With the changes in lifestyle and living environment as well as the improvement of testing methods, thyroid diseases have been growing rapidly in recent years. Compared with hyperthyroidism, people seem to know less about hypothyroidism, below, the author will talk to you about those things about hypothyroidism. First, what is hypothyroidism? Hypothyroidism (hypothyroidism, referred to as “hypothyroidism”) is a generalized hypometabolic syndrome caused by a variety of causes of thyroid hormone (including T3, T4) synthesis, secretion, or biological effects due to insufficient. The pathology of hypothyroidism is characterized by the accumulation of mucopolysaccharides in tissues and skin, which in severe cases manifests as “mucous edema”. The main causes of hypothyroidism include autoimmune damage (e.g. autoimmune thyroiditis) and thyroid destruction (e.g. surgery, radioactive iodine treatment). In addition, the incidence of hypothyroidism in iodine-deficient areas is significantly higher than that in iodine-supplying areas, and it is more common in females than in males. What are the dangers of hypothyroidism? If hypothyroidism is not well controlled, it can jeopardize various systems of the whole body: 1. Central nervous system: memory loss, slow response, depression, sleepiness, mental decline and dementia. 2. 2, cardiovascular system: bradycardia, weak heart sound, heart enlargement, often accompanied by pericardial effusion, which is called “hypothyroidism heart disease”. 3, digestive system: loss of appetite, constipation, abdominal distension, and even paralytic intestinal obstruction in severe cases. 4. Reproductive system: men may suffer from hypogonadism, impotence, testicular atrophy and infertility; women may suffer from irregular menstruation, excessive menstrual bleeding, amenorrhea and infertility. 5.Endocrine system: adrenocortical hypoplasia, decreased blood and urine cortisol. 6. Muscle and joint system: muscle weakness and pain, joint stiffness and inflexibility, slow bone metabolism, decreased bone formation and resorption. In addition, for the occurrence of hypothyroidism in different age groups, its main hazards are different: occurring in the fetus and infancy hypothyroidism, mainly affecting the child’s intelligence and growth and development, resulting in short stature, mental retardation, known as “cretinism”; occurring in the early childhood hypothyroidism, also affect the child’s physical and intellectual development, only to a relatively lesser extent, this type of hypothyroidism is also affected by the physical and intellectual development, but the degree of the disease is relatively mild. The degree of hypothyroidism in early childhood will also affect the child’s physical and intellectual development, only to a lesser extent, such children are later than children of the same age in height, teething, toddlerhood, and learning to speak; hypothyroidism that occurs in puberty will lead to delayed puberty, growth stagnation, resulting in short height, impaired sexual development, and in serious cases, infertility due to immaturity; hypothyroidism that occurs in pregnant women can lead to abnormalities of the offspring’s intellectual and growth development, increase the chances of children with birth defects, and also significantly increase the risk of miscarriage in pregnant women. The occurrence of hypothyroidism in pregnant women can lead to abnormalities in the intelligence and growth of their offspring, increase the chances of birth defects in their children, and significantly increase the incidence of miscarriage, preterm labor, placental abruption, perinatal fetal death and other adverse events; hypothyroidism occurs in adults, the most common clinical (accounting for 90-95%), the main clinical manifestations of low metabolic syndrome, such as weight gain, fatigue, fear of cold, memory loss, lethargy, anemia, depression, constipation, skin dryness, swelling, menstrual irregularities, and so on. Third, how to categorize hypothyroidism according to the age of onset is divided into: ① cretinism (starting in the fetus or newborn); ② juvenile-type hypothyroidism (starting in the pre-pubertal development of children); ③ adult-type hypothyroidism (starting in adulthood). According to the lesion site can be divided into: ① primary hypothyroidism, accounting for more than 95% of all hypothyroidism, common causes include autoimmune, thyroid surgery and hyperthyroidism radioactive iodine treatment; ② central