Chronic lymphocytic thyroiditis

An overview of chronic lymphocytic thyroiditis (chronic lymphocytic thy - roid itis), also known as Hashimoto's thyroiditis (Hashimoto thyroiditis), is an autoimmune disease. A cause. From the course of serum were detected in a high titer of anti-thyroid various components of autoantibodies. If thyroid microsomal antibodies, thyroglobulin antibodies, and some patients with thyroid stimulation blocking antibody (TsBAb) values. 2. Immune cells as evidence of thyroid tissue, a large plasma cells and lymphocytes and lymphoid follicles. Had a mother cell (blastcell) formation, migration inhibitory factor and lymphocytes produce toxins, The patient's T cells are sensitized to the activity of the corresponding antigen mainly thyroid cells. 3. Some were accompanied by other autoimmune diseases, such as pernicious anemia, the Red Scars disseminated tumors, rheumatoid arthritis, Sjogren's syndrome, type I diabetes, chronic active hepatitis. The disease late low thyroid function, the clinic was myxedema. With the inhibition of T-lymphocyte genetic defects lead to thyroid autoantibodies. In light of the disease still K cell-mediated immunity, including the release of Lymphotoxin soluble cells, Thyroid lead to cell damage. In addition to genetic factors and the incidence of autoimmune mechanism closely related. The disease is familial clustering phenomenon, and multiple women. Foreign HLA genetic factor in the study found that whites DBW3 Europe and the United States, DR5, And for the Japanese DBW53 there is a higher frequency. Most of the pathological changes glands showed diffuse swelling, solid texture, surface pale, uniform plane was lobulated, no necrosis or calcification. Thyroid early acinar epithelium was inflammatory damage, membrane rupture, the cytoplasm showed varying degrees of eosin staining, said normal cell function, and thyroid hyperplasia acinar changes, the disease is the characteristic pathology. Late thyroid atrophy, acinar change and a decrease in the number of small, very small cavity containing glue-like substance. The most characteristic change of mesenchymal throughout a large number of plasma cells and lymphocytes and lymphoid follicles, which can be found even foreign body giant cells. Additionally, there are middle-of connective tissue. Clinical manifestations of the disease more common in middle-aged women, the performance of goiter, slow onset, often unwittingly found, normal thyroid volume of about 2 ~ 3 times, the smooth surface, texture and resilience flexible as rubber, obviously nodules were rare. no tenderness, no adhesion with the surroundings, which can swallow campaign activities. Advanced there will be a few mild symptoms of partial oppression. The disease develops slowly, sometimes goiter in a few years may not change significantly. Early normal thyroid function. Course sometimes there may hyperthyroidism, and then normal, hypothyroidism, and then normal, similar to the process of subacute thyroiditis. but not with pain, fever, it said this state of painless thyroiditis, were called postpartum incidence of postpartum thyroiditis. But thyroid damage to a certain level, many patients began to emerge hypothyroidism, a few submissions myxedema. The disease can sometimes with pernicious anemia, which exist for patients with gastric parietal cell autoantibodies.