When you notice thickening or a lump in your neck, even if you have no uncomfortable symptoms, you should think about whether an enlarged thyroid or other thyroid disorder has occurred. You should go to the hospital promptly at this time. Your doctor can usually tell you whether your thyroid gland is enlarged and whether there is a lump by palpating the thyroid gland. There are many different thyroid disorders, and those who have an enlarged thyroid gland or a swollen thyroid gland generally need further tests to determine the nature of the thyroid disorder, such as blood tests to check thyroid function and, if necessary, radionuclide and ultrasound examinations of the thyroid gland, or even cytology of thyroid puncture. You should think about the possibility of hyperthyroidism when you have symptoms such as fear of heat, excessive sweating, palpitations, anxious temperament, hyperphagia, and weight loss. When you notice symptoms such as fear of cold, swelling, weight gain, dry skin and loss of appetite, you should be aware of the possibility of hypothyroidism. When you feel pain and fever in the neck, especially when you can feel a lump in the thyroid gland and have pressure pain, you should think about the possibility of acute or subacute thyroiditis. In these cases, you should visit the endocrinology department of the hospital in time for further examination so that you can get timely diagnosis and reasonable treatment. Thyroiditis is a less that clinical condition caused by destruction of the thyroid follicular structure, tissue degeneration, exudation, necrosis, and hyperplasia due to autoimmunity and other causes. Very rarely it is caused by infection. Classification: Hashimoto’s thyroiditis, acute suppurative thyroiditis, subacute thyroiditis, painless thyroiditis, infectious thyroiditis and other causes of thyroid, most commonly chronic lymphocytic and subacute thyroiditis. 1. Subacute thyroiditis (subacute thyroiditis) Subacute thyroiditis, also known as acute nonsuppurative thyroiditis, viral thyroiditis, and giant cell thyroiditis, makes it one of the more common types of thyroiditis. The cause of the disease is unknown, but it is related to viral infection or viral metaplasia. The age of onset is usually 20 – 60 years old, with a high incidence in middle age and more women than men. The thyroid gland may be 2-3 times larger or larger than normal, with significant pressure pain within 1 week of the onset of the disease. These symptoms are caused by the release of excessive thyroid hormones from the thyroid gland during acute inflammation. In the course of disease resolution, a few patients may develop hypothyroidism such as swelling, constipation, coldness, and drowsiness, but these manifestations do not last long eventually thyroid function returns to normal. Diagnosis In the early stages of the disease, laboratory tests reveal increased T3 and T4, decreased TSH and thyroid radioiodine uptake, and increased blood sedimentation. After a few weeks, the thyroid T3 and T4 stores are depleted and transient hypothyroidism occurs with decreased T3 and T4, increased TSH and normal thyroid radioiodine uptake. Weakly positive antibodies may be present during the onset of the disease. Treatment High-dose aspirin or NSAIDs are used. corticosteroids (prednisone 30-40 mg/d, decreasing over 6 weeks) are recommended for more severe and prolonged cases, and all symptoms disappear within 24-48 hours. Treatment is terminated when radioiodine uptake in the thyroid gland returns to normal. 2. Hashimoto’s thyroiditis is also known as chronic lymphocytic thyroiditis, Hashimoto’s goiter, and autoimmune thyroiditis. The disease occurs mostly in women around 40 years of age and is rare in men, with a male to female ratio of about 1:20. There are no exact incidence statistics, but in the past 20 or 30 years, domestic and foreign data suggest that the incidence of the disease has increased, and the incidence in the population can be as high as 22.5 to 40.7/100,000, which shows that this disease is not rare. The number of cases of chronic lymphocytic thyroiditis admitted to Shanghai Medical University from 1975 to 1986 accounted for 3.88% of the number of cases of thyroid disease in the same period. Etiology According to many clinical and experimental data in recent years, this disease is an autoimmune disease. In most patients, the serum and thyroid tissue contain antibodies against thyroid antigens, mainly known as thyroglobulin antibodies (TGA), thyroid microsomal antibodies (MCA), thyroid cell surface antibodies (FCA), and thyroid glial second component (CA2). The first two are of clinically useful value. In normal human serum, the thyroglobulin antibody value is 1:32, rarely exceeding 1:256, and the microsomal antibody value is below 1:4; in patients with chronic lymphocytic thyroiditis, these two antibody values can be as high as 1:2500 and 1:640 or more, respectively. One is that the target organ has changed antigenically for some reason, making itself “non-self” and rejecting it; the other is that the immunologically active cells have mutated, reducing the number of suppressive T cells and making the B cells more active, producing an excess of antibodies. When antibody-antigen binding occurs, an antigen-antibody complex is formed that covers the surface of the thyroid cells and is activated by the binding of K cells, a type of killer lymphocyte that has a cytotoxic effect on antibody-dependent cell-mediated immunity and releases cytotoxicity upon activation, resulting in destruction of thyroid cells. In addition, genetic factors must be taken into account