Subacute thyroiditis, also known as granulomatous thyroiditis, giant cell thyroiditis and de Quervain’s thyroiditis, is a self-limiting (curable) thyroiditis associated with viral infection, often preceded by an upper respiratory tract infection and usually without residual hypothyroidism. There is a tendency for seasonal onset, male to female ratio: 1:3-6, with women aged 40 to 50 years being the most common.
Etiology and pathology
The onset of subacute thyroiditis is associated with viral infections, such as influenza virus, coxsackievirus and mumps virus infections. These viruses can be found in the patient’s thyroid tissue or in patients with increased titers of antibodies to these viruses in the serum. In about 10-20% of cases, serum thyroid autoantibody titers increase during the subacute phase of the disease and disappear after remission of the disease, presumably associated with thyroid autoantibody production induced by thyroiditis. Patients with this disease may have a viral susceptibility genome and are therefore susceptible to the disease. The onset is transient and only rarely eventually progresses to permanent hypothyroidism.
The pathology of the disease is mainly the destruction of the thyroid follicular epithelium and the loss of follicular integrity. The general presentation is a hard, pale lesion that lacks boundaries with the normal thyroid gland. The characteristic histological features are a central nucleus of follicular glia surrounded by polymorphonuclear giant cells and follicular changes leading to granulomas.
Clinical manifestations
1, symptoms: 1 to 3 weeks before the onset of the disease often have symptoms of viral pharyngitis, mumps, measles or other viral infections. The typical manifestation is obvious pain in the anterior neck area (thyroid area), which can radiate to the ear area and worsen when swallowing. Rarely, the pain may be absent. It may be accompanied by general malaise, lethargy, fever, palpitations, excessive sweating, and neurosis.
Physical examination: The thyroid gland can be found to be enlarged, sometimes more obvious on one side, hard to palpate and painful to touch. Some patients may have palpable enlarged cervical lymph nodes.
Laboratory tests]
According to the results of laboratory tests on thyroid function, subacute thyroiditis can be divided into three stages: the hyperthyroid phase (hyperthyroidism), the hypothyroid phase (hypothyroidism) and the recovery phase (recovery) of thyroid function.
1. Hyperthyroid phase: Blood sedimentation is accelerated and can be >100mm/hour. Serum T3 and T4 levels are increased and TSH levels are decreased. Decreased thyroid iodine uptake rate (<2% in 24 hours).
This is a characteristic “separation” between serum thyroid hormone levels and the iodine uptake capacity of the thyroid gland in subacute thyroiditis, which occurs when the thyroid follicles are destroyed by inflammation and the stored thyroid hormones are released into the bloodstream, resulting in “destructive thyrotoxicosis “At this time, the thyroid follicular cells are destroyed and iodine uptake capacity is significantly reduced.
2. Hypothyroidism stage: Serum T3 and T4 levels drop below normal levels, while TSH levels rise back above normal. The iodine uptake rate of the thyroid gland is gradually restored.
The reason is that all thyroid hormones stored in the thyroid gland have been released and the thyroid follicular cells are recovering and have not yet fully recovered their normal thyroid function.
3. Recovery period: Serum T3, T4, TSH levels and thyroid iodine uptake rate return to normal.
Diagnosis and differential diagnosis
Diagnosis based on.
1. systemic manifestations of acute inflammation.
2. enlargement, hardness and pressure pain of the thyroid gland.
3. Laboratory tests for the above three manifestations (varying with the time of consultation and duration of the disease).
Subacute thyroiditis needs to be differentiated from acute hemorrhage of thyroid nodules, acute onset of Hashimoto’s thyroiditis, and painless thyroiditis.
[Treatment].
Subacute thyroiditis is a self-limiting disease with a good prognosis. There is no specific treatment for this disease. Treatment consists of two aspects: reducing local symptoms and targeting abnormal thyroid function.
In mild cases, only non-steroidal anti-inflammatory drugs, such as aspirin, indomethacin, and ibuprofen, should be used. Glucocorticoids are indicated for those with severe pain, persistently elevated body temperature, and ineffective treatment with NSAIDs, which can rapidly relieve pain and reduce symptoms of thyrotoxicosis. Generally, the initial prednisone is 20-40mg per day, divided into three doses, and then gradually reduced to discontinued after 1-2 weeks according to the improvement of the disease, with a total treatment course of 6-8 weeks. The total duration of treatment is 6-8 weeks. Rapid dose reduction and premature discontinuation may lead to recurrence of the disease.
For thyrotoxicosis, Genericol can be given. In the presence of transient hypothyroidism, levothyroxine replacement therapy may be given as appropriate.
A small number of patients can relapse and treatment remains the same as above.
Prevention
Strengthening the body’s immunity and avoiding upper respiratory tract infections and pharyngitis are important in preventing the occurrence of subacute thyroiditis.