietveld, A. P., & Elte, J. W. F. (2010). Four patients with hypothyroid Graves’ disease. The Netherlands Journal of Medicine, 68(4), 178–180.
Takasu, N., & Matsushita, M. (2012). Changes of TSH-Stimulation Blocking Antibody (TSBAb) and Thyroid Stimulating Antibody (TSAb) Over 10 Years in 34 TSBAb-Positive Patients with Hypothyroidism and in 98 TSAb-Positive Graves’ Patients with Hyperthyroidism: Reevaluation of TSBAb and TSAb in TSH-Receptor-Antibody (TRAb)-Positive Patients. Journal of Thyroid Research, 2012, 182176.


See this blog post for a link to our larger collection of sources on this topic:

Categories: Atrophic Thyroiditis, TSHR-Antibody

7 replies

  1. Je le suis aussi et n’était pas bien soignée depuis près de 10 ans.
    I am too and have not been nicely treated since 10 years.


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