Chronic lymphocytic thyroiditis
Chronic lymphocytic thyroiditis, also known as autoimmune thyroiditis, is a chronic inflammatory autoimmune disease that uses its own thyroid tissue as the antigen. Hashimoto’s thyroiditis was first reported by Hashimoto at Kyushu University in Japan (1912) in a German medical journal and was named Hashimoto’s thyroiditis, the most common clinical inflammation of the thyroid gland.
Hashimoto thyroiditis is a chronic lymphocytic thyroiditis, which is an autoimmune disease.
Differentiation
I. Medical history and symptoms.
Etiology and mechanism
The main manifestation is an enlarged thyroid gland, most of which is diffuse and a few of which can be limited, and some of which start with swelling of the face and limbs. The disease can be divided into eight types.
(a) Hashimoto’s hyperthyroidism: Patients have typical hyperthyroid symptoms and positive laboratory test results. Hyperthyroidism and Hashimoto’s disease can co-exist or occur sequentially, co-exist and transform each other.
(ii) Pseudohyperthyroidism: A few may have symptoms of hyperthyroidism, but no evidence of hyperthyroidism in thyroid function tests and positive TGAb and TMAb.
(iii) Proptosis type: the eyes are protruding, and the thyroid function may be normal, hyper or hypo.
(iv) Subacute thyroiditis type: more rapid onset, swollen and painful thyroid gland with fever, accelerated blood sedimentation, but normal or increased 131 iodine uptake rate, positive thyroid antibody titer.
(v) Adolescent type: accounting for about 40% of adolescent goiter, with normal thyroid function and low antibody titers.
(vi) Fibrotic type: The disease is of longer duration and may present with extensive or partial fibrosis of the thyroid gland, thyroid atrophy, and hypothyroidism.
(vii) With thyroid adenoma or cancer: often isolated nodules with high TGAb and TMAb titers.
(viii) Associated with other autoimmune diseases.
Thyroid gland
II. Physical examination reveals.
The thyroid gland is diffusely or restrictively enlarged, hard and elastic in texture, with clear borders, no tenderness, smooth surface, some of the thyroid gland may be nodular, the lymph nodes in the neck are not enlarged, and some may have mucinous edema of the extremities.
III. Ancillary tests.
(1) Determination of anti-thyroid antibodies: serum anti-thyroid peroxidase antibody (TMAb) (anti-TPO) and serum thyroglobulin antibody (TGAb) (Anti-tg) are often significantly increased and have diagnostic significance for this disease. In some patients, multiple tests are required.
(2) Early thyroid function may be normal, and in Hashimoto hyperthyroidism, thyroid function is mildly elevated. As the disease progresses, T3 and T4 may decrease and TSH may increase.
(3) Irregular concentrations or sparse areas on radionuclide imaging of the thyroid gland, with a few appearing as “cold nodules”.
(4) Positive potassium perchlorate release test.
(5) Blood sedimentation may be accelerated, serum gammaglobulin may be increased, and albumin may be decreased.
(6) Thyroid puncture shows a large number of lymphocytic infiltrates.
IV. Differential diagnosis.
It should be differentiated from other causes of goiter and thyroiditis.
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.
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3. Some patients are accompanied by other autoimmune diseases such as pernicious anemia, disseminated erythema scarum, rheumatoid arthritis, dry syndrome, type I diabetes, chronic active hepatitis, etc. 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 the stomach lining cells in the patient.
Diagnosis
Detailed diagram
I. Basic tests
1. Thyroid function tests may vary depending on the course of the disease.
(1) Serum T4 and T3 are normal in the early stage, but TSH is elevated; in the later stage, serum T4 decreases, T3 is normal or decreases, and TSH is elevated.
(2) The iodine uptake rate of thyroid gland is normal or increased in the early stage, but can be suppressed by T3; in the later stage, the iodine uptake rate decreases and TSH is not increased by injection.
2. Immunological examination The titers of thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) in blood are significantly elevated, and both of them are diagnostic when they are greater than 50% (immunoassay double antibody method), which can last for several years or more than ten years. These two antibodies are the only basis for the diagnosis of this disease.
3. Other tests: increased sedimentation up to 100 mm/h, decreased serum albumin and increased r-globulin.
Further tests
1. SPECT thyroid scan may be uniform or heterogeneous, and may appear as “cold nodules”.
For those with atypical clinical manifestations and low or negative antibody titers, fine needle aspiration cytology or tissue biopsy may be used to confirm the diagnosis.
Diagnostic points
1. Middle-aged women with diffuse enlargement of the thyroid gland with a tough texture should be considered for this disease regardless of thyroid function.
2, serum TGA and TMA titers are significantly elevated (>50%), which can basically confirm the diagnosis.
3. For atypical clinical manifestations, antibody titers >= 60% for two consecutive times, and for those with hyperthyroidism, antibody titers >= 60 for more than six months.
4. The disease should be differentiated from thyroid cancer, which is antibody negative. The incidence of thyroid cancer in this disease is reported to be 5%-17% in the literature.