Acute radiation thyroiditis

Introduction to acute radiation thyroiditis Acute radiation thyroiditis (acuteradiothyroiditis) refers to inflammation of the thyroid that occurs within two weeks after acute radiation. Usually, the thyroid is less sensitive to direct effects of radiation, but the thyroid in a proliferative state is more sensitive to radiation. Therefore, the thyroid gland of patients with minors and hyperthyroidism is more sensitive to radiation and is prone to thyroiditis. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: hyperthyroidism

Cause of acute radiation thyroiditis

(1) Causes of the disease

The main causes of thyroid radiation damage are:

1. 131I treatment of thyroid disease such as hyperthyroidism in patients taking 131I treatment, about 1 to 5% of patients with acute radiation thyroiditis; after thyroid cancer patients undergoing radionuclide treatment, due to residual thyroid tissue How much different, the incidence of acute radiation thyroiditis can reach 2% to 30%.

2. Radioactive iodine contaminates radioactive iodine that enters the body through the respiratory tract or digestive tract. It is ingested by the thyroid gland and locally concentrated to cause radioactive damage.

3. The nuclear accident causes acute systemic radiation damage. The patient's local manifestations are neck skin itch and discomfort, neck pressure, dysphagia, thyroid pain, and systemic reactions may be slightly hot, fatigue, palpitations, sweating, Dizziness, hand tremor and other symptoms of hyperthyroidism.

(two) pathogenesis

The pathological changes in the acute phase are mainly thyroid tissue congestion and edema, follicular cells damaged, neutrophil infiltration, followed by follicular disintegration, follicular epithelium with epithelial nest without certain structure, gel-like overflow follicle, filtration The epithelial cells undergo eosinophilic changes, cytoplasm is abundant, and eosinophilic granules appear, vacuoles become obvious, cell size, arrangement, nuclear staining are inconsistent, nuclear size is different, often nuclear hypertrophy, deformity or deep staining, juvenile patients The follicle becomes smaller, and it is a small follicle that does not contain glia. In a few cases, thyroid nodules or adenomas may form, small blood vessels may dilate, the wall may be thickened, and there may be cellulose-like necrosis and thrombosis. Follicular cell and interlobular fibrous tissue hyperplasia, mild inflammatory cell infiltration, fibrous tissue hyperplasia increased with time, and finally the entire thyroid follicle atrophy, the volume became smaller, grayish white scar, leaving small irregular and not Glia-containing follicles remain in large fibrous tissue, called postradiation fibrosis, and Kennedy and Thomson treat 131I and remove the thyroid to treat hyperthyroidism. The thyroid gland was observed by histological observation. It was found that the follicular epithelium after irradiation had obvious eosinophilic changes, while the thyroiditis was not obvious after radiotherapy. The survivors were often accompanied by hypothyroidism and the occurrence of post-radiation papillary carcinoma. The rate is increasing.

Acute radiation thyroiditis prevention

Early detection and early diagnosis are the key to the prevention and treatment of this disease.

Acute radiation thyroiditis complications Complications

In some patients with hyperthyroidism treated with 131I, there will be aggravation of hyperthyroidism and even thyroid crisis. This is mainly due to the rapid release of a large amount of thyroid hormone into the blood after thyroid follicular destruction. Therefore, 2 to 8 weeks before 131I treatment of hyperthyroidism Routine anti-thyroid drug treatment should be performed first to deplete the stored thyroid hormone, and radioactive iodine treatment should be started after about 5 days of treatment. After 2 to 7 days after treatment, anti-thyroid drugs can still be given again. In addition, at 131I Before and after treatment, there is no need to stop beta blockers, such as propranolol (propranolol).

Acute radiation thyroid symptoms common symptoms skin tenderness neck muscles swelling hard

Radioactive thyroiditis has a history of radiotherapy, often occurring within 1 to 2 weeks after 131I or 125I treatment of hyperthyroidism and thyroid cancer. Symptoms in the acute phase are generally mild, manifested as sudden onset of local thyroid pain, tenderness, neck swelling, etc. Sometimes, transient hyperthyroidism can occur.

Examination of acute radiation thyroiditis

Laboratory examination: thyroid absorption 131I rate is reduced. Other ancillary examinations: thyroid fine needle aspiration cytology. Patients with subclinical hypothyroidism should be followed up for a few months, and TSH should be measured to determine whether L-T4 is treated. It is suggested that L-T4 should be used in the subclinical reduction phase. Other laboratory tests are also helpful in diagnosing hyperthyroidism and thyroiditis, iodine uptake, TGAb, TPOAb, TRAb, fine needle aspiration cytology for thyroid nodules, and thyroid scans and ultrasound for identification.

Diagnosis and diagnosis of acute radiation thyroiditis

One to two weeks before the onset of the disease, the patient has a history of radionuclide exposure or a history of radionuclide treatment; a sudden onset of pain in the thyroid gland, tenderness and swelling of the neck, or a transient hyperthyroidism, can be clearly diagnosed.

Diagnostic criteria:

1 There is a history of ray exposure, and the thyroid dose is 0.3 Gy or more.

2 incubation period of more than 1 year.

3 thyroid enlargement, most of them have no tenderness.

4 Thyroid microsomal antibodies (Tm-Ab) and/or thyroglobulin antibody (Tg-Ab) are positive, and thyroid stimulating hormone (TSH) is increased.

5 may be associated with hypothyroidism. Fine needle aspiration cytology: 131I affected thyroid gland in addition to typical nodular goiter and/or chronic lymphocytic thyroiditis, smear with follicular cells, massive glial, fibrovascular matrix and lymph Cell composition. Follicular cells are mainly loose monolayer plexus, occasionally forming tiny follicles with distinct nuclear size and pleomorphism, large volume of large, but not typical follicular cells, mainly single or plexiform and fibrous substrates. Mixed with blood vessels, these cells have large nuclear chromatin, occasionally visible nucleoli, no nuclear groove and nuclear inclusions, a slight increase in nuclear/plasma ratio, abundant cytoplasm, and many nuclear giant nuclei. Therefore, smear can be Misdiagnosed as undifferentiated cancer. The pathology of the surgical specimen confirmed that all glandular structures were formed by nodule formation, lymphocytic infiltration, fibrosis, follicular atrophy, and obvious polymorphism of follicular cells.

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