What Is Subacute Thyroiditis?

Subacute thyroiditis, also known as subacute granulomatous thyroiditis, (false) giant cell thyroiditis, non-infective thyroiditis, transitional thyroiditis, viral thyroiditis, DeQuervain thyroiditis, granulomatous thyroiditis, anatomical deconstruction Picture or giant cell thyroiditis, etc., was first reported by DeQuervain in 1904. The disease has gradually increased in recent years, with complicated clinical changes, misdiagnosis and missed diagnosis, and easy recurrence, leading to a decline in health, but most patients can be cured. The disease may be characterized by population onset due to seasonal or viral epidemics.

Basic Information

nickname

Subacute granulomatous thyroiditis, (false) giant cell thyroiditis

English name

subacute thyroiditis

Visiting department

Endocrinology

Multiple groups

Middle-aged women

Common locations

thyroid

Common causes

Related to viral infection

Contagious

no

Causes of subacute thyroiditis

It has not been fully clarified and is generally considered to be related to viral infection. Evidence is that patients have a history of upper respiratory infections before onset, the incidence often changes with the season, and has a certain epidemic.

Viral antibodies are present in the patient's blood (the antibody titer is highly consistent with the disease stage). The most common are Coxsackievirus antibodies, followed by adenovirus antibodies, influenza virus antibodies, and mumps antibodies. Although mumps virus has been isolated from thyroid tissue in patients with subacute thyroiditis, tangible evidence that the cause of subacute thyroiditis is the virus has not been found.

In addition, Chinese and Japanese subacute thyroiditis are related to HLA-Bw35, suggesting that there is a genetic factor for the susceptibility to the virus, but there are patients who are not related to the above HLA-Bw35.

Clinical manifestations of subacute thyroiditis

More common in middle-aged women. The incidence is seasonal, such as the peak in summer. Patients often have upper respiratory tract infections at the onset. Onset of virus infection 1 to 3 weeks, the typical disease period can be divided into early stage with hyperthyroidism, middle stage with hypothyroidism, and the third stage of recovery.

Early

Onset is rapid and feverish, accompanied by fear of cold, chills, fatigue, and loss of appetite. The most characteristic manifestation is pain and tenderness in the thyroid area, which is often radiated to the submandibular, behind the ear or neck, etc. The pain worsens the range of thyroid lesions during chewing and swallowing. To another leaf, or always limited to one leaf. The diseased glands are swollen, hard, and tender. When the lesions are extensive, intravesicular thyroid hormones and non-hormonal iodinated proteins are temporarily released into the blood in large quantities, so in addition to the general manifestations of infections, they can also be accompanied by common manifestations of hyperthyroidism.

Mid-term

When the thyroid hormones in the thyroid acinar are depleted due to infection and destruction, and the thyroid parenchymal cells are not repaired, the serum thyroid hormone concentration can be reduced to hypothyroidism level, and clinically, it can be transformed into hypothyroidism.

3. Recovery period

Symptoms gradually improved, goiter or nodules gradually disappeared, and in many cases, the remaining small nodules were slowly absorbed. If treatment is prompt, most patients can fully recover, and very few patients become permanent hypothyroidism.

In mild or atypical cases, the thyroid gland is only slightly enlarged, pain and tenderness are mild, fever is not high, systemic symptoms are mild, and clinical signs of hyperthyroidism or hypothyroidism may not be present. The duration of the disease varies from several weeks to more than half a year, usually about 2 to 3 months, so it is called subacute thyroiditis. After remission, relapse may still occur.

Subacute thyroiditis

Subacute thyroiditis should be drawn for blood sedimentation, blood routine, total T ₃ , total T ₄ , free T ₃ , free T ₄ , TSH, thyroglobulin antibody (TRAb), thyroid peroxidase antibody (TPO), B-ultrasound, thyroid iodine uptake and thyroid radionuclide scans were performed. White blood cell count and neutrophils are normal or high, red blood cell sedimentation rate increases, often> 50mm / h, serum protein bound iodine or serum T ₃ , T ₄ , FT ₃ and FT ₄ concentrations increase, and thyroid iodine uptake decreases Scanning of the thyroid showed thyroid enlargement, but the image was unevenly developed or incomplete, and some were completely undeveloped. Protein electrophoresis showed a decrease in albumin and an increase in globulin, mainly an increase in r and 1 globulin.

Subacute thyroiditis diagnosis

1. Systemic symptoms such as acute onset and fever;

2. Thyroid pain, swelling and stiffness;

3. ESR significantly increased;

4. Two-way separation of elevated serum thyroid hormone concentration and decreased thyroid iodine uptake rate can diagnose the disease.

