The THIRD type of autoimmune thyroid disease: Atrophic Thyroiditis

atrophic thyroiditis

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

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

Myths and lack of knowledge

Most doctors and patients have never heard about Atrophic Thyroiditis (AT). That’s because it’s not taught in medical 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 still repeated in publications that repeat earlier misinformed publications.

As a result of these myths and lack of knowledge, most of us are misclassified as Hashimoto’s thyroiditis when we also have TPO (thyroid peroxidase) or TG (thyroglobulin) antibodies, or as cases of hypothyroidism of unknown cause when Hashimoto’s antibodies are absent or not elevated.

The surprising facts

AT is a HYPOthyroid form of Graves’ disease. Jara, et al, 2008, explains that Atrophic Thyroiditis patients usually have a Graves’ disease genetic profile, which is quite distinct genetically from Hashimoto’s.

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

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.

You can flip between hypo and hyper status

According to Takasu et al, 2012, a small percentage of hypothyroid patients with the blocking antibody, as well as 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 — My thyroid and failed therapy

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

I was without hypothyroid symptoms until my late 20s. In my early 30s I presented with a TSH over 150.

In my final 3 years of therapy on Synthroid, I had a TSH receptor blocking antibody attack. Previously, records show I had a TSH that ranged from low-normal to almost suppressed by a FT4 at top of reference range and a FT3 level in the lower half of reference.

When the antibody attack arrived (or returned after many years), after a small dose reduction, my TSH suddenly rose to 18.8 mU/L while my FT4 was still in the upper part of reference. I continued to have a high and variable TSH level despite a high-normal FT4. Meanwhile, the Total and Free T3 level remained almost flatlined below reference range.

T4 monotherapy finally became unsustainable after I fell into a severe health crisis for three months including random daily and nightly chest pain and tachycardia that triggered a numb or weak arm, legs, or severe lightheadedness. Walking, standing, and normal cognitive tasks became difficult. T3 levels fell even lower. Reverse T3 elevated far above reference. Reducing T4 dose offered temporary relief from chest pain but worsened hypothyroidism. Several attempts to return the T4 dose back to normal levels ended in severe pain and hospital emergency visits. Transition to therapy with T3 hormone finally resolved the crisis.

How the antibody warps TSH-FT4-FT3 relationships

What I experienced is a fluctuating pattern seen in others with active blocking antibodies during thyroid therapy (Tagami et al, 2019).

The loss of normal T4 feedback on TSH happens partly because the antibody blocks the ultrashort feedback loop at the pituitary gland. The “ultrashort feedback loop” has also been called the “Brokken-Prummel-Wiersinga” feedback loop after the team that published a few articles about it in the early 2000s. This pituitary TSH feedback loop has been more extensively studied in hyperthyroid Graves’ disease, but the inverse happens at the same receptor in patients with blocking antibodies.

As with cases of fluctuating Graves’ disease during treatment, as the antibody varies, TSH can be variable, unrelated to FT4 and FT3 levels, fluctuating mainly with the antibody level (Alzahrani et al, 2005). TSH becomes a distraction, not a useful measure of treatment effectiveness.

The TSH receptor blocking antibody functions as an “inverse agonist” of TSH receptor signaling (McLachlan & Rapoport, 2013). Even baseline TSH-receptor signaling is cut off in a severe blocking antibody attack, and high levels of circulating TSH in blood cannot signal at the blocked receptors in the thyroid and elsewhere across the entire body.

TSH signaling usually upregulates the deiodinases that perform T4-T3 conversion. Without even the basal signal produced by an empty TSH receptor, the conversion rate drops throughout the body, and likely even in the pituitary and hypothalamus. This could be the second reason why the TSH can become abnormally elevated in relationship to FT4 during therapy.

Common signs and diagnosis

A very high TSH (over 50) at diagnosis with no goiter (no thyroid swelling) is a common finding in studies of Atrophic Thyroiditis.

Atrophic Thyroiditis can also be diagnosed by ultrasound measurements showing the telltale signs of the TSH receptor antibody that signals cell death (apoptosis) — this is the TSH receptor “cleavage” or “neutral” antibody (Morshed et al, 2015). Glands will show abnormal shrinkage in relationship to the person’s sex and body surface area, and sometimes an abnormal pattern of shrinkage. (Vitti et al, 1994; Carle et al, 2009; Turicos et al, 2015)

The best antibody test is (or was) the TBII test — Thyrotropin-Binding Inhibitory Immunoglobulin (Khoo et al, 1999), even though the test does not reveal the blocking antibody alone. TBII tests measure both stimulating and blocking TSHR antibodies and add them together to yield a single number. The number is higher in Atrophic Thyroiditis when blocking antibodies are active than when only a mild attack of stimulating antibody antibodies is present.

Unfortunately, the old technology TBII test is being replaced by newer TRAb (thyroid receptor antibody) tests. Some of these TRAb tests falsely claim to offer what the TBII test used to provide. Unfortunately, most of these test developers have decided that the hypothyroid form of the TRAb antibody is not important to diagnose. Most of them simply measure the net difference between stimulating and blocking, giving a number only for the stimulating effect (McLachlan & Rapoport, 2013).

Read more

Read more recent articles that cover the TSH-receptor blocking antibody and Atrophic Thyroiditis:


Alzahrani, A. S., Aldasouqi, S., Abdel Salam, S., & Sultan, A. (2005). Autoimmune Thyroid Disease with Fluctuating Thyroid Function. PLoS Medicine, 2(5).

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.

Morshed, S. A., & Davies, T. F. (2015). Graves’ Disease Mechanisms: The Role of Stimulating, Blocking, and Cleavage Region TSH Receptor Antibodies. Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones et Metabolisme, 47(10), 727–734.

Tagami, T., Hiroshima-Hamanaka, K., Umakoshi, H., Tsuiki-Naruse, M., Kusakabe, T., Satoh-Asahara, N., Shimatsu, A., & Moriyama, K. (2019). Experimental Reproduction of Dynamic Fluctuation of TSH Receptor-Binding Antibodies Between Stimulation and Inhibition. Journal of the Endocrine Society, 3(12), 2361–2373.

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.

Turcios, S., Lence-Anta, J. J., Santana, J.-L., Pereda, C. M., Velasco, M., Chappe, M., Infante, I., Bustillo, M., García, A., Clero, E., Maillard, S., Rodriguez, R., Xhaard, C., Ren, Y., Rubino, C., Ortiz, R. M., & de Vathaire, F. (2015). Thyroid Volume and Its Relation to Anthropometric Measures in a Healthy Cuban Population. European Thyroid Journal, 4(1), 55–61.

Vitti, P., Lampis, M., Piga, M., Loviselli, A., Brogioni, S., Rago, T., Pinchera, A., & Martino, E. (1994). Diagnostic usefulness of thyroid ultrasonography in atrophic thyroiditis. Journal of Clinical Ultrasound: JCU, 22(6), 375–379.

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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