Overview of Radiation Thyroiditis
Radiation thyroiditis is the result of varying degrees of inflammatory changes in the thyroid gland due to ionizing radiation and causes different changes in thyroid function with corresponding clinical symptoms. These changes are related to the dose and type of radiation, the duration of exposure, and individual differences such as age, gender, and genetics. Hypothyroidism is the most common manifestation of direct thyroid irradiation injury. Radiation thyroiditis can present with hyperthyroidism, hypothyroidism, and a painful sensation in the thyroid gland. High doses of ionizing radiation to the thyroid gland in childhood can lead to thyroid nodules and thyroid tumors, with papillary and follicular carcinomas being the most common.
Etiology
Radiation thyroiditis is divided into external and internal irradiation. External irradiation refers to thyroiditis caused by X-ray radiation treatment of neck lesions; internal irradiation history refers to thyroiditis manifested when radioactive iodine is used to treat hyperthyroidism.
Ionizing radiation can cause different changes in the human thyroid gland. The incidence of benign and malignant tumors is significantly increased with low-dose irradiation, whereas changes in thyroid function and thyroiditis are more common with higher-dose irradiation A history of neck X-ray irradiation in childhood for the treatment of acne or enlarged tonsils is a risk factor for the development of papillary carcinoma of the thyroid gland in adults, and the treatment of neck X-ray irradiation is now banned.
Symptoms
1. high dose radiation to the thyroid gland or iodine 131 treatment for thyroid disease 1 to 2 weeks ago.
2. Neck discomfort, pressure sensation, localized pain in the thyroid gland, difficulty in swallowing, fever, malaise, panic, hand tremor and other manifestations of transient hyperthyroidism. Thyroid gland tenderness is obvious, skin surface erythema, skin itching and edema. The clinical severity of radiogenic thyroiditis does not necessarily correlate with the radiation dose.
Radiation-induced thyroiditis occurs 4 to 12 weeks after treatment, unlike acute radiation reaction, which occurs one week after treatment and manifests as neck pain, erythema, and edema. Radiation thyroiditis is a longer process, delayed for several weeks, with thyroid hormone release, mild hyperthyroidism manifestation, and no iodine uptake by the thyroid gland in the hyperthyroid phase. Hypothyroidism occurs in 40% of patients receiving external neck radiation after 2 years. Patients with autoimmune thyroiditis are more likely to develop hypothyroidism after external irradiation.
Excessive radioiodine therapy for hyperthyroidism or thyroid tumors can cause acute painful swelling of the thyroid gland and discomfort in the salivary glands, most of which resolve within a few days. A complication of chronic radioiodine is permanent hypothyroidism requiring lifelong thyroxine replacement therapy.
Examination
The iodine 131-affected thyroid gland has a smear consisting of follicular cells, large amounts of colloid, fibrovascular stroma, and lymphocytes, in addition to the typical findings of nodular goiter and chronic lymphocytic thyroiditis. The follicular cells are mainly in loose monolayer clumps, occasionally forming tiny follicles with markedly unequal nuclear sizes and pleomorphism, and a large number of bulky but atypical follicular cells, mainly single or clumped and with a fibrovascular stroma intermixed with blood vessels, which are characterized by coarse nuclear chromatin, occasional marked nucleoli, absence of nuclear grooves and intranuclear inclusions, a slight increase in the nuclear/plasma ratio, and an abundance of cytoplasm, many of which are huge and show naked nuclei The smear can therefore be misdiagnosed as undifferentiated carcinoma. Pathology of surgical specimens confirms that all glandular structures are destroyed by nodule formation, lymphocytic infiltration, fibrosis, follicular atrophy, and marked polymorphism of follicular cells.
Diagnosis.
Radiation thyroiditis is an autoimmune thyroid injury resulting from multiple or prolonged radiation exposure of the thyroid gland at one time or over a short period of time (weeks).
1. history of radiation exposure with a thyroid dose of 0.3 grams or more.
3. enlarged thyroid gland, mostly without tenderness.
4. Positive thyroid microsomal antibodies (Tm-Ab) and thyroglobulin antibodies (Tg-Ab), and increased thyroid-stimulating hormone (TSH).
5. May be accompanied by hypothyroidism.
Complications
1. Radiation hypothyroidism
Radioactive hypothyroidism refers to hypothyroidism caused by a single localized or multiple high-dose irradiation of the thyroid gland within a short period of time (several weeks), or systemic irradiation that exceeds the equivalent dose limit for a long period of time. Treatment principles:
(1) Closely observe the condition and review once a year (nuclide imaging is prohibited).
(2) If TSH and blood lipids are persistently elevated, thyroid preparations should be given as replacement therapy.
(3) Temporarily disengage from radiation work, and continue to engage in radioactive work after recovery.
2. Radioactive benign thyroid nodules
Radioactive benign thyroid nodules refer to nodular lesions induced by irradiation of thyroid tissues with high dose or long-term over-equivalent dose limit:
(1) Disengage from radiation work.
(2) Treatment with thyroid preparations and yearly reexamination (nuclear imaging is prohibited).
(3) Surgical excision of cancerous lesions should be treated as radioactive thyroid cancer.
Treatment
1. Immediately disengage from the radioactive source and stop the treatment with nuclide. Generally, the symptoms can be relieved after a few days.
2. Mild aseptic thyroiditis may occur 2-3 weeks after radioactive iodine administration, and the symptoms may subside in about 1 week without treatment or simple analgesic. High-dose radioactive iodine treatment causes excessive release of thyroid hormones in the form of transient exacerbation of hyperthyroidism, often due to inadequate preparation before treatment, should be symptomatic treatment, with severe symptoms, sedation, analgesia, and adrenal cortical steroid hormone therapy. β-blocking drugs such as propranolol can be used to advocate the use of antithyroid medication, the disease is often self-limiting. Amiodarone propionate combined with beta-blockers treats severe destructive-induced thyrotoxicosis by inhibiting 5-deiodinase reducing blood T3 attenuating the peripheral effects of thyroid hormones.
3. Tracheotomy is required in the presence of severe laryngeal edema.
4. Disconnect from radiation, review once a year (prohibit nuclear imaging), surgical resection for cancerous lesions, and treat as radiological thyroid cancer.
Prognosis
Immediately detach from the radiation source and stop the treatment with nuclide, usually the symptoms can be relieved after a few days.