Antithyroid antibodies


Antithyroid autoantibodies, antithyroid antibodies, are autoantibodies targeted against one or more components on the thyroid. 

The most clinically relevant anti-thyroid autoantibodies are anti-thyroid peroxidase antibodies (anti-TPO antibodies), thyrotropin receptor antibodies (TRAb) and thyroglobulin antibodies (TgAb). 

Graves’ disease and Hashimoto’s thyroiditis are commonly associated with the presence of anti-thyroid autoantibodies. 

Although there is overlap, anti-TPO antibodies are most commonly associated with Hashimoto’s thyroiditis and activating TRAb’s are most commonly associated with Graves’ disease. 

Anti-thyroid antibodies can be subdivided into groups according to their target antigen.

Anti-thyroid peroxidase (anti-TPO) antibodies are specific for the autoantigen TPO.

TPO is a 105kDa glycoprotein that catalyses iodine oxidation and thyroglobulin tyrosyl iodination reactions in the thyroid gland.

Anti-TPO antibodies are the most common anti-thyroid autoantibody, present in approximately 90% of Hashimoto’s thyroiditis, 75% of Graves’ disease and 10-20% of nodular goiter or thyroid carcinoma. 

10-15% of normal individuals can have high level anti-TPO antibody titers.

High serum antibodies are found in active phase chronic autoimmune thyroiditis, and can be used to assess disease activity in patients that have developed such antibodies.

The majority of anti-TPO antibodies are produced by thyroid infiltrating lymphocytes, with minor contributions from lymph nodes and the bone marrow.

Anti-TPO antibodies cause thyroid cell damage by complement activation and antibody dependent cell cytotoxicity.

The thyrotropin receptor is the antigen for TSH receptor antibodies (TRAbs). 

TRAbs are present in 70-100% of Graves’ disease (85-100% for activating antibodies and 75-96% for blocking antibodies) and 1-2% of normal individuals.

TPO antibody is more easily measured than the TSH receptor antibody, and so is often used as a surrogate in the diagnosis of Graves’ disease. 

These antibodies activate adenylate cyclase by binding to the TSH receptor, causing the production of thyroid hormones and subsequent growth and vascularisation of the thyroid.

In TRAbs induce Graves’ ophthalmopathy it is likely that the antibodies bind to TSH receptors in retro-orbital tissues, causing infiltration of lymphocytes, cytokine production causing fibroblasts to produce glycosaminoglycans, leading to ophthalmopathy.

Blocking TRAbs competitively block the activity of TSH on the receptor. 

This can cause hypothyroidism by reducing the thyrotropic effects of TSH. 

They are found in Hashimoto’s thyroiditis and Graves’ disease and may be cause of fluctuation of thyroid function in the latter. 

Thyroglobulin antibodies are specific for thyroglobulin, a 660kDa matrix protein involved in the process of thyroid hormone production. 

Thyroglobulin antibodies are found in 70% of Hashimoto’s thyroiditis, 60% of idiopathic hypothyroidism, 30% of Graves’ disease, a small proportion of thyroid carcinoma and 3% of normal individuals.

Anti-TPO antibodies are present in 99% of cases where thyroglobulin antibodies are present, however only 35% of anti-TPO antibody positive cases also demonstrate thyroglobulin antibodies.

Anti-Na+/I− symporter antibodies are present in approximately 20% of Graves’ disease and 24% of Hashimoto’s thyroiditis.

Antibodies in Graves’ disease is thought to arise by activation of CD4+ T-cells, followed by B-cell recruitment into the thyroid producing antibodies specific to the thyroid antigens. 

Anti-thyroid antibodies are used to track the presence of autoimmune thyroiditis, but are not considered to contribute directly to the destruction of the thyroid.

Anti-thyroid antibodies is associated with an increased risk of unexplained subfertility, miscarriage, preterm birth and maternal postpartum thyroiditis.

Leave a Reply

Your email address will not be published. Required fields are marked *