Causes of postpartum hyperthyroidism

Causes of postpartum hyperthyroidism, a disease that is more common in women. Excessive thyroid hormone can cause a range of clinical manifestations, such as heat intolerance and sweating, increased appetite and weight loss, palpitations, and emotional tension and irritability. Hyperthyroidism is an endocrine disease caused by excessive secretion of thyroid hormone in the body. Clinically, it manifests itself in the digestive system, endocrine system, and nervous system.

1. Direct evidence of the immune mechanism of hyperthyroidism includes:

(1) In terms of humoral immunity, there are many known antibodies against thyroid cell components, such as thyroid stimulating antibodies (TISI) against TSH receptors, or TSH receptor antibodies (TRAb), which can bind to TSH receptors or their related tissues, further activate cAMP, and enhance thyroid function. This antibody can pass through the placental tissue and cause hyperthyroidism in the newborn, or if the hyperthyroidism is not treated thoroughly, the antibody will remain positive and lead to recurrence of hyperthyroidism.

(2) In terms of cellular immunity, it has been confirmed that these antibodies are produced by B lymphocytes. There are sensitized T lymphocytes against thyroid antigens in the blood of patients with hyperthyroidism. When hyperthyroidism occurs, lymphocytes can produce LATS under the activation of phytohemagglutinin (PHA). PHA excites T lymphocytes and then stimulates B lymphocytes, thereby producing immunoglobulins that can excite the thyroid gland, such as TSI, and induce hyperthyroidism. Organ-specific autoimmune diseases are all caused by immune regulation disorders due to functional defects of suppressor T lymphocytes (Ts). Therefore, the immune response is a complex result involving the interaction of T and B lymphocytes and phagocytes. It is now believed that it is mainly related to the reduced function of suppressor T lymphocytes associated with gene defects. Ts function defects can lead to T cell sensitization, causing B cells to produce TRAb and cause hyperthyroidism.

2. Indirect evidence includes:

(1) There is a large infiltration of lymphocytes and plasma cells in the thyroid gland and behind the eyeball.

(2) The number of lymphocytes in the peripheral blood circulation increases, which may be accompanied by hyperplasia of the reticuloendothelial tissue of the lymph nodes, liver, and spleen.

(3) The patient and his relatives may develop other autoimmune diseases at the same time or successively.

(4) The blood of patients and their relatives is positive for anti-thyroid antibodies, TRAb, anti-gastric parietal cell antibodies, and anti-myocardial antibodies.

(5) Elevated levels of IgG, IgA, and IgM in the thyroid gland and blood.

The initiation cause of Graves' disease is currently believed to be due to genetic defects in the immune monitoring and regulatory functions of the patient's Ts cells. When there are external factors such as mental trauma or infection, the body's immunity is destroyed, the "forbidden strain" cells are out of control, and the B lymphocytes that produce TSI proliferate and mutate in function. Under the action of Ts cells, a large amount of TSI autoantibodies are secreted, causing disease. People with mental trauma and family history are more likely to develop the disease, which is a predisposing factor. In recent years, it has been found that the HLA-B8 of Caucasians with hyperthyroidism is twice as high as that of normal people, the HLA-BW35 of Asian Japanese is increased, the susceptibility of overseas Chinese to HIA-BW46 positivity is increased, and B13 and B40 are more obvious. These have attracted attention.