bubble_chart Overview

Subacute thyroiditis, also known as de Quervain's thyroiditis, granulomatous thyroiditis, or giant cell thyroiditis.

bubble_chart Etiology

It has not yet been fully elucidated, but it is generally believed to be related to viral infection. The evidence includes:

1. Patients often have a history of upper respiratory tract infection before the onset of the disease, and the onset often varies with the seasons and exhibits a certain degree of epidemicity.

2. Viral antibodies are present in the blood of patients (the titer of the antibodies corresponds to the disease stage), with the most common being Coxsackie virus antibodies, followed by adenovirus antibodies, influenza virus antibodies, mumps virus antibodies, etc. Although there have been reports of isolating mumps virus from the thyroid tissue of patients with subacute thyroiditis, definitive evidence that the cause of subacute thyroiditis is viral has not yet been found.

Additionally, subacute thyroiditis in Chinese and Japanese individuals is associated with HLA-Bw35, suggesting a genetic predisposition to viral susceptibility. However, some patients are not linked to the aforementioned HLA-Bw35.

bubble_chart Pathological Changes

The thyroid gland is enlarged with a firm texture. The cut surface still shows translucent colloid with scattered gray lesions. Microscopically, the affected thyroid follicles are replaced by granulomatous tissue, containing numerous chronic inflammatory cells, histiocytes, and giant cells that have phagocytosed colloid particles. The lesion resembles subcutaneous nodules, hence it is referred to as granulomatous or giant cell thyroiditis.

bubble_chart Clinical Manifestations

It is commonly seen in middle-aged women. The onset has a seasonal pattern, with summer being the peak period. Patients often have an upper respiratory tract infection at the onset. Typically, the entire course of the disease can be divided into an early stage with hyperthyroidism, an intermediate stage [second stage] with hypothyroidism, and a stage of convalescence or late stage [third stage].

(1) Early Stage: The onset is usually abrupt, presenting with fever accompanied by chills, shivering, fatigue, and loss of appetite. The most characteristic manifestation is pain and tenderness in the thyroid area, often radiating to the jaw, behind the ears, or the neck, with aggravated pain during chewing and swallowing. The extent of thyroid involvement varies—it may start in one lobe and later expand or shift to the other lobe, or remain confined to one lobe. The affected gland is swollen, firm, and markedly tender. When the lesion is extensive, thyroid hormones and non-hormonal iodinated proteins in the follicles are transiently released into the bloodstream in large quantities, leading to common manifestations of hyperthyroidism in addition to general signs of infection.

(2) Intermediate Stage [Second Stage]: When thyroid hormones in the follicles are depleted due to infection-induced destruction and the thyroid parenchymal cells have not yet repaired, serum thyroid hormone levels may drop to hypothyroid levels, and clinical manifestations may shift to hypothyroidism.

(3) Stage of Convalescence: Symptoms gradually improve, and thyroid swelling or nodules gradually disappear. However, in many cases, small nodules may remain and slowly resolve. If treated promptly, most patients can fully recover, with very few progressing to permanent hypothyroidism.

In mild or atypical cases, the thyroid may only be slightly enlarged, with mild pain and tenderness, no fever, and minimal systemic symptoms. Clinically, there may be no obvious signs of hyperthyroidism or hypothyroidism. The duration of the disease varies, ranging from a few weeks to over half a year, typically around 2–3 months, hence the name subacute thyroiditis. After remission, the condition may recur.

bubble_chart Diagnosis

If the patient has fever, accompanied by short-term thyroid enlargement with single or multiple nodules that are hard to the touch and significantly tender, the disease can be preliminarily diagnosed clinically. Laboratory tests in the early stage show increased erythrocyte sedimentation rate, and normal or decreased white blood cell count. Blood T₃ and T₄ levels are elevated, while blood TSH is decreased. The iodine uptake rate may drop below 5–10%, a feature that is of significant importance for diagnosing this disease. Blood thyroid immunoglobulin levels are also elevated in the initial stage [first stage], and their return to normal occurs later than that of thyroid hormones. Ultrasound examination is a good diagnostic method for determining the active phase of the disease. Ultrasound imaging often shows low-density lesions in tender areas. Fine-needle aspiration or tissue biopsy can confirm the presence of giant cells.

bubble_chart Treatment Measures

Adrenal glucocorticoids have a significant effect on this disease, often rapidly relieving fever and thyroid pain within 1 to 2 days of medication, with the thyroid usually shrinking noticeably after one week. Initially, prednisone can be administered at 10mg, 3 to 4 times daily for 1 to 2 weeks, followed by a gradual reduction of 5mg per day each week, with the entire course lasting 1 to 2 months. If recurrence occurs after discontinuation, prednisone can be used again, and thyroid tablets may be added, especially for those with hypothyroidism, at a dosage of 40 to 120mg daily, tapering off gradually after several months. Analgesic and antipyretic drugs such as indomethacin are also effective for this condition.