I. Incidence and etiology of subclinical hypothyroidism Due to the improvement of people’s living standard and health awareness, and also due to the improvement of public medical conditions. The typical clinical symptoms of severe hypothyroidism described in medical textbooks in the past, such as lethargy and mucinous edema, are less commonly seen in today’s clinical practice. Instead, clinicians often see patients with mild hypothyroidism. Unlike patients with severe hypothyroidism, patients with subclinical hypothyroidism have normal serum T4 and T3 levels and only mildly increased serum TSH levels, and most patients have no obvious clinical symptoms, and only a few have mild or non-specific symptoms. These patients are often detected by routine health check-ups or by the presence of non-specific symptoms or by visiting a doctor for hypercholesterolemia and having their nail function checked. Foreign epidemiological findings show that the prevalence of subclinical hypothyroidism in North America ranges from 1% to 10%; the prevalence is about 20% in women over 60 years of age. 16% in men over 74 years of age, and the prevalence is higher in women than in men. In patients with subclinical hypothyroidism, about 75% of patients have only mildly elevated serum TSH levels, (5-10 mU/L), and 50% to 80% of patients have positive anti-thyroid peroxidase antibodies. The main causes of subclinical hypothyroidism are: treatment in patients with hyperthyroidism (antithyroid drugs, 131 iodine, surgery), history of external neck irradiation in patients with tumors, goiter, Hashimoto’s thyroiditis, postpartum thyroiditis, certain natural immune damage, especially type I diabetes. Subclinical hypothyroidism can also occur in patients taking etanercept for arrhythmias, taking lithium salts, or using immunomodulatory factors such as interferon. Some severe non-thyroidal diseases may also present with increased serum TSH levels and normal serum free T4 levels, such as chronic renal insufficiency and primary hypoadrenocorticism. Artificial artifacts due to laboratory errors. In some patients, there is no clear pathogenic factor. Second, the impact of subclinical hypothyroidism on health 1, subclinical hypothyroidism will gradually develop into hypothyroidism: foreign scholars randomly selected 2800 adults in North America from 1972 to 1974 to analyze the report of nail function and follow up 20 years, found that patients with increased serum TSH levels and positive anti-thyroid antibodies at the same time are more prone to hypothyroidism, with an average annual increment of 4.3%, is TSH levels The average annual increase was 4.3%, 38 times higher than that of patients with normal TSH levels and negative antithyroid antibodies. In contrast, patients with only elevated serum TSH levels or positive antithyroid antibodies are also more likely to develop hypothyroidism, with an annual increase of 2.6% and 2.1%, respectively. 33% of the former and 27% of the latter develop hypothyroidism over a 20-year period. 2, subclinical hypothyroidism caused by lipid metabolism disorders, causing coronary heart disease: some scholars conducted a survey of Dutch women and followed up 4.6 years, the information shows that the incidence of coronary heart disease in patients with subclinical hypothyroidism with increased lipids is two times higher than that of patients with normal A function and normal lipids. The study suggested that serum total cholesterol and low-density lipoprotein (LDL) levels were higher in patients with subclinical hypothyroidism than in those with normal A function. Serum total cholesterol and low-density lipoprotein (LDL) levels decreased after treatment in patients with subclinical hypothyroidism, while high-density lipoprotein (HDL) levels did not decrease significantly. Patients with subclinical hypothyroidism whose total cholesterol level is greater than 6.2 mmol/L can significantly reduce their total serum cholesterol level after treatment. In contrast, serum total cholesterol levels in patients with recent subclinical hypothyroidism with serum total cholesterol levels less than 6.2 mmol/L do not decrease significantly after treatment. A few studies have also shown that thyroxine (T4) therapy has no lipid-lowering effect in patients with serum TSH levels below 10 mU/L. 3. Subclinical hypothyroidism causes neurosis: patients show mental symptoms such as fatigue, emotional instability, depression, paranoia and nervousness. 4. Subclinical hypothyroidism is associated with ovarian hypovulation and infertility. C. Screening of subclinical hypothyroidism Since most patients with subclinical hypothyroidism have mild or no symptoms, a routine health screening of the public is necessary to detect patients with subclinical hypothyroidism. Some scholars suggest that women aged 35 years or older and men aged 65 years or older should be screened every 5 years, and pregnant women should be screened once before and once after delivery to detect subclinical hypothyroidism in a timely manner. Fourth, the treatment of subclinical hypothyroidism The benefits of subclinical hypothyroidism treatment are as follows: First, thyroxine (T4) treatment can effectively prevent the occurrence of hypothyroidism. Secondly, thyroxine treatment can improve the lipid profile and thus reduce the morbidity and mortality of coronary heart disease. Secondly, thyroxine treatment improves the symptoms of subclinical hypothyroidism, and patients may experience significant improvements in anxiety levels, as well as improvements in perceptual function and memory. Finally, thyroxine treatment is useful in the treatment of ovarian hypovulation and infertility. Hypothyroidism has a greater impact on the health of patients because of the ease of conversion of subclinical hypothyroidism to hypothyroidism. Only about 5% of patients with subclinical hypothyroidism can normalize their serum TSH levels on their own without treatment, so treatment of subclinical hypothyroidism is necessary. The initial dose of thyroxine is 50-75µg per day, and if the patient has coronary artery disease, the dose of thyroxine should be 12.5-25µg. The serum TSH level should be checked after 4-6 weeks of treatment, and the dose should be adjusted according to the change of TSH level. After the TSH level is normalized, the dosage should be kept constant. Follow up annually thereafter. If the patient develops progressive hypothyroidism, long-term replacement therapy will be required. Although thyroxine treatment does not lower the blood lipids in all patients with subclinical hypothyroidism who have elevated blood lipids, it can effectively stop the onset of hypothyroidism and reduce the patient’s symptoms. V. Opposing views on treatment of subclinical hypothyroidism The benefits and dangers of subclinical hypothyroidism treatment have been debated in the medical community for the past 20 years. A few scholars have argued that thyroxine treatment is prone to overdose situations. Some studies have shown that overdose on hypothyroidism replacement therapy can occur in up to 21% of cases. Treatment overdose is prone to induce medical hyperthyroidism, cause osteoporosis or induce atrial fibrillation in patients, so treatment is viewed with caution. Nevertheless, most scholars still advocate treatment of subclinical hypothyroidism because of the many advantages of thyroxine therapy.