hypothyroidism, commonly caused by pituitary external irradiation, pituitary macroadenoma, craniopharyngioma and post-partum hemorrhage, etc. Thyrotropin-releasing hormone (TRH) or thyrotropic stimulating hormone (TSH) production and secretion of reduced; ③ thyroid hormone resistance syndrome, refers to the thyroid hormone resistance syndrome, refers to the thyroid hormone resistance syndrome, refers to the thyroid hormone resistance syndrome. Hormone Resistance Syndrome (HRS), which refers to the defective functioning of thyroid hormones in peripheral tissues. According to the severity can be divided into: ① subclinical hypothyroidism; ② clinical hypothyroidism; ③ mucous edema coma. How to diagnose hypothyroidism Clinical diagnosis of hypothyroidism mainly relies on clinical manifestations and thyroid function tests, thyroid function tests are an important basis for the diagnosis of hypothyroidism. 1, the symptoms and signs of hypothyroidism: common symptoms are easy to fatigue, fear of cold, weight gain, memory loss, slow reaction, sleepiness, depression, constipation, menstrual irregularities, muscle cramps and so on. Typical physical signs include apathetic expression, dull gaze, pale face with deficiency swelling, hoarse voice, dry skin, and thinning hair. “Mucous edema” is the characteristic clinical manifestation of hypothyroidism. Laboratory tests: ① Increase in serum TSH and decrease in FT4, consider “primary hypothyroidism”. Further search for the cause of hypothyroidism. If TPOAb is positive, consider the cause of hypothyroidism to be autoimmune thyroiditis. If serum TSH is low or normal, and TT4 and FT4 are low, consider “central hypothyroidism”. Do a TRH stimulation test to confirm. Further search for pituitary and hypothalamic lesions. Attachment: TRH stimulation test: after intravenous injection of TRH, serum TSH does not increase suggests pituitary hypothyroidism; delayed increase for hypothalamic hypothyroidism; serum TSH in the base value of the increase on the basis of further increase, suggesting primary hypothyroidism. Fifth, hypothyroidism is easily confused with what diseases? Hypothyroidism has a slow onset, many symptoms and non-specific, it is easy to be clinically misdiagnosed as the following diseases: 1, chronic nephritis patients with hypothyroidism due to water and sodium retention manifested as facial edema, skin pallor, anemia, blood cholesterol elevation, and some patients with positive urine protein, so it is often considered to be a kidney disease. However, patients with hypothyroidism usually do not have high blood pressure, normal renal function, generally no hematuria and large amounts of proteinuria, and hypothyroidism. 2, anemia About 25-30% of patients with hypothyroidism have anemia, which is often misdiagnosed as iron deficiency anemia, aplastic anemia or pernicious anemia. The possible causes of anemia in hypothyroidism include heavy menstrual flow and long menstrual period, which leads to excessive blood loss, and anemia is aggravated by decreased appetite, nutritional deficiencies and lack of gastric acid. 3, plasma cavity effusion plasma cavity effusion occurs in hypothyroidism (such as pericardial effusion, pleural effusion, etc.) is often misdiagnosed as tuberculosis, malignant tumors, uremia, pericarditis and connective tissue disease. Hypothyroidism in the plasma cavity fluid in the high protein content, low cell count, cholesterol content and high immunoglobulin content, insensitive to diuretic treatment. 4, idiopathic edema Hypothyroidism patient’s fibroblast secretion of mucopolysaccharides in the subcutaneous excessive accumulation, can cause “mucous edema”, often due to the symptoms are not specific, easy to be misdiagnosed as “idiopathic edema”. With “idiopathic edema” is different, “mucous edema” for non-fingerprinted edema, and patients with hypothyroidism. 5, depression hypothyroidism patients occur more in the elderly, elderly patients symptoms are not specific, slow progression of the disease, not easy to be detected, fear of cold, sluggishness, loss of appetite, depressed, poor sleep and depression and other symptoms, was diagnosed as “geriatric depression”. 6.Pituitary tumor: Long-term hypothyroidism patients, especially children, pituitary gland can be enlarged, sometimes misdiagnosed as pituitary tumor; primary hypothyroidism, long-term blood T4 drop, pituitary cell hyperplasia and hypertrophy, resulting in the enlargement of the pterygoid saddle, some female patients due to menstrual disorders and lactation, the laboratory found that the prolactin is mildly elevated, was misdiagnosed as pituitary prolactinoma. 