Thyroiditis

The term thyroiditis relates to diverse group of inflammatory diseases of the thyroid gland, usually caused by autoimmune factors, and sometimes by infectious agents (e.g. mumps virus).

Hashimoto’s thyroiditis

Hashimoto’s thyroiditis is a chronic inflammatory disorder of the thyroid characterized by the infiltration of thyroid by auto-antibodies. It is thought to be the most common cause of primary hypothyroidism in the Western world, and is eight times more prevalent in women than in men. (Berkow 1992, 1083; Rubin 2001, 606)

The pathogenesis of Hashimoto’s thyroiditis relates to high circulating autoantibodies against thyroid peroxidase (which acts to oxidize iodide into organic iodine), thyroglobulin (which serves as a substrate for the iodination of tyrosine in the thyroid), and the TSH receptor. There is a familial tendency for Hashimoto’s thyroistis, with both patients and their relatives having a higher incidence of other autoimmune diseases (e.g. IDDM, Addison’s disease, myasthenia gravis, pernicious anemia, RA, SLE, Sjögren's syndrome). (Berkow 1992, 1083; Rubin 2001, 606)

Patients with Hashimoto’s typically present with a non-tender enlargement of the thyroid gland or fullness of the throat that can promote some discomfort in swallowing. Upon examination the thyroid is enlarged, smooth or nodular, and firm. Many patients have hypothyroidism when first seen, and may present with other autoimmune diseases such as SLE and RA. Laboratory investigation typically yields normal T4 and TSH levels, with high levels of thyroid peroxidase antibodies and sometimes anti-thyroglobulin antibodies. As the disease progresses the patient develops clinically evident hypothyroidism, with decreased T4, decreased thyroid radioactive iodine uptake, and increased TSH. (Berkow 1992, 1083; Rubin 2001, 606)

Holistic treatment

Please review the section on hypothyroidism and autoimmune disease. Treatment should attempt to address the underlying autoimmune factors and support normal thyroid function.