for the development of these immune abnormalities. Many cases illustrate that half of the siblings in the same family have significantly elevated antibody levels and multiple cases of Hashimoto’s disease occur. Symptoms and signs The onset of Hashimoto’s disease is insidious, often without specific symptoms, and the main manifestation in 80-90% of patients is an enlarged thyroid gland, mostly diffuse and asymmetrical, with lesions involving one or both sides, but still clearly palpable in the isthmus or conus lobe. The thyroid gland is tough and rubbery, with a relatively flat surface and no adhesions to surrounding tissues. However, later in the course of the disease, due to gradual fibrosis of the thyroid gland, the surface of the thyroid gland may become multilobular and inconsistent in hardness, giving it a multinodular appearance, resembling a new thyroid organism, without enlargement of the nearby lymph nodes. Some patients start with hyperthyroidism and later feel generalized weakness due to atrophy of the thyroid gland and the development of mucinous edema. They also feel a slight pressure in the neck and swallowing discomfort. Ancillary tests: thyroglobulin and microsomal antibodies are positive; 131I uptake is generally normal and can be suppressed by T3 when increased. Thyroid isotope scans show a symmetrical morphology, but the distribution of radioactivity is often uneven, with patchy sparse areas; T3 and T4 values are normal; TSH values are decreased, but increase in hypothyroidism. Diagnosis Laboratory tests early in the disease include normal T3, T4 and increased titers of thyroid peroxidase antibodies and, less commonly, thyroglobulin antibodies. Thyroid radioactive iodine uptake can be increased, most often due to thyroid iodine organic disorders with persistent iodine uptake by the thyroid gland. Later in the course of the disease, hypothyroidism develops with decreased T4, decreased thyroid radioiodine uptake and increased TSH. Treatment Since Hashimoto’s thyroiditis is a chronic disease, once the neck is found to be enlarged and the diagnosis is confirmed, do not take the risk of having the enlarged thyroid removed. This is because it is easier for patients with Hashimoto’s thyroiditis to go into early hypothyroidism and require long-term thyroxine. The correct approach to Hashimoto’s thyroiditis is to exercise more, eat less iodine-containing foods, and have regular blood tests and ultrasound follow-ups. Patients who are already on medication should have regular follow-up visits to make appropriate medication adjustments. Although Hashimoto’s hyperthyroidism has several characteristic clinical manifestations as described above, histological examination is indispensable to diagnose Hashimoto’s hyperthyroidism. The diagnosis can be established by the presence of both histological signs of typical Hashimoto’s disease and toxic diffuse goiter on thyroid puncture biopsy histology. Both are seen on the same specimen, in completely different areas, sometimes independently, and in most cases still both overlap. They are usually treated with small doses of antithyroid drugs and appropriate doses of thyroid hormones, often for a longer period of time. Due to low thyroid reserve function, multiple doses of antithyroid medications can easily fall into hypothyroidism. Hyperthyroidism can last for many years and often progresses to mucinous edema in those with long duration of disease. Therefore, surgery and radioactive iodine therapy are contraindicated in the treatment of hyperthyroidism, otherwise permanent hypothyroidism is likely to occur. Another manifestation of Hashimoto’s hyperthyroidism is Hashimoto’s disease with transient hyperthyroidism. Hashimoto’s disease is an autoimmune thyroid disease in which the pathological changes are mainly lymphocytic infiltration of the thyroid tissue, which results in destruction of the thyroid tissue and often leads to hypothyroidism. However, when chronic lymphocytic thyroiditis progresses to a certain stage, the thyroid follicles are destroyed due to immune factors and other factors, and the thyroid hormones stored in the follicles are released into the bloodstream, resulting in an increase in the concentration of thyroid hormones in the bloodstream and causing hyperthyroidism. This type of hyperthyroidism is often transient, and when the thyroid hormones released into the bloodstream are metabolized (consumed), the symptoms of hyperthyroidism disappear. Treatment is symptomatic only, and anti-thyroid medication is generally not used. Radioactive iodine therapy and surgery are prohibited. There are also a few patients who can develop Hashimoto’s disease into mucinous edema and then into Graves’ disease, because Hashimoto’s disease, Graves’ disease and mucinous edema are all autoimmune thyroid diseases, and the pathogenesis of the three is similar and can be clinically transformed into each other. Notes on patient’s diet: 1. Eat less and eat more, do not overeat. Avoid spicy, tobacco and alcohol. 2, replenish sufficient water, drink about 2500ml of water per day, avoid coffee, strong tea and other excitatory drinks. 3, appropriate control of high-fiber foods, especially when diarrhea. 4.Pay attention to the reasonable combination of nutrients. 5.Forbid to eat seaweed, sea fish, sea jelly skin and other foods with high iodine content. Since iodine is very easy to volatilize in the air or after being heated, iodized salt can be used by simply putting it in the air or heating it slightly. 6.Eat foods rich in potassium and calcium. 7.Control the diet appropriately after the condition is reduced.