7.Low T3 syndrome: clinically, some patients with acute and chronic severe diseases or advanced tumor malignant stroma patients, there can be a decrease in blood free T3 (FT3), which is called “low T3 syndrome”, and it is often mistaken as “hypothyroidism”. However, the blood free T4 (FT4) of these patients is generally normal, sometimes slightly decreased or elevated, serum anti-T3 (rT3) is elevated, TSH is normal, which can be identified. Sixth, hypothyroidism in pregnancy and general population hypothyroidism control standard is the same? The normal range of serum thyroid stimulating hormone (TSH) in the general population is 0.3~5.0 mIU/L. During pregnancy, the reference range of TSH is different from that of the general population due to the influence of many factors. There is currently no pregnancy-specific TSH reference range, but the consensus at home and abroad is that in early pregnancy (before 12 weeks of gestation) the TSH reference range should be 20-30% lower than that of the non-pregnant population. The American Thyroid Association (ATA) recommends TSH 2.5 mIU/L as the upper limit of TSH in early pregnancy, and more than 2.5 mU/L can be diagnosed as “hypothyroidism in pregnancy”. The treatment goal of hypothyroidism in pregnancy is that the serum TSH level should be <2.5 mIU/L in early pregnancy, <3.0 mIU/L in mid and late pregnancy, and the FT4 should be kept in the upper third of the normal range for non-pregnant women. VII. Can I take thyroxine for maternal hypothyroidism? Despite the widespread use of levothyroxine (L-T4) in women with hypothyroidism, there is no evidence that this product poses a risk to the fetus. As far as safety is concerned, L-T4 has the highest safety class A in the FDA Drug Safety Classification. Even with higher doses of L-T4 therapy, the amount of thyroid hormone secreted into the lotion during breastfeeding is not sufficient to cause the infant to develop hyperthyroidism or suppressed TSH secretion, so L-T4 can be safely taken by hypothyroidism patients during pregnancy and breastfeeding as well. viii, Does "subclinical hypothyroidism" need treatment? "Subclinical hypothyroidism" refers to the situation where serum thyroid hormone (T4, T3, FT4, FT3) levels are normal and TSH is elevated, which is a transitional state between normal and hypothyroidism. If no intervention is made, about 5-15% of "subclinical hypothyroidism" develops into "clinical hypothyroidism" every year. There is a large body of evidence suggesting that subclinical hypothyroidism is associated with hyperlipidemia, cardiovascular and cerebrovascular diseases, the chances of conception, safety during pregnancy and delivery, and mental abnormalities in the offspring. The benefits of subclinical hypothyroidism treatment are mainly reflected in the following aspects: firstly, thyroxine (L-T4) treatment can effectively prevent the occurrence of hypothyroidism; secondly, thyroxine treatment can improve the condition of blood lipids and reduce the morbidity and mortality of cardiovascular diseases; thirdly, thyroxine treatment can improve the symptoms of subclinical hypothyroidism to a certain extent, such as fatigue, lethargy, chills, depression, memory loss and so on. Finally, thyroxine therapy is helpful in the treatment of ovarian hypo-ovulation and infertility. However, it should also be noted that thyroid hormone replacement therapy may increase the risk of atrial fibrillation in patients and bone loss in postmenopausal women. In conclusion, the need for treatment of subclinical hypothyroidism must be weighed against the pros and cons and differentiated according to each patient's individual situation. At present, it is recognized that the following patients with subclinical hypothyroidism need treatment: ①TSH>10 mIU/L; ②combined goiter; ③significantly elevated cholesterol; ④preparing to get pregnant or pregnant women. Replacement therapy is not recommended for patients with subclinical hypothyroidism and coronary artery disease. Is the initial dose of replacement therapy and its adjustment the same for all patients with hypothyroidism? Hypothyroidism replacement therapy program should be individualized, the starting dose size should be based on the patient’s age, the presence of comorbidities and the severity of the disease, etc., depending on the individual. 