Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis, Hashimoto's disease and autoimmune thyroiditis, is an autoimmune disease in which the thyroid gland is gradually destroyed.

Early on, symptoms may not be noticed. Over time, the thyroid may enlarge, forming a painless goiter. Most people eventually develop hypothyroidism with accompanying weight gain, fatigue, constipation, hair loss, and general pains. After many years, the thyroid typically shrinks in size. Potential complications include thyroid lymphoma. Further complications of hypothyroidism can include high cholesterol, heart disease, heart failure, high blood pressure, myxedema, and potential problems in pregnancy.

Hashimoto's thyroiditis is thought to be due to a combination of genetic and environmental factors. Risk factors include a family history of the condition and having another autoimmune disease. Diagnosis is confirmed with blood tests for TSH, thyroxine (T₄), antithyroid autoantibodies, and ultrasound. Other conditions that can produce similar symptoms include Graves' disease and nontoxic nodular goiter.

Hashimoto's is typically not treated unless there is hypothyroidism or the presence of a goiter, when it may be treated with levothyroxine. Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy. Surgery is rarely required to treat the goiter.

Hashimoto's thyroiditis has a global prevalence of 7.5%, and varies greatly by region. The highest rate is in Africa, and the lowest is in Asia. In the US, white people are affected more often than black people. It is more common in low to middle-income groups. Females are more susceptible, with a 17.5% rate of prevalence compared to 6% in males. It is the most common cause of hypothyroidism in developed countries. It typically begins between the ages of 30 and 50. Rates of the disease have increased. It was first described by the Japanese physician Hakaru Hashimoto in 1912. Studies in 1956 discovered that it was an autoimmune disorder.

In the early stages of autoimmune thyroiditis, patients may have normal thyroid hormone levels and no goiter or a small one. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis. Early on, thyroid autoantibodies in the blood may be the only indication of Hashimoto's disease. They are thought to be the secondary products of the T cell-mediated destruction of the gland.

As lymphocytic infiltration progresses, patients may exhibit signs of hypothyroidism in multiple bodily systems, including, but not limited to, a larger goiter, weight gain, cold intolerance, fatigue, myxedema, constipation, menstrual disturbances, pale or dry skin, and dry, brittle hair, depression, and ataxia. Extended thyroid hormone deficiency may lead to muscle fibre changes, resulting in muscle weakness, muscle pain, stiffness, and rarely, pseudohypertrophy. Patients with goiters who have had autoimmune thyroiditis for many years might see their goiter shrink in the later stages of the disease due to destruction of the thyroid. Graves disease may occur before or after the development of autoimmune thyroiditis.

While rare, more serious complications of the hypothyroidism resulting from autoimmune thyroiditis are pericardial effusion, pleural effusion, both of which require further medical attention, and myxedema coma, which is an endocrine emergency.