radiation thyroiditis
Introduction
Introduction to radiation thyroiditis Ionizing radiation can cause different changes in human thyroid gland. The incidence of benign and malignant tumors is significantly increased at low doses (10-1500 rad), while thyroid function changes and thyroiditis are more common in larger doses. These changes are related to the dose and type of radiation. Exposure time, individual differences such as age, gender, genetics, hypothyroidism is the most common manifestation of direct thyroid injury. Direct thyroid gland can produce a variety of thyroid diseases, including autoimmune thyroiditis, Graves disease, Grayes eye with normal thyroid function, syndrome similar to asymptomatic thyroiditis, thyroid cyst, single or multiple benign nodules, nipple Thyroid, follicular or mixed thyroid cancer. basic knowledge The proportion of illness: the incidence rate is about 0.006% - 0.009% Susceptible people: no special people Mode of infection: non-infectious Complications: thyroid cancer
Cause
Causes of radiation thyroiditis
(1) Causes of the disease
1. Ionizing radiation can cause different changes in human thyroid gland. The incidence of benign and malignant tumors is significantly increased in low doses, while thyroid function changes and thyroiditis are more common in larger doses.
2. Changes in thyroid function are related to dose, type, exposure, time, individual differences, age, gender, and genetics of the radiation.
3. Radioactive iodine treatment, that is, acute and chronic thyroiditis can be caused by external irradiation treatment of head and neck diseases.
(two) pathogenesis
In theory, radiation can inhibit follicular epithelial function, reduce the number of functional follicles, alter blood supply or vascular permeability, and induce immune responses to produce various thyroid dysfunctions. However, the exact mechanism of any form of radiation damage is not Clearly, acute changes in the 3 to 6 weeks of a lethal dose nuclear explosion include follicular reduction with flattened, cubic epithelium, higher radiation doses such as therapeutic doses of 131I producing follicular necrosis, acute vasculitis, thrombosis and hemorrhage, Subsequent lymphocytic infiltration, hardening of the arteries, and chronic changes caused by low doses include local irregular follicular hyperplasia, vascular hyalinosis and fibrosis, and lymphocytic infiltration.
A prospective study showed that serum TSH decreased significantly during radiation therapy (thyrotoxicosis) because radiation promoted thyroid hormone release, inhibited TSH secretion, increased TSH after radiation therapy (hypothyroidism), and thyroid received therapeutic dose The external irradiation can cause thyrotoxicosis. The serum TSH increases 4 to 12 months after the start of radiation therapy, and the latency of the first 3 months is stable. Among the thyroid hormones, free T4 is the most sensitive indicator of radiation-induced thyroid dysfunction. Thyroidosis is mild. No thyroid histological changes have been observed after administration of small doses of radiation such as 40 Gy for 4 weeks. Therefore, it is believed that excessive hormone release may be caused by increased cell membrane permeability, after radiation therapy 2 Weekly decreased TSH levels began to rise, at this time, still significantly lower than before treatment, after which TSH continued to rise, similar changes are also seen in the course of subacute thyroiditis, that thyroid inflammatory changes during radiotherapy, that is, acute radiation thyroid Inflammation, TSH levels were higher than 6 months after radiation thyroiditis, during follow-up Restoration to baseline levels suggests that irreversible damage to follicles may occur. Some studies have shown an increased incidence of hypothyroidism in the years following radiation therapy, probably due to the killing of thyroid stem cells after radiation therapy, resulting in reduced mitosis and progressive hypothyroidism. Vascular injury also plays a role.
Typical pathological changes: follicular destruction and atrophy, eosinophilic changes, nuclear abnormalities, nodule formation, lymphocytic infiltration, large amounts of gelatinous follicles, fibrosis.
Acute phase changes: early thyroid congestion, edema, follicular cell shedding, glial phagocytosis; thereafter, follicular cell fragments, a small amount of inflammatory cells (such as neutrophils) infiltration, loss of colloid, followed by follicular disintegration, filtration The epithelial cells of the vesicle epithelium are not structured, the glial overflows the follicles, extensive necrosis, nuclear pyknosis, eosinophilic changes in the follicular epithelium, cytoplasm rich and eosinophilic granules, cell size arrangement, staining are inconsistent The size of the nucleus is different. It often has nuclear hypertrophy, deep staining and deformity. It should be differentiated from cancer cells. Radiation may damage connective tissue. Some follicles become smaller. They are small follicles without glia. In a few cases, there may be thyroid. Nodule or adenoma formation may be caused by hyperplasia of thyroid tissue that is still proliferative after radioactive iodine damage. Small blood vessels dilate, blood vessel wall thickens, may have cellulose-like changes, and may also have thrombosis, interstitial Or mild inflammatory cell infiltration, some cases have lymphoma-like goiter-like structure, interstitial often fibrous tissue hyperplasia, especially between the follicular and interlobular regions, fibrous tissue hyperplasia at any time The increase in growth, and finally the entire thyroid volume is reduced, leaving a small irregular and lack of colloid-like follicles remaining in large fibrous tissue, called post-radiation fibrosis, Kennedy and Thomson believe that follicular epithelium The eosinophilic changes without significant thyroiditis are more specific changes after radiation.
