Does hyperthyroidism affect menstruation?

Does hyperthyroidism affect menstruation? It will definitely affect endocrine system. What I want to say is that the principle of antithyroid hormone therapy is to suppress thyroid hormone. It usually takes more than 2 years and needs to be maintained at a low dose. Relapse is common after stopping or reducing the dose. I don't know if you have any children now. If you don't have children and you still have symptoms of irregular menstruation, you should take them seriously. If the condition is serious, you need to go to the hospital for examination.

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.

Genetic factors (20%):

Clinically, familial Graves' disease is not uncommon. The rate of identical twins suffering from Graves' disease simultaneously can reach 30% to 60%, while that of fraternal twins is only 3% to 9%. Family history surveys show that in addition to hyperthyroidism, other thyroid diseases such as hypothyroidism may also be present, or TSI may be positive in family relatives. This shows that Graves' disease has a familial genetic tendency, and this inheritance pattern may be autosomal recessive, autosomal dominant, or polygenic.

Other causes (10%):

(1) Hyperfunctioning nodular goiter or adenoma. In the past, it was believed that this disease was not an autoimmune disease because no immune evidence such as IgG, TSI, and IATS was detected in the blood. In 1988, the country reported that serum thyroglobulin antibodies and microsomal antibodies were detected in single nodules, with a positive rate of 16.9% (62/383) and a positive rate of 54.7% (104/190) in multiple nodules. The proliferating thyroid tissue in these nodules was not regulated by TSI and became autonomous hyperfunctioning or hyperfunctional thyroid nodules or adenomas. It is currently believed that the onset of thyroid adenoma and carcinoma is also due to tumor genes.

(2) Pituitary tumors increase TSH secretion, causing pituitary hyperthyroidism, such as hyperthyroidism associated with TSH-secreting tumors or acromegaly.

(3) Subacute thyroiditis, chronic lymphocytic thyroiditis, painless thyroiditis, etc. may all be associated with hyperthyroidism.

(4) Increased exogenous iodine causes hyperthyroidism, which is called iodine-induced hyperthyroidism. If a patient with goiter takes too much iodine, too much thyroid tablets or too much levothyroxine sodium (L-T4), it may cause hyperthyroidism. In a small number of patients, taking amiodarone may also cause hyperthyroidism.

(5) Ectopic endocrine tumors can cause hyperthyroidism, such as ovarian tumors, choriocarcinoma, digestive system tumors, respiratory system tumors and breast cancer, which secrete thyroid-stimulating hormone and can cause clinical hyperthyroidism.