Prevention and treatment of subclinical hyperthyroidism Subclinical hyperthyroidism has a negative impact on the cardiovascular system and bones, predisposes to atrial fibrillation and can also lead to fractures. Low TSH increases mortality in people over 60 years of age, and about 5% of patients progress to clinical hyperthyroidism each year. How to prevent and treat subclinical hyperthyroidism as well as prevent the progression of subclinical hyperthyroidism to clinical hyperthyroidism is a question that every endocrinologist should consider. TSH decreases during stress, and stress is an important factor in causing subclinical hyperthyroidism. Health education is the primary and basic measure for the prevention and treatment of subclinical hyperthyroidism. Its purpose is to eliminate the stressors that cause subclinical hyperthyroidism. Its main content is to educate patients to actively improve their lifestyles, avoid bad emotions and harmful mental stimuli, avoid excessive and persistent mental tension, and avoid various unexpected serious damages of somatic nature. Treatment can be started for the persistence of subclinical hyperthyroidism with TSH 0.1 mU/L when the effect is not significant after health education intervention. As the incidence of hyperthyroidism increases, the number of cases of subclinical hyperthyroidism is increasing, and its prevention and treatment are discussed in this paper. Subclinical hyperthyroidism is characterized by normal T3 and T4 and reduced TSH. It may be a temporary clinical phenomenon that occurs in the early stage of Graves’ disease (GD), after surgery or radioiodine treatment for GD, and during the recovery period of various thyroid infections. However, it can also persist and become a specific clinical type of hyperthyroidism (including GD), and in a few cases it can progress to clinical hyperthyroidism. It can be diagnosed after exclusion of hypothalamic-pituitary disorders, non-thyroidal somatic disorders and other causes of TSH reduction]. Subclinical hyperthyroidism occurring on the basis of various thyroid disorders is endogenous subclinical hyperthyroidism. It is commonly seen in the early stages of GD, a stage in the recovery process after treatment for GD or in Graves’ ophthalmopathy, autonomic adenoma of thyroid function, and multinodular goiter. It is a temporary clinical phenomenon, but some can last for a relatively long period of time. TSH returns to normal in some patients, and progresses to clinical hyperthyroidism in about 5% of patients each year. Subclinical hyperthyroidism caused by high intake of L-T4 due to replacement therapy or suppression therapy is exogenous subclinical hyperthyroidism, which is commonly seen in patients with thyroid nodules, goiter, thyroid tumor and hypothyroidism replacement therapy. The symptoms of subclinical hyperthyroidism are usually not obvious or non-specific. There may be mild psychiatric symptoms or mood disturbances. Regardless of the type of subclinical hyperthyroidism, it has a negative impact on the cardiovascular system and bone iliac. It may cause atrial fibrillation and left ventricular hypertrophy, which affect the systolic and diastolic functions of the heart and may lead to fractures. The pathogenesis of subclinical hyperthyroidism has various causes, and treatment varies from disease to disease. This article focuses on the most common early stage of GD and the ongoing phase of recovery after treatment of GD, an autoimmune thyroid disease whose cause is not fully understood. It is currently thought to be an autoimmune disease with a genetic basis and the involvement of stress factors. Although the mode of inheritance is not certain, there is a consensus on the various stress factors that can trigger the disease. The endocrine system of the body undergoes a series of changes under stressful conditions. Primarily, the immune response is regulated through the hypothalamic-pituitary-adrenocortical axis and the sympathetic-adrenomedullary axis. Somatic and mental stimuli acting on the nervous system can regulate the function of the immune system and systemic organs and tissues through neuroendocrine responses that produce various hormones or stress immunomodulators. In contrast, viruses, toxins, tumors, heterogeneous proteins and other stimuli act on the immune system to produce various cytokines and immune response hormones, which can also act on the neuroendocrine system to stimulate or regulate, and the latter then acts on the tissues and organs of the body to mobilize various functional activities in response to the stimuli. This is the interaction between the stress response and the immune response. In stressful conditions, autoimmune diseases can be induced by attenuating the activation of suppressive T lymphocytes. The vast majority of autoimmune endocrinopathies cause damage to the endocrine cells involved and hypofunction occurs, with the exception of GD, because the antigen targeted by the autoantibodies that appear (thyroid excitatory antibody TSAb) is the TSH receptor on the surface of thyroid cells, and the latter activation by TSAb can cause thyroid cell hyperplasia and hyperfunction. The activation of hypothalamic-pituitary-thyroid under stress leads to elevation of thyroid hormones in blood. Stress causes a dramatic decrease in serum TSH concentrations in rats. Surgical stress causes a temporary acute decrease in human serum TSH and causes a nocturnal increase in serum TSH to disappear. The endocrine function of the hypothalamus is in turn influenced by other parts of the nervous system. The hypothalamus is extensively connected to both the higher poles of the central nervous system and the surrounding sensory nerves. Excessively strong or too persistent stressors, such as bad emotions and harmful mental stimuli, excessive and persistent mental tension, apprehension, fear, anger, excitement, etc., are important factors in triggering GD. Mental stimuli can alter the normal regulation of thyroid function and the body’s immune system and contribute to the occurrence of GD. Psychological stress induced GD is the result of the interaction between neuroendocrine and immune systems. Prevention and treatment of subclinical hyperthyroidism With the accelerated pace of work and life, the incidence of hyperthyroidism has increased, and the number of subclinical hyperthyroidism has increased significantly. The main goal of prevention and treatment of subclinical hyperthyroidism is to prevent the progression of subclinical hyperthyroidism to clinical hyperthyroidism and to reduce the damage to cardiovascular and bone iliac. Primary intervention: Health education is the primary and basic measure to prevent subclinical hyperthyroidism. Stress can cause hyperthyroidism and the thyroid gland itself is already defective in subclinical hyperthyroidism patients, so the main goal of health education is to eliminate the stressors in subclinical hyperthyroidism patients. The main content is to educate patients to avoid too strong or persistent stressors, such as avoiding bad emotions and harmful mental stimuli, excessive and persistent mental stress, and avoiding various accidental serious physical injuries. For patients with high mental stress or chronic worries or depression, it is recommended to seek counseling from a psychological consultant. Implement a healthy lifestyle, live a regular life and pay attention to proper exercise. Pay attention to reducing iodine intake, not eating iodine-rich foods such as kelp and nori, eating less food with high levels of anisotropic proteins such as shrimp and crab, and eating less goiter-causing foods such as radish and cabbage. You should keep your clothes loose and forbid to squeeze the thyroid gland with your hands to avoid an increase in thyroid hormone secretion when the thyroid gland is under pressure. Thyroid function should be measured every 1-2 months at outpatient visits. Secondary intervention: Exogenous subclinical hyperthyroidism is due to L-T4 overdose, so adjusting L-T4 dose can normalize TSH. In patients with endogenous subclinical hyperthyroidism who do not achieve significant results after health education intervention, the expert committee considers that treatment may be recommended when TSH is 0.1 mU/L, the patient is 60 years old, at risk of heart disease, osteoporosis or has clinical manifestations of hyperthyroidism. Early GD, continuous phase after GD treatment with low-dose antithyroid drugs. Autonomous adenoma of thyroid function and multinodular goiter can be treated surgically.