Progression changes: Proliferation gradually stops, the repair process begins, vascular damage continues, follicular and paravascular edema gradually disappear, cell accumulation decreases, acute necrosis is replaced by chronic deformation, follicular cell vacuoles are formed, and nuclear deep staining is reduced , hypertrophy and local hyperplasia appear.
Late changes: thyroid atrophy, hyperplasia, tumor formation or normal.
Prevention
Radioactive thyroiditis prevention
Individuals who have received radiation exposure need to have a systematic, clinical evaluation of thyroid or pituitary function, at least once a year, including symptoms of thyroid dysfunction, such as weight changes, heat resistance, menstrual function, skin or hair changes and physical changes, thyroid Signs of hypofunction or hyperthyroidism, careful palpation of the thyroid gland to assess size, nodules, pericardial or pleural effusion after chest and neck irradiation, arrhythmia or hypercholesterolemia patients should evaluate thyroid function, serum TSH As with FT4 concentrations, asymptomatic individuals should also be examined once a year to diagnose subclinical hypothyroidism.
Complication
Radioactive thyroiditis complications Complications thyroid cancer
1. Radiation hypothyroidism Radiation hypothyroidism refers to thyroid function caused by multiple high-dose exposure or long-term super-equivalent dose limit of whole body irradiation in one or a short period of time (weeks). Low, the principle of treatment:
1 Close observation of the condition, review once a year (disabling radionuclide imaging),
2TSH and elevated blood lipids are given to thyroid preparation replacement therapy,
3 Temporarily out of the ray work, after the recovery can continue to engage in radioactive work.
Clinical hypothyroidism:
1 work off the ray,
2 thyroid preparation replacement and adjuvant treatment, regular review every year,
3 After the recovery, you can continue to work on radiation, and continue to replace the lifelong replacement therapy.
2. Radioactive thyroid benign nodules (radiation benign thyroid nodule) Radioactive thyroid benign nodules refer to nodular lesions induced by irradiation of large doses or long-term super-equivalent dose limits of thyroid tissue.
(1) Working off the ray.
(2) Treatment of thyroid preparations, review once a year (disabling radionuclide imaging).
(3) The cancerous patients are surgically removed and treated according to radioactive thyroid cancer.
Symptom
Radioactive thyroid symptoms common symptoms skin itching, fatigue, palpitation, difficulty swallowing
1.1 to 2 weeks before the thyroid gland received high doses of radiation or 131I treatment of thyroid disease.
2. Neck discomfort, pressure, thyroid local pain, difficulty swallowing, fever, fatigue, palpitation, hand shake and other transient hyperthyroidism, a small number of thyroid crisis, thyroid tenderness, erythema on the skin surface, itchy skin And edema, the clinical severity of radiation thyroiditis is not necessarily related to radiation dose.
Examine
Radioactive thyroiditis
Thyroid absorbing 131I rate is reduced.
Fine needle aspiration cytology.
Diagnosis
Diagnostic identification of radiation thyroiditis
Diagnostic criteria
1. There is a history of ray exposure, and the thyroid dose is above 200Gy.
2. The disease occurs within 2 weeks after the general irradiation line.
3. There is local tenderness and swelling of the thyroid gland.
4. There are symptoms and signs of hyperthyroidism, thyroid crisis can occur in severe cases.
5. Triiodothyronine (T3), elevated serum thyroxine (T4) and thyroglobulin (Tg).
6. Reference indicators Blood routine white blood cell count decreased, erythrocyte sedimentation rate increased, lymphocyte chromosome aberration rate and micronucleus rate increased.
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.
Patients with subclinical hypothyroidism should be followed up for a few months. TSH is measured to determine whether L-T4 is treated. It is recommended to use L-T4 in the subclinical hypothyroidism stage. Other laboratory tests can also help diagnose hyperthyroidism. And thyroiditis, iodine uptake rate, TGAb, TPOAb, TRAb, fine needle aspiration cytology for thyroid nodules, thyroid scan and ultrasound are also used for identification.
