Definition
Hypothyroidism (hypothyroidism), is a group of endocrine disorders caused by inadequate synthesis, secretion or biological effect of thyroid hormone (TH) due to multiple causes. Its pathology is characterized by the accumulation of mucopolysaccharides in the tissues and skin, which manifests as mucinous edema (myxedema).
Epidemiology
The prevalence of hypothyroidism in the normal population is 0.8% to 1.0%, and it is more common in women than in men.
The prevalence of hypothyroidism in newborns is about 1/7000, and increases with age in adults.
Primary hypothyroidism accounts for 95% of cases, and less than 5% of cases are due to TSH deficiency.
Classification
1. There are three types according to the age of onset of the disease. If the disease starts in fetus or newborn, it is called cretinism; if the disease starts in children, it is called juvenile hypothyroidism; if the disease starts in adults, it is adult hypothyroidism. In severe cases, all types of hypothyroidism can be manifested as mucinous edema.
2, according to the onset of the site is divided into primary hypothyroidism and secondary hypothyroidism. Primary hypothyroidism is the most common, followed by pituitary hypothyroidism.
Etiology
The etiology is complex and the pathogenesis varies with the cause and type.
1, primary hypothyroidism.
It accounts for about 95% or more of the cases, and is caused by diseases of the thyroid gland itself, mostly as a consequence of acquired thyroid tissue being destroyed.
(1) Inflammation, due to autoimmune reactions or viral infections, etc. In particular, chronic lymphocytic thyroiditis has a high incidence of occult onset.
②After iodine-131 treatment.
(iii) After removal of a large part or all of the thyroid gland.
(④Iodine deficiency is most common in areas with endemic goiter, and goiter and hypothyroidism can occur in a few areas with high iodine levels.
⑤ Many salts containing monovalent anions (such as ClO4- and NO3-) can inhibit iodine uptake by the thyroid gland, causing goiter and hypothyroidism.
(6) Hypothyroidism caused by genetic factors or genetic mutations.
2.Secondary hypothyroidism.
Secondary hypothyroidism occurs due to TSH deficiency caused by pituitary or hypothalamic diseases. It is often caused by tumor, surgery, radiotherapy or postpartum ischemic necrosis of the pituitary gland. In addition to hypothyroidism, hypoadrenocorticism and hypogonadism are often present in those with extensive destruction of the anterior pituitary gland, manifesting as a decrease in compound pituitary hormone secretion; hypothalamic TRH secretion deficiency can lead to hypothyroidism due to successive decreases in TSH and TH. It can be caused by hypothalamic tumor, sarcoidosis, chronic inflammation or radiotherapy, etc.
3. Thyrotropic hormone or thyroid hormone insensitivity syndrome.
TSH insensitivity syndrome is a type of hypothyroidism caused by the thyroid gland being resistant to TSH. Some cases are genetically related and the family findings are autosomal recessive. It may be due to mutations in the TSH receptor gene or impaired cAMP production in TSH messaging. TH insensitivity syndrome is a form of hypothyroidism caused by reduced tissue sensitivity to thyroid hormones. It is often familial in origin and is autosomal dominant or recessive. It may be due to mutations in the TH receptor gene, reduced TH receptors or post-receptor defects.
Clinical presentation
In adult hypothyroidism, for example, hypothyroidism occurs more rapidly after surgical resection or iodine-131 treatment, while spontaneous hypothyroidism mostly starts insidiously and develops slowly, with some patients showing typical manifestations only after more than 10 years of illness.
1, general manifestations: fear of cold, less sweating, weakness, less speech and laziness, slow movement, low body temperature, loss of appetite and weight gain, yellow face, puffy eyelids, thick lips and large tongue, dry and cold skin, rough and flaky. Due to anemia and carotenemia, the palms of the hands and feet are often ginger.
2, neuropsychiatric system: indifferent expression, memory loss, mental retardation. Slow reaction, drowsiness, mental depression.
3, muscle and joint: muscle weakness, there may also be temporary muscle ankylosis, spasm, pain, etc. Occasionally, severe muscle weakness is seen. Patients with mucinous edema may have arthropathy and occasional joint effusion.