If the patient has a fever, a goiter accompanied by single or multiple nodules in a short period of time, the touch is hard and marked tenderness, and the clinical diagnosis of this disease may be preliminary. Laboratory tests showed increased erythrocyte sedimentation and normal or slightly elevated white blood cells. Blood T ₃ and T ₄ increase, while blood TSH decreases, and the iodine measurement rate can be reduced to less than 5% to 10%. This feature is of great significance for the diagnosis of this disease. Blood thyroid immunoglobulin is also elevated in the early stage, and it returns to normal later than thyroid hormone. Ultrasound examination is a better method to diagnose and judge its active period. Low-density lesions often appear on the tenderness of ultrasound imaging. Cytocentesis or tissue biopsy can confirm the presence of megakaryocytes.

Differential diagnosis of subacute thyroiditis

Subacute thyroiditis needs to be distinguished from acute bleeding of thyroid nodules, acute onset silent or painless thyroiditis of chronic lymphocytic thyroiditis, and acute purulent thyroiditis. It is not difficult to identify when the bleeding from multiple nodular goiters reaches the nodule, because at this time you can touch the nodules on the thyroid; if the bleeding is to a single thyroid nodule, it is more difficult to identify. In this type of hemorrhage, the function of thyroid tissue other than the lesion still exists, and the erythrocyte sedimentation rate is rarely increased. The acute onset of chronic lymphocytic thyroiditis can be accompanied by thyroid pain and tenderness, but the glands are mostly widely invaded, and most of the blood's antithyroid antibodies are elevated. Patients with hyperthyroidism need to be distinguished from toxic diffuse goiter. However, the latter has an increased rate of ¹³¹ iodine uptake, painless thyroiditis with hyperthyroidism, and a decreasing rate of radioactive iodine uptake. The pathology shows chronic Thyroiditis, which is often referred to as high-functioning thyroiditis without the presence of giant cells, is difficult to distinguish from painless thyroiditis. The erythrocyte sedimentation rate does not increase during the test, and antithyroid antibodies are significantly increased. . It can be seen that there are sepsis lesions in other parts of the body, there is a significant infection reaction in the adjacent tissues of the thyroid, leukocytes are significantly increased, and there is a fever reaction. The radioiodine uptake function of acute purulent thyroiditis still exists, and subacute thyroiditis rarely needs to be distinguished from thyroid cancer where the thyroid is widely involved, because the clinical and laboratory examinations of the two are very different.

Subacute thyroiditis treatment

There are several treatment options for subacute thyroiditis, including thioureas, thyroid-stimulating hormones, and inhibitory amounts of thyroid hormones. The evidence that the use of these drugs affects the disease process is not yet conclusive.

Treatment includes two aspects: reducing local symptoms and targeting the effects of thyroid dysfunction. Generally speaking, most patients can only treat symptomatically. Use aspirin or other analgesics for mild cases. Symptoms can be controlled by using paracetamol or salicylate; in severe cases, such as pain and fever, other non-steroidal anti-inflammatory drugs can be used for a short time, or glucocorticoids such as prednisone can be used quickly Relieve clinical manifestations, about 5% of patients need to use corticosteroids to reduce symptoms, continue to take medicine for 1 to 2 weeks or even 4 to 8 weeks after reducing the dose, sharing for 6 to 8 weeks. If the patient does not respond to prednisone for 24 to 48 hours, the diagnosis of subacute thyroiditis should be reassessed. Changes in blood sedimentation during treatment can guide medication such as the need for the disease. Restarting prednisone is still effective, but corticosteroids will not affect the natural course of the disease. Fast, but it will make the condition worse. It has also been suggested that if glucocorticoids are continuously used, the dose is used so that the patients do not show symptoms until their radioactive iodine uptake rate returns to normal, which may avoid relapses. Patients with hyperthyroidism are generally not treated with antithyroid drugs. Non-specific drugs, such as propranolol, an oral blocker. Hyperthyroidism with this disease is temporary, and low thyroid iodine uptake is not an indication for radioiodine treatment. These drugs disrupt the synthesis of thyroid hormones, but the excess thyroid hormones in subacute thyroiditis are due to T ₄ and T ₃ leaked from the damaged follicles, not due to increased synthesis and secretion, without the need for sulfur Urea antithyroid drugs. The hypothyroidism of this disease is often temporary, and usually there are not many symptoms of hypothyroidism, so thyroid hormone replacement therapy is not needed. At this time, increased TSH secretion is important for the recovery of thyroid function. Unless the patient has hypothyroidism, thyroid hormone therapy should be contraindicated. Those with mild hypothyroidism need not deal with it. However, some people have suggested that when there is hypothyroidism, thyroid preparations such as L-type sodium thyroxine can be used to prevent the disease from being aggravated by elevated TSH. In severe cases, thyroid hormone can be used for a period of time. About 10% of patients can have permanent hypothyroidism, and long-term thyroid replacement therapy is required. Traditional Chinese medicine is said to have a better effect on the acute stage of the disease.