Hashimoto thyroiditis is an autoimmune disease that destroys thyroid cells by cell and antibody-mediated immune processes. It is the most common cause of hypothyroidism in developed countries. In contrast, worldwide, the most common cause of hypothyroidism is an inadequate dietary intake of iodine. This disease is also known as chronic autoimmune thyroiditis and chronic lymphocytic thyroiditis. The pathology of the disease involves the formation of antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis. The diagnosis is often challenging and may take time until later in the disease process. The most common laboratory findings demonstrate an elevated thyroid-stimulating hormone (TSH) and low levels of free thyroxine (fT4), coupled with increased antithyroid peroxidase (TPO) antibodies. However, earlier on in the course of the disease, patients may exhibit signs, symptoms, and laboratory findings of hyperthyroidism or normal values. This is because the destruction of the thyroid gland cells may be intermittent. Women are more often affected. The female-to-male ratio is at least 10:1. Although some sources cite diagnosis happening more so in the fifth decade of life, most women are diagnosed between the ages of 30 to 50 years. Conventional treatment is comprised of levothyroxine at the recommended dose of 1.6 to 1.8 mcg/kg/day. The T4 converts to T3, which is the active form of thyroid hormone in the human body. Excessive supplementation can lead to deleterious and morbid effects, such as arrhythmias (the most common being atrial fibrillation) and osteoporosis. In this chapter, we review the pathogenesis, diagnosis, and management of Hashimoto thyroiditis.
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