What Is Autoimmune Thyroid Disease?
The prevalence of women with autoimmune thyroid disease is significantly higher than that of men. Most women think that estrogen plays a very important role. The positive rate of thyroid peroxidase antibody (TPOAb) in women under 70 years of age is significantly higher than that in men. High but some studies have also obtained very different results, such as the significant reduction in the incidence of thyroid autoantibodies and some AITD such as Graves disease (GD) in women after estrogen replacement therapy (HRT) or the use of contraceptives.
Autoimmune thyroid disease
- The prevalence of women with autoimmune thyroid disease is significantly higher than that of men. Most women think that estrogen plays a very important role. The positive rate of thyroid peroxidase antibody (TPOAb) in women under 70 years of age is significantly higher than that in men. High but some studies have also obtained very different results, such as the significant reduction in the incidence of thyroid autoantibodies and some AITD such as Graves disease (GD) in women after estrogen replacement therapy (HRT) or the use of contraceptives.
Autoimmune thyroid disease pathology
- Autoimmune thyroid disease (AITD) is an autoimmune antibody against thyroid antigens that can be detected in the blood of patients with thyroid disease caused by autoimmune disorders, including globin antibodies and thyroid microsomal antibodies. Patients may be accompanied by mild proteinuria and even nephrotic syndrome. There have been reports in the literature of 85 patients with AITD, and proteinuria was found to be as high as 40%. Studies suggest that the occurrence of this type of proteinuria may be related to autoimmunity. Many renal biopsy reports about AITD combined with proteinuria show that thyroid antigen is deposited in the kidney tissue. It is believed that it may be caused by the thyroid antigen-antibody complex deposited on the kidney tissue through blood circulation. Immune complex nephritis.
- Autoimmune thyroid disease
Autoimmune thyroid disease symptoms
- There are mainly clinical manifestations of AITD and two symptoms of proteinuria, most of which are mild, but sometimes manifested as nephrotic syndrome. AITD and proteinuria occur simultaneously or successively, sometimes AITD manifests first, and sometimes proteinuria manifests first. The occurrence interval of this person can even reach more than 10 years.
Clinical diagnosis of autoimmune thyroid disease
- When AITD is combined with proteinuria, this disease should be considered, but attention should be paid to identify whether the two are two independent diseases. The diagnosis of proteinuria is caused by AITD, and it depends on renal biopsy to detect the deposition of thyroid antigen in renal tissue. Because AITD and proteinuria do not necessarily occur at the same time, attention should be paid to the exclusion of AITD when diagnosing AITD in the presence of proteinuria and various immune complex nephritis.
- Differential diagnosis: AITD should be distinguished from various immune complex nephritis.
Autoimmune thyroid disease test
- Laboratory tests: Laboratory manifestations of nephrotic syndrome may be present. Proteinuria and AITD can occur at the same time or successively with occasional microscopic hematuria without hypertension and renal impairment
- Other auxiliary inspections:
- Renal biopsy The most common pathological type in patients with AITD-related nephrotic syndrome is membranous nephropathy and focal glomerulosclerosis with mesangial proliferative nephritis. Specific changes were thyroid antigen deposition on renal biopsy.
Autoimmune thyroid disease treatment
- There is still no consensus on the treatment of AITD-related nephrotic syndrome. Foreign literature reports that immunosuppressants and thyroidectomy may be effective. However, the treatment of AITD itself should be emphasized in this disease. Because a large amount of proteinuria in clinical nephrotic syndrome can cause loss of thyroid binding globulin and can often increase hypothyroidism, the dose of thyroid replacement therapy for such patients usually needs to be increased. Eliminating thyroid antibodies and abnormal thyroid antigens is the main link of treatment. 1. Graves disease due to the treatment of hyperthyroidism drugs pyrimidines and imidazoles have a slight inhibition of Grayes disease autoimmune response can reduce thyroid autoantibodies in the blood circulation can reduce proteinuria.
- 2. The application of immunosuppressive drugs and steroid hormones and azathioprine (emulin) can reduce proteinuria in some patients.
- 3. The effect of thyroidectomy on proteinuria is not clear. However, in the first case of Graves' disease with nephrotic syndrome, long-term use of methimazole (tabazole) had poor efficacy. The proteinuria was significantly reduced after thyroidectomy and follow-up for 11 months. There was no change in glomerular filtration rate. What is important is the timing of thyroidectomy, and its relief is almost limited to patients with stage to meningeal nephritis.
- 4. The effect of radioactive iodine treatment on proteinuria is not clear and can even worsen proteinuria.
Autoimmune thyroid disease cell apoptosis
- Autoimmune thyroid diseases include Graves disease (GD) and Hashimoto's thyroiditis (HT). Although it is currently believed that the occurrence of this type of disease is caused by the disorder of the body's immune system, there are many clinical phenomena that are difficult to explain. In the study of its pathogenesis, apoptosis has become a research hotspot. Studies have shown that the Fas pathway-mediated apoptosis may be involved in the pathogenesis of autoimmune thyroid disease.
