Chronic lymphocytic thyroiditis, also known as Hashimoto thyroiditis, is an autoimmune disease.

bubble_chart Etiology

1. During the course of the disease, high-titer autoantibodies against various thyroid components can be detected in the patient's serum. These include thyroid microsomal antibodies, thyroglobulin antibodies, and elevated levels of thyroid-stimulating blocking antibodies (TsBAb) in some patients.

2. Evidence of cellular immunity includes the presence of a large number of plasma cells and lymphocyte infiltration in thyroid tissue, as well as the formation of lymphoid follicles. Blast cells are observed, along with the production of migration inhibition factors and lymphotoxins. The T lymphocytes of affected patients exhibit sensitization activity, with the corresponding antigen primarily being the thyroid cell membrane.

3. Some patients may also present with other autoimmune diseases, such as pernicious anemia, systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, type 1 diabetes, and chronic active hepatitis. In the late stage (third stage) of the disease, when thyroid function is significantly impaired, clinical manifestations include myxedema. A hereditary defect in the patient's suppressor T lymphocytes leads to the production of thyroid autoantibodies. Additionally, K-cell-mediated immunity is involved in this disease, releasing soluble factors, including lymphotoxins, which contribute to thyroid cell damage. Furthermore, genetic factors are closely associated with the mechanism of autoimmune disease development. This condition exhibits familial clustering and is more prevalent in women. Studies on HLA genetic factors abroad have shown that in Caucasians of European descent, DBW₃ and DR₅ are more common, whereas in Japanese populations, DBW₅₃ appears with higher frequency.

bubble_chart Pathological Changes

Most glands exhibit diffuse enlargement, with a firm texture, pale surface, and uniformly lobulated cut surface, without necrosis or calcification. **Initial stage [first stage]**: The thyroid follicular epithelium shows inflammatory destruction, basement membrane rupture, and varying degrees of eosinophilic staining in the cytoplasm, indicating normal cell function. There is also hyperplasia of thyroid follicles, which is characteristic of the disease's pathology. **Late stage [third stage]**: The thyroid gland shows significant atrophy, with smaller and fewer follicles, and the lumina contain minimal colloid. The most characteristic changes include extensive infiltration of plasma cells and lymphocytes throughout the stroma, along with the formation of lymphoid follicles, occasionally containing foreign-body giant cells. Additionally, there is moderate connective tissue hyperplasia.

This disease is more common in middle-aged women and manifests as goiter. The onset is slow and often discovered incidentally, with the thyroid gland being about 2–3 times the normal size. The surface is smooth, the texture is tough and elastic like rubber, and obvious nodules are rare. There is no tenderness, no adhesion to surrounding tissues, and it moves with swallowing. In the

advanced stage, a few cases may exhibit grade I local compressive symptoms. The progression of the disease is slow, and sometimes the goiter shows no significant changes over several years. In the initial stage [first stage], thyroid function is normal. During the course of the disease, hyperthyroidism may occasionally occur, followed by normalization, hypothyroidism, and then normalization again—a process similar to subacute thyroiditis but without pain, fever, etc. Hence, this condition is called painless thyroiditis. If it occurs postpartum, it is termed postpartum thyroiditis. However, when thyroid destruction reaches a certain extent, many patients gradually develop hypothyroidism, and a few may present with myxedema. This disease may sometimes be complicated by pernicious anemia due to the presence of autoantibodies against gastric parietal cells in the patient's body.

bubble_chart Diagnosis

1. Medical History and Symptoms:

More common in women aged 30 to 50, the onset is insidious, progresses slowly, and has a prolonged course. The main manifestation is thyroid enlargement, mostly diffuse, with a few cases being localized. Some patients may present with a sensation of facial or limb swelling. The disease can be divided into eight types:

(1) Hashitoxicosis: Patients exhibit typical hyperthyroidism symptoms and positive laboratory test results. Hyperthyroidism and Hashimoto's disease may coexist or occur sequentially, transforming into each other.

(2) Pseudo-hyperthyroidism: A few patients may show hyperthyroidism symptoms, but thyroid function tests reveal no evidence of hyperthyroidism, with positive TGAb and TMAb.

(3) Exophthalmic type: Protrusion of the eyeballs, with thyroid function that may be normal, hyperactive, or hypofunctioning.

(4) Subacute thyroiditis-like type: Acute onset with thyroid swelling and pain, accompanied by fever and increased erythrocyte sedimentation rate, but ¹³¹

(5) Juvenile type: Accounts for about 40% of thyroid enlargement in adolescents, with normal thyroid function and lower antibody titers.

(6) Fibrotic type: Prolonged course, may present with extensive or partial thyroid fibrosis, thyroid atrophy, and hypothyroidism.

(7) Accompanied by thyroid adenoma or cancer: Usually presents as a solitary nodule, with higher TGAb and TMAb titers. (8) Associated with other autoimmune diseases.

2. Physical Examination Findings:

The thyroid is diffusely or locally enlarged, firm yet elastic, with clear borders, non-tender, and a smooth surface. Some thyroids may appear nodular, with no enlargement of cervical lymph nodes. Some patients may exhibit limb myxedema.

3. Auxiliary Examinations:

(1) Early thyroid function may be normal. In Hashitoxicosis, thyroid function is grade I elevated. As the disease progresses, T3 and T4 may decrease, TSH increases, and TMAb and TGAb are positive. (2) Thyroid radionuclide imaging shows irregular areas of concentration or sparsity, with a few cases presenting as "cold nodules." (3) Positive perchlorate discharge test. (4) Increased serum gamma globulin and decreased albumin. (5) Thyroid puncture reveals extensive lymphocyte infiltration.

4. Differential Diagnosis:

Should be distinguished from thyroid enlargement and thyroiditis caused by other etiologies.

bubble_chart Treatment Measures

Patients with hypothyroidism are treated with thyroid tablets as replacement therapy. Generally, 80–160 mg of thyroid tablets or 100–300 μg of L-T₄ can be administered daily, which provides more stable and reliable effects. For elderly patients, especially those with heart blood vessel disease, treatment should start with a small dose (10–20 mg of thyroid tablets or 12.5–25 μg of L-T₄ ).