Chronic lymphocytic thyroiditis, also known as Hashimoto’s thyroiditis or Hashimoto’s disease, is an autoimmune disease.
Diagnosis
I. Medical history and symptoms.
Mostly seen in women aged 30 to 50 years, the onset is insidious, the development is slow and the course is long, the main manifestation is enlargement of the thyroid gland, most of which is diffuse, a few can be limited, and some start with a feeling of swelling of the face and extremities. The histological features are a large number of lymphocytes and plasma cells infiltrating the thyroid gland tissue and forming lymphoid follicles.
II. Physical examination findings.
The thyroid gland is diffusely or restrictively enlarged, hard and elastic in texture, with clear borders, no tenderness, smooth surface, some of the thyroid glands may be nodular, the lymph nodes in the neck are not enlarged, and some of them may have mucinous edema of the extremities.
Third, auxiliary examination.
In early stage, thyroid function may be normal, and in Hashimoto hyperthyroidism, thyroid function may be mildly elevated. There are irregular concentrations or sparse areas on radionuclide imaging of the thyroid gland, with a few showing “cold nodules”. Positive potassium perchlorate release test. Serum gammaglobulin is elevated and albumin is decreased. Thyroid puncture shows a large number of lymphocytic infiltrates.
Treatment measures
Surgical removal is generally not indicated. Treatment with thyroxine tablets or levothyroxine T4 is indicated. Surgery may be considered if it causes pressure symptoms or other.
Etiology
1. High potency autoantibodies against various components of the thyroid gland can be detected in the patient’s serum during the course of the disease. For example, thyroid microsomal antibodies, thyroglobulin antibodies, and elevated serum thyroid stimulating blocking antibody (TsBAb) values in some patients.
2. Evidence of cellular immunity is the presence of a large number of plasma cell and lymphocyte infiltrates and lymphoid follicle formation in the thyroid tissue. There is blastcell formation, mobile inhibitory factor and lymphatic fine toxin production. T lymphocytes in patients with this disease are sensitized and the corresponding antigens are mainly thyroid cell membranes.
Some patients are accompanied by other autoimmune diseases such as pernicious anemia, disseminated erythema scarum, rheumatoid arthritis, dry syndrome, type I diabetes, and chronic active hepatitis. In the later stages of the disease, when thyroid function is markedly low, the clinical picture is one of mucinous edema. The patient has a genetic defect in suppressor T lymphocytes leading to the production of thyroid autoantibodies. In combination with K-cell mediated immunity, which is still present in this disease, lysable cells, including lymphotoxins, are released, leading to thyroid cell damage.
In addition genetic factors are closely related to the pathogenesis of autoimmunity. There are family clusters of the disease and it is more prevalent in women. In foreign studies on HLA genetic factors, it was found that DBW3 and DR5 are increased in European and American whites, while DBW53 appears more frequently in Japanese.
Pathological changes
Most of the glands are diffusely enlarged, firm in texture, pale on the surface, uniformly lobulated in cut surface, without necrosis or calcification. Initially, the thyroid follicular epithelium showed inflammatory destruction, basement membrane fracture, and varying degrees of eosin staining of the cytoplasm, indicating normal cell function and changes such as thyroid follicular hyperplasia, which are characteristic pathology of the disease. In the later stages, the thyroid gland is markedly atrophied, with smaller and less numerous alveoli and a cavity containing very little gelatinous material. The most characteristic changes are massive plasma cell and lymphocyte infiltration and lymphoid follicle formation in various parts of the interstitium, with occasional foreign body giant cells. There is also a moderate degree of connective tissue hyperplasia.
Clinical presentation
The disease is most common in middle-aged women and presents as a goiter that starts slowly, often unintentionally, and is approximately two to three times the size of the normal thyroid gland, with a smooth surface and a firm, elastic texture like rubber. In the late stage, a few may have mild local pressure symptoms.
The disease develops slowly, and sometimes the goiter does not seem to change significantly over several years. In the initial stage, thyroid function is normal. The process is similar to subacute thyroiditis, but is not accompanied by pain, fever, etc. Therefore, this state is called painless thyroiditis, and postpartum onset is called postpartum thyroiditis. However, when the thyroid gland is destroyed to a certain extent, many patients gradually develop hypothyroidism, and a few show mucinous edema. The disease can sometimes be combined with pernicious anemia due to the presence of autoantibodies to gastric lining cells in the patient.