1. Young patients with mild to moderate hypothyroidism without cardiovascular or other diseases should be given a complete replacement dose, i.e., 0.5~1.3 μg/kg of standard body weight. Elderly patients, especially those with cardiovascular disease, should start with a small dose of 12.5~50 μg per day, and slowly increase the dose by 25~50 μg (or even 12.5 μg) every 2~4 weeks until the disappearance of systemic symptoms and the normalization of thyroid function (TSH and FT4), and then use this as the maintenance dose for a long period of time. If the initial replacement dose is too large and the increment is too fast, the metabolic rate can be suddenly increased, increasing the burden on the heart and easily inducing angina pectoris, arrhythmia, heart failure, and even myocardial infarction. Generally speaking, blood free T4 returns to normal after 6 weeks of adequate replacement therapy, and blood TSH takes a longer time, about 3 months. 3, hypothyroidism in pregnancy, as long as the patient’s own condition allows, should take one-step supplemental treatment, so that the patient’s serum TSH level as soon as possible to reach the standard, in order to avoid hypothyroidism on the fetus to cause adverse effects. 4, mucous edema coma, combined with acute infection or other serious diseases of hypothyroidism patients need to quickly correct the thyroid function, the general adult can be a single intravenous administration of levothyroxine sodium 300 ~ 500 μg, can be within 24h to make the blood T4 rise to normal levels. The second day with 100 μg, the third day after the daily administration of 50 μg, until the condition improves to reduce the maintenance dose. 5.A rapid increase in metabolic rate in patients receiving large doses of thyroid hormone may lead to pituitary-adrenocortical overload, available hydrocortisone 5 mg/h intravenous infusion to prevent adrenocortical insufficiency or crisis. X. Do all hypothyroid patients need to eat more iodine-containing foods? First of all, it should be emphasized that not all “hypothyroidism” is related to iodine deficiency. Whether patients with hypothyroidism need iodine supplementation depends on the cause of hypothyroidism. Only hypothyroidism caused by simple iodine deficiency needs iodine supplementation under the guidance of a doctor. In fact, most of the clinical “hypothyroidism” is caused by chronic lymphocytic thyroiditis (i.e., “Hashimoto’s disease”), the cause of which is autoimmune disorders, and at this time, it is not only inappropriate to eat high iodine foods such as kelp, seaweed, seaweed and other seaweed, but also to appropriately control daily life in the This is because a high iodine diet will activate the thyroid gland. This is because a high iodine diet will activate the autoimmune mechanism of the thyroid gland, destroying the thyroid tissue, inducing and aggravating thyroiditis, and leading to a further reduction in the patient’s thyroid function. Of course, there is no need to ban iodine, just eat normally. In short, we usually eat iodized salt is already appropriate, do not need to take additional iodine. Can I stop taking medication after my hypothyroidism is corrected? There are many causes of hypothyroidism, such as chronic lymphocytic thyroiditis, thyroid surgery or radiotherapy, overdose of antithyroid medication, iodine deficiency, subacute thyroiditis and so on. Most cases of hypothyroidism (e.g. chronic lymphocytic thyroiditis, after thyroid surgery or radiotherapy) are permanent and require lifelong medication. Only a small proportion of hypothyroidism (e.g., subacute thyroiditis, pharmacogenetic hypothyroidism or iodine-deficiency hypothyroidism) is temporary and can be cured with treatment without lifelong medication. Many patients see lifelong medication as a burden, but in fact it is not necessary. “Hypothyroidism is a condition in which the body does not have enough thyroid hormone, and the purpose of replacement therapy is to replenish the body’s lack of thyroid hormone. Generally take a few weeks after the thyroid function can be basically restored to the normal level, but if you stop taking the medicine, the original disappearance of the symptoms (such as fear of cold, less sweat, fatigue, lethargy, mental instability, etc.) can be reappeared in 1 ~ 3 months. Especially during pregnancy, when the mother’s demand for thyroxine increases, if the supplement is insufficient, it will affect the growth and development of the fetus.