4. Cardiovascular system: sinus bradycardia. The cardiac turbinate is enlarged and the heart sound is weakened. Ultrasonography may reveal pericardial effusion, and there may be pleural or abdominal effusion at the same time. Long-term patients are prone to complications of coronary heart disease due to increased blood cholesterol, but angina pectoris and heart failure are rare due to reduced myocardial oxygen consumption.
5, digestive system: often anorexia, abdominal distension, constipation, severe cases may appear paralytic intestinal obstruction or mucus edema megacolon. Due to the lack of gastric acid or vitamin B12 malabsorption, iron deficiency anemia or pernicious anemia may result.
6, endocrine system: loss of libido, impotence in men, women often have excessive menstruation, prolonged periods and infertility. About l/3 patients may have overflowing breast.
7. Mucinous edema coma: seen in those with severe disease. Triggers are severe physical illness, interruption of thyroid hormone replacement therapy, cold, infection, surgery and the use of anesthetics and sedatives. Clinical appearance is drowsiness, hypothermia (<35ºC), tachypnea, bradycardia, decreased blood pressure, muscle relaxation in the limbs, weakened or absent reflexes, and even coma, shock, and life-threatening cardiac and renal insufficiency.
Prevention of hypothyroidism
Since the occurrence of early onset hypothyroidism is related to the severity of hyperthyroidism, the type of goiter, the size of the thyroid gland, the dose of iodine-131, the number of iodine-131 treatments, and the treatment methods used before iodine-131 treatment (such as surgery and antithyroid drugs), proper selection of patients with hyperthyroidism and careful decision on the dose of iodine-131 treatment are effective in reducing the incidence of early onset hypothyroidism after iodine-131 treatment. Therefore, proper selection of patients with hyperthyroidism and careful decision of the dose of iodine-131 treatment are effective in reducing the incidence of early-onset hypothyroidism after iodine-131 treatment.
However, the occurrence of early-onset hypothyroidism depends more on the sensitivity of individual hyperthyroid patients, and the above treatment measures can only reduce the occurrence of early-onset hypothyroidism to a certain extent, but cannot eliminate it fundamentally.
Late onset hypothyroidism is not related to the dose of iodine-131, but to the autoimmune process and to the natural history of hyperthyroidism. There is even no good solution to reduce late onset hypothyroidism. Although some scholars have attempted to predict the individual susceptibility of hyperthyroid patients by measuring certain immunological indicators, no breakthrough has been achieved. Therefore, neither early-onset nor late-onset hypothyroidism can be prevented at this time. This remains an important topic for future clinical research on iodine-131 treatment of hyperthyroidism.
Thyroid hormone replacement therapy
Since the occurrence of hypothyroidism after iodine-131 treatment for hyperthyroidism is inevitable and unpredictable, the principle of management of hypothyroidism is early diagnosis and timely thyroid hormone replacement therapy. The important thing for early diagnosis is follow-up, with special emphasis on follow-up before 3 months and regular follow-up thereafter.
Although there is no evidence-based basis for the initial dose of thyroid hormone replacement therapy, in the clinical practice of nuclear medicine, hypothyroid patients are classified as mild, moderate or severe according to the severity of their own symptoms and signs and their thyroid gong results.
1. Mild hypothyroidism: serum TSH <45mU/L, mild hypothyroid symptoms and signs, and mildly reduced thyroid function. Administer levothyroxine (L-T4), such as Raitis or Eugenol 25~50ugqd for 3 months.
2. Moderate hypothyroidism: serum TSH 46~100mU/L, obvious signs and symptoms of hypothyroidism, and reduced thyroid function. Administration of levothyroxine (L-T4) 75~100ugqd for 3 months.
3. Severe hypothyroidism: serum TSH>100mU/L, severe hypothyroidism symptoms and signs, and significantly reduced thyroid function. Give levothyroxine (L-T4) 150ugqd for 3 months.
In all three cases mentioned above, the thyroid function should be reviewed once a month to adjust the dosage of medication. For patients who tend to have temporary hypothyroidism, levothyroxine (L-T4) may be discontinued for observation after 3 months of administration.