Hypothyroidism (hypothyroidism) is a systemic hypometabolic syndrome caused by decreased synthesis and secretion of thyroid hormones or inadequate tissue utilization. If hypothyroidism begins in the fetus or newborn, it is called cretinism; in children before sexual development, it is called juvenile hypothyroidism; in adults, it is called adult hypothyroidism. According to the location of the lesion: 1. Hypothyroidism caused by the lesion of the thyroid gland itself is called primary hypothyroidism. It accounts for more than 95% of all hypothyroidism. The three main causes of primary hypothyroidism are autoimmunity, thyroid surgery and hyperthyroidism 131I treatment, which account for more than 90% of all hypothyroidism. 2. Hypothyroidism caused by hypothalamic and pituitary lesions that reduce the production and secretion of thyrotropin-releasing hormone (TRH) or thyroid stimulating hormone (TSH) is called central hypothyroidism. External pituitary irradiation, pituitary macroadenoma, craniopharyngioma and postpartum hemorrhage are the more common causes. 3. The syndrome caused by impairment of the biological effect of thyroid hormone in peripheral tissues is called thyroid hormone resistance syndrome. The syndrome is classified according to the degree of hypothyroidism: clinical hypothyroidism and subclinical hypothyroidism. Clinical manifestations: Symptoms are mainly based on reduced metabolic rate and decreased sympathetic excitability, and early patients with mild disease may have no specific symptoms. Typical patients have chills, fatigue, swelling of the hands and feet, drowsiness, memory loss, low sweating, joint pain, weight gain, constipation, menstrual disorders in women, or excessive menstruation, or infertility. Physical examination: Typical patients may have dull expression, unresponsiveness, puffiness of the face and/or eyelids, thick lips and large tongue, dry, rough skin, low skin temperature, puffiness, ginger skin on the palms of the hands and feet, sparse and dry hair, prolonged Achilles tendon reflex, and slow pulse rate. In a few cases, anterior tibial mucinous edema is present. The disease may involve the heart with pericardial effusion and heart failure. In severe cases, mucinous edema coma may occur. Laboratory diagnosis: Primary hypothyroidism has increased serum TSH and decreased TT4 and FT4. The level of increased TSH and decreased TT4 and FT4 correlates with the extent of the disease. Serum TT3 and FT3 were normal in the early stage and decreased in the late stage. Subclinical hypothyroidism has only increased TSH and normal TT4 and FT4. Thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TgAb) are the main indicators for the diagnosis of autoimmune thyroiditis (including Hashimoto’s thyroiditis and atrophic thyroiditis). If TPOAb is positive with increased serum TSH levels, it indicates that damage to thyroid cells has occurred. The incidence of clinical hypothyroidism and subclinical hypothyroidism increases significantly when TPOAb > 50 IU/ml and TgAb > 40 IU/ml at the initial visit. Treatment: Levothyroxine (L-T4, eugenol) is the main replacement therapy for this disease. Lifetime replacement is usually required. Hypothyroidism occurring during the treatment of hyperthyroidism, hypothyroidism due to subthyroiditis and a small number of hypothyroidisms due to Hashimoto’s thyroiditis may be recovered. The goal of treatment is the disappearance of clinical signs and symptoms of hypothyroidism and the maintenance of TSH, TT4 and FT4 values within normal limits. In hypothyroidism secondary to hypothalamus and pituitary gland, TSH cannot be used as a therapeutic indicator, but the goal of treatment is to achieve normal range of serum TT4 and FT4. The dose of treatment depends on the patient’s condition, age, weight and individual differences. The replacement dose of eugenol (levothyroxine sodium) in adult patients is 50-200µg/day, with an average of 125µg/day. The dose based on body weight is 1.6-1.8µg/kg/day; children need a higher dose of about 2.0µg/kg/day; elderly patients need a lower dose of about 1.0µg/kg/day; the replacement dose in pregnancy needs to be increased by 30-50%; patients with postoperative thyroid cancer need a high dose replacement of about 2.2µg/kg/day to control TSH at the level needed to prevent tumor recurrence. It is generally started at 25-50 μg/day orally once daily and increased by 25 μg every 1-2 weeks until the therapeutic goal is reached. The starting dose should be small for those who suffer from ischemic heart disease, and the dose should be adjusted slowly to prevent inducing and aggravating heart disease. T4 has a half-life of 7 days, so it can be taken once a day in the morning. Thyroid tablets are a dry preparation of the thyroid gland of animals and are rarely used because of their unstable thyroid hormone content and high T3 content. It usually takes 4-6 weeks to re-establish the hypothalamic-pituitary-thyroid axis balance, so at the beginning of treatment, hormone indicators are measured at 4-6 week intervals. The L-T4 dose is then adjusted according to the test results until the target of treatment is reached. After the treatment target is reached, hormone indicators need to be rechecked every 6-12 months.