eMedicine Specialties > Endocrinology > Thyroid

Thyroiditis, Subacute

Author: Mark R Allee, MD, Assistant Professor, Department of Medicine, University of Oklahoma Health Sciences Center
Coauthor(s): Mary Zoe Baker, MD, Professor, Department of Medicine, Section of Endocrinology, Metabolism and Hypertension, University of Oklahoma; Medical Director, University of Oklahoma Physicians, Medicine Specialty Clinic, General Medicine Clinic and Medicine Residents' Clinic
Contributor Information and Disclosures

Updated: Feb 7, 2007

Introduction

Background

Thyroiditis refers to inflammation of the thyroid gland. Subacute thyroiditis (SAT) is a self-limited condition characterized by a triphasic course of hyperthyroidism followed by hypothyroidism and ending with euthyroidism. Subacute thyroiditis may account for 15-20% of thyrotoxicosis presentations and 10% of hypothyroidism presentations. The thyrotoxicosis results from release of preformed thyroid hormone. This phase lasts 4-10 weeks. The disease undergoes remission in 2-4 months. At this time, the thyroid is depleted of colloid and is now incapable of producing thyroid hormone, resulting in hypothyroidism. The hypothyroidism may be mild and not requiring any therapy. As the follicles regenerate, the euthyroid state is restored. Up to 95% of patients return to this normal thyroid state. 

The term subacute thyroiditis (SAT) conventionally has been used interchangeably with subacute granulomatous (de Quervain) thyroiditis, which was the first syndrome described as causing inflammation and release of preformed hormone from the gland.

Pathophysiology

Subacute thyroiditis has been thought to have viral origins. Most patients have a history of an upper respiratory infection 2-8 weeks prior to the onset of thyroiditis. Therefore, more cases occur in the summer. The search for a viral cause is often unrewarding. A few cases appear to be associated with the mumps virus. High titers of mumps antibodies have been found in some patients with subacute thyroiditis, and, occasionally, parotitis or orchitis is associated with thyroiditis. The mumps virus has been cultured directly from thyroid tissue involved with subacute thyroiditis. The disease has also been reported in association with other viral conditions, including measles, influenza, adenovirus, infectious mononucleosis, myocarditis, cat scratch fever, and coxsackievirus. 

Numerous attempts to culture viruses from cases not associated with mumps have failed. However, viral antibody titers to common respiratory tract pathogens often are elevated in these patients. Because the titers fall promptly and multiple viral antibodies may appear in the same patient, the elevation probably is an anamnestic response to the inflammatory condition.

An autoimmune reaction is unlikely. During the illness, the development of cell-mediated immunity against various thyroid cell particulate fractions or crude antigens appears to be related to the release of these materials during tissue destruction. Data on the mechanism of inflammation and the pathogenesis of subacute thyroiditis at the cellular level are sparse.

The role of growth factors has received some attention. In the granulomatous stage of subacute thyroiditis, growth factor–rich monocytes and/or macrophages infiltrating into follicle lumina are thought to trigger the granulomatous reaction, and vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), and transforming growth factor beta 1 (TGF-β1) produced by the stromal cells probably mediate the reaction. In the regenerative phase, endothelial growth factor (EGF) mediates follicle regeneration through its mitogenic effect on thyrocytes, along with cofactors. In addition, the decreased expression of TGF-β1, a fibrogenic factor, contributes to thyroid tissue repair. VEGF and bFGF may be responsible for angiogenesis in both stages.

Frequency

United States

Subacute thyroiditis is uncommon. The reported incidence is 1 case in 10,000. The presence of the HLA-Bw35 haplotype confers a greater predilection for subacute thyroiditis by 6-fold, when compared to the general population.

Sex

A female preponderance exists, with a female-to-male ratio of 3-5:1.

Age

The disease has been reported in persons of all ages. Subacute thyroiditis is more common between the third and fifth decades of life. It is uncommon in childhood.

Clinical

History

• Pain is the predominant symptom. While the pain may be limited to the region of the thyroid, it may also involve the upper neck, throat, jaw or ears.  Some patients may first consult an otolaryngologist. The pain may be so severe that the patient cannot tolerate palpation of the neck.  The pain is most commonly bilateral.  Occasionally, the pain may be unilateral, beginning in one lobe and spreading to the opposite side (creeping thyroiditis). Coughing, swallowing, or even tightening a necktie aggravates pain.
• Systemic symptoms, including fatigue, malaise, and myalgia, are common. Fever (up to 104ºF) may also be present.
• Thyrotoxic symptoms may be absent, mild, or moderate but rarely are severe. Up to 50% of the patients present with hyperthyroidism. Patients may complain of nervousness, heat intolerance, palpitations, tremulousness, and increased sweating.

Physical

• The thyroid is mildly to moderately enlarged, usually 2-3 times its