Postpartum Thyroiditis: Not Just a Worn Out Mom

Katherine Pereira; Ann J. Brown

Disclosures

Journal for Nurse Practitioners. 2008;4(3):175-182. 

In This Article

Pathophysiology

PPT thyroiditis is the result of an autoimmune process. Pathologic examination shows lymphocytic infiltration of the thyroid gland by B cells and cytotoxic T cells.[9] There is widespread inflammation and apoptosis of thyroid cells, which causes release of preformed thyroxine (T4) and triiodothyronine (T3) into the circulation. Production of new thyroid hormone ceases for an interval because of damage to thyroid cells and the subsequent drop in TSH in response to elevations in T4 and T3. After inflammation resolves, TSH rises and production of thyroid hormone resumes. However, if there is significant thyroid damage, permanent hypothyroidism can ensue.

It is not clear what triggers this autoimmune process, though it is clear that it is initiated by activation of thyroid antigen-specific helper T cells. One theory suggests that certain viruses contain a protein that activates thyroid-specific T cells.[10] Another theory is that thyroid epithelial cells present their intracellular proteins to T cells. T cells activated in this way induce B cells to secrete thyroid antibodies (thyroid peroxidase antibodies). Thyroid peroxidase (TPO) antibodies are cytotoxic to thyrocytes, the thyroid hormone-producing cells in the thyroid.

Approximately half of all women with PPT have a family history of autoimmune thyroid dysfunction, indicating a genetic link to risk for the condition.[11] Molecular studies have identified the major histocompatibility (MHC) region, located on chromosome 6, as important in determining T cell and antigen response in autoimmune thyroiditis.[1] There also appears to be a link between the HLA-DR3, HLA-DR4, and HLA-DR5 antigens and risk for both PPT and Hashimoto's thyroiditis.[12,13]

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