- Cell Apoptosis in Thyroid Tissue of Autoimmune Thyroid Disease People have observed the situation of cell apoptosis in thyroid tissue of autoimmune thyroid disease from various angles using various methods. Apoptosis occurs in normal thyroid tissue, but the degree of apoptosis is very weak. In HT and thyroid cancer tissues, the number of follicular cell apoptosis increased significantly. Most apoptosis occurs in thyroid follicles that are destroyed by infiltrating lymphocytes. In intact thyroid follicles far from the germinal center of lymphocytes, the number of apoptosis was significantly reduced. In GD with slight lymphocyte infiltration, apoptosis is reduced, but also tends to be associated with local infiltration of lymphocytes. These findings suggest that the occurrence of HT in autoimmune thyroid disease is related to immune-mediated apoptosis.
- The relationship between Fas and its regulators and autoimmune thyroid diseases was inspired by the important role of the Fas pathway in immune-mediated cytotoxicity. In recent years, research on autoimmune thyroid diseases has focused on Fas proteins and their regulation. On the thing.
- Current research generally suggests that thyroid cells have the ability to express Fas. Immunohistochemical studies found that Fas protein was expressed in normal thyroid cells, thyroid cancer, HT, and GD tissues, while the expression in HT was significantly stronger than that in normal tissues or GD and non-autoimmune thyroid diseases. Different from the above view, Giordano et al. Found no expression of Fas protein in normal thyroid cells, and they believed that Fas was expressed only in thyroid cells affected by cytokines. Whether this contradiction is related to the normal control tissue selected by the latter as a non-toxic nodule remains to be further studied.
- How Fas expression is regulated in thyroid cells is unclear. The accumulation of lymphocytes in thyroiditis tissues suggests that certain cytokines may regulate the expression of Fas antigen. Kawakami et al. Showed that the expression of Fas was increased in normal thyroid and GD tissues treated with interferon (IFN) - or interleukin (IL) -1. Giordano et al. Did not find Fas antigen expression in normal thyroid tissue, but after IL-1 treatment, Fas antigen expression appeared in normal thyroid tissue.
- In addition, the effect of Tsh on the expression of Fas antigen has also attracted people's attention. Kawakami et al. Believe that Tsh inhibits the expression of Fas antigen. They found that Tsh stimulated thyroid cell proliferation while increasing the number of thyroid cells by hindering the apoptotic process.
- FasL and Bcl-2 expression in autoimmune thyroid disease. Fas can induce apoptosis after combining with FasL, but whether thyroid cells express FasL is controversial. Some studies suggest that there is only weak or no FasL expression on normal thyroid cells. Some studies have found that only normal thyroid tissues can express FasL after being exposed to IL-1. FasL has potential expression in HT, non-toxic thyroid nodules, GD, and papillary carcinoma. Or there is expression. These studies suggest a possible relationship between FasL and specific thyroid diseases.
- Because Bcl-2 can inhibit cell apoptosis in many ways, Bcl-2 has also received much attention in the study of thyroid apoptosis. Although it does not have a specific blocking effect on Fas-mediated apoptosis, it still plays a role in the pathogenesis of thyroid disease. Many studies have found that Bcl-2 is underexpressed in thyroid tissues (such as HT) that have a high degree of apoptosis. In non-autoimmune thyroid disease tissues and GD tissues, Bcl-2 was positively expressed, and in GD tissues, Bcl-2 positive expression was stronger. It is speculated that the expression of Bcl-2 may be related to certain diseases such as HT, GD, and thyroid cancer.
- In summary, apoptosis is an autonomous physiological death process and an important negative feedback mechanism to maintain the body's own stability. Apoptosis plays an important role in both thyroid physiology and pathology. Apoptosis is closely related to the occurrence of HT. There is a Fas death pathway in thyroid tissue. Fas protein is expressed in thyroid tissue. Fas protein is expressed in different intensity in different thyroid disease tissues. FasL expression is a potential threat to thyroid tissue. At present, there are still different opinions on the regulation mechanism of Fas protein expression. Arscott et al. Believe that neither IFN-, IL-1 or Tsh can significantly increase the expression of Fas mRNA or protein, and found that Tsh did not change the thyroid cell's effect on Fas-mediated cell apoptosis Death sensitivity. The relationship between FasL and specific thyroid disease has not been confirmed. Through the study of apoptosis, people can have a deeper understanding of the pathogenesis of autoimmune thyroid diseases, so as to lay a theoretical foundation for the clinical search for new treatments for some autoimmune thyroid diseases.
Autoimmune thyroid disease prevention
- There are no reports on the prevention of AITD, but in the topical discussion of autoimmunity and pregnancy, some scholars have suggested that taking selenium during pregnancy can prevent the occurrence of postpartum thyroiditis.