Thyroiditis is a general term for different types of thyroiditis caused by different causes.
The main types of thyroiditis are as follows.
(1) Chronic lymphatic thyroiditis.
(2) Subacute thyroiditis.
(3) Painless thyroiditis.
(4) Acute thyroiditis.
(5) Sclerosing thyroiditis.
Among the above thyroiditis, chronic lymphatic thyroiditis is the most common, subacute thyroiditis is the second most common, painless thyroiditis is the third most common, and the other two types of thyroiditis are rare. The following will describe the characteristics of the first three types of thyroiditis respectively.
I. Chronic lymphocytic thyroiditis
Chronic lymphocytic thyroiditis is also known as Hashimoto’s disease or Hashimoto’s thyroiditis. It is now believed that the disease is autoimmune related and is also known as autoimmune thyroiditis. The disease is most often seen in middle-aged women and has a tendency to develop into hypothyroidism, which is more common in clinical practice.
Etiology and pathogenesis: It is believed that the cause of this disease is related to autoimmunity. Anti-thyroid antibodies, including thyroglobulin antibodies and thyroid microsomal antibodies, are often significantly elevated in the serum of patients with this disease. There is a large infiltration of lymphocytes and plasma cells in the thyroid tissue. The disease may coexist with other autoimmune diseases such as pernicious anemia, dry syndrome, chronic active hepatitis, and systemic lupus erythematosus. Lymphocytes from patients with this disease can produce leukocyte movement inhibitory factors after contact with thyroid tissue antigens in vitro. All of the above can be seen in patients with Graves’ disease and idiopathic mucinous edema, suggesting a common pathogenetic factor for all three. Therefore, Graves’ disease, idiopathic mucinous edema and this disease are collectively referred to as autoimmune thyroid disease. Autoimmune thyroid disease can also occur in the same family.
The development of chronic lymphocytic thyroiditis is associated with HLA-DR3 and -DR5.
The mechanisms that contribute to thyroid damage in this disease have not been clarified to date. It may be due to a genetic defect in T lymphocytes, especially suppressor T lymphocytes, which do not exert a normal inhibitory effect on the formation of autoantibodies to B lymphocytes, leading to the formation of thyroid autoantibodies. Antibody-antigen complexes can be deposited on the basement membrane of cells and activate K cells (killer cells) to exert their cytotoxic effects, resulting in the destruction of autologous thyroid cells.
Clinical manifestations: The disease starts slowly, with goiter being the prominent clinical manifestation. It is usually moderately diffusely enlarged, still maintaining the shape of the thyroid gland, but the sides are asymmetrical, tough like rubber, with a smooth surface that moves with swallowing. The surface is smooth and moves with swallowing. However, sometimes it can be nodular in shape and hard, which can be easily confused with thyroid cancer. The localized thyroid gland is usually painless, but some patients with rapid enlargement of the thyroid gland may have localized pain and pressure. In early cases, thyroid function can still be maintained within the normal range, but serum TSH can be increased, indicating that thyroid reserve function has decreased at that time. As the disease progresses, clinical manifestations of hypothyroidism or mucinous edema may occur. The disease may occasionally present with pressure symptoms such as difficulty breathing or swallowing. However, in some patients, the thyroid gland does not become enlarged, but rather shrinks, while its main manifestation is hypothyroidism.
Chronic lymphocytic thyroiditis may also present with transient thyrotoxicosis, and a few patients may have proptosis, but this is usually mild. The disease may coexist with Graves’ disease.
Diagnosis and differential diagnosis: Any middle-aged woman who presents with diffuse enlargement of the thyroid gland with a firm texture should be considered for this disease, regardless of her thyroid function. If the serum thyroid microsomal antibodies and thyroglobulin antibodies are significantly elevated, the diagnosis is basically confirmed. A positive perchlorate release test may also help in the diagnosis of this disease. A needle biopsy of the thyroid gland is recommended in suspected cases to clarify the diagnosis.
In patients with chronic lymphocytic thyroiditis, the thyroid gland can sometimes have multiple nodules with a hard texture, which should be differentiated from thyroid cancer. The latter is often negative for serum anti-thyroid antibodies and can be examined with a thyroid needle biopsy if necessary. A small number of patients with chronic lymphocytic thyroiditis may present with localized thyroid pain, nodules and accelerated erythrocyte sedimentation rate, which should be differentiated from subacute thyroiditis. The latter often resolves on its own, and the iodine uptake rate of the thyroid gland is often significantly reduced. After treatment with prednisone, clinical symptoms often disappear rapidly and are generally not difficult to differentiate.
Treatment: Early patients with insignificant enlargement or symptoms of the thyroid gland are not necessarily treated and can be followed up and observed. However, if there is hypothyroidism, even if there is only an increase in serum TSH and the symptoms are not obvious, they should be treated with thyroid preparations. Generally, dry thyroid tablets or levothyroxine (L-T4) are used, and the dose depends on the response of the disease. It is advisable to start with a small dose, 20 mg/d of dry thyroid tablets or L-T425-50 μg/d, and gradually increase it later. The maintenance dose is 60-180mg/d of dry thyroid tablets or 100-150μg/d of L-T4, taken orally in divided doses. The thyroid gland may shrink significantly in some patients after medication. The duration of treatment depends on the condition, and sometimes it is necessary to take it for life.
Patients with hyperthyroidism should be treated with anti-thyroid drugs, but the dose should be small, otherwise hypothyroidism is likely to occur. Radioactive iodine or surgical treatment is not usually used, otherwise severe mucinous edema may occur. Although glucocorticoids can shrink the thyroid gland and reduce the titration of anti-thyroid antibodies, they have certain side effects and can recur after discontinuation, so they are generally not used. However, if the thyroid gland is rapidly enlarging or accompanied by pain and pressure symptoms, short-term application can be used to relieve the symptoms more quickly. Prednisone 30mg daily, divided into oral doses. It can be gradually reduced and used for 1 to 2 months. Stop the drug after the disease is stabilized. If the thyroid gland does not shrink after treatment with thyroid preparations and other drugs, or if thyroid cancer is suspected, surgical treatment can be considered, and thyroid preparations should continue to be supplemented after surgery.
II. Subacute thyroiditis
Subacute thyroiditis is more common in clinical practice. It is mostly seen in adults between 20 and 50 years of age, but also in young and old, and is more common in women, 3 to 4 times more common than in men.
Etiology: The disease may be related to viral infection. The onset of the disease is often preceded by an upper respiratory tract infection. At the onset of the disease, the patient has an increased titer of antibodies to certain viruses in the serum, including influenza virus, coxsackievirus, adenovirus, mumps virus, etc.
Clinical manifestations: The onset of the disease is usually acute. The disease is often preceded by an upper respiratory tract infection. The first symptoms are weakness and general malaise, and pain in the thyroid gland, which may be radiated to the jaw, ear, or occipital region, but sometimes there is no pain. Systemic symptoms, including chills, fever, and decreased appetite, may also be present. Many patients may also have palpitations, nervousness, and other manifestations of thyrotoxicosis, but they last for a short period of time, usually no more than 2 weeks. Physical examination may reveal mild enlargement of the thyroid gland, often with nodules of medium texture and significant pressure pain, located on one side, which may disappear after a certain period of time and later appear on the other side. Most of the disease lasts only a few weeks and can resolve on its own, but it can recur. The entire course of the disease can last for several months, usually 2 to 3 months, and can be prolonged to 1 to 2 years in a few patients, but it usually recovers completely without affecting thyroid function. Some patients may develop transient hypothyroidism with mild symptoms, and permanent hypothyroidism is rare.
Diagnosis and differential diagnosis: The diagnosis of this disease is mainly based on its clinical manifestations and laboratory tests. Patients with enlarged thyroid gland, nodules, pain and tenderness, with systemic symptoms, significantly accelerated erythrocyte sedimentation rate, and significantly reduced iodine uptake by the thyroid gland usually below 10%, the diagnosis is often not difficult to establish.
However, sometimes the main symptom in the early stage is “pharyngeal” pain, which can be misdiagnosed as upper respiratory tract infection or pharyngitis, etc. The diagnosis can be clarified only when local symptoms of thyroid gland appear. In some cases, sudden bleeding in the thyroid adenoma may cause pain in the thyroid gland, but it is often rapidly relieved, and the iodine uptake rate of the thyroid gland does not decrease. Chronic lymphocytic thyroiditis sometimes has an acute onset, with localized pain and tenderness, and can be confused with subacute thyroiditis, but the former often presents with diffuse goiter, no significant increase in erythrocyte sedimentation rate, and a significant increase in thyroglobulin and microsomal antibodies. Sometimes, local pain and pressure can also be seen in thyroid cancer, while thyroid hormone enters the blood circulation to inhibit TSH secretion due to the destruction of thyroid tissue, and the iodine uptake rate of thyroid gland is reduced. If necessary, thyroid needle biopsy or close follow-up may be performed.
Treatment: In mild cases, aspirin, indomethacin and other non-steroidal anti-inflammatory drugs are used to control symptoms. Aspirin 0.5 to 1.0g, 2 or 3 times a day, orally, the course of treatment is usually in about 2 weeks. If the symptoms are more severe, prednisone 20-40mg/d can be given orally in divided doses, the symptoms can be relieved quickly, the body temperature will drop, the pain will disappear, and the thyroid nodules will shrink or disappear soon. The dosage can be gradually reduced after 1 to 2 weeks, and the course of treatment is usually 1 to 2 months, but after stopping the drug can be relapsed, and the treatment is still effective again. Those with thyrotoxicosis may be given propranolol to control symptoms. If the iodine uptake rate of the thyroid gland has returned to normal, relapse is usually not repeated after discontinuation of the drug. A small number of patients may develop transient hypothyroidism, and if symptoms are significant, thyroid preparations may be supplemented appropriately. Those with obvious infection should be treated accordingly.
Painless thyroiditis
It is a type of thyroiditis that has only been recognized in recent years. The cause of the disease is not well understood and may be related to immune dysfunction. This disease is distinctly different from subacute thyroiditis because there is no history of viral infection before the onset of the disease and there is no thyroid pain at the time of onset. The disease is also different from chronic lymphatic thyroiditis because there is a transient change in thyroid function during the onset of the disease and thyroid function returns to normal after the disease.
Clinical manifestations: Early manifestations of hyperthyroidism last for about 2-5 months, then the hyperthyroidism disappears. In some patients, the hyperthyroidism disappears and the patient is cured; in some patients, hypothyroidism may occur after the disappearance of the hyperthyroidism, and the patient may recover after a period of normalization. There is no thyroid pain during the onset of the disease. Blood tests for thyroglobulin antibodies and thyroid microsomal antibodies are normal or elevated, and blood sedimentation is increased. In hyperthyroidism, the blood T3 and T4 are increased, but the rate of iodine uptake by the thyroid gland is reduced. In hypothyroidism, blood T3 and T4 are decreased, and the rate of 131 iodine uptake by the thyroid gland is reduced. After thyroid function is normalized, blood sedimentation is normalized, and blood T3 and T4 and thyroid 131 iodine uptake rate are normalized.
Treatment: Adrenocorticosteroids such as prednisone can be used in doses and methods similar to those used for subacute thyroiditis. If no medication is used, the disease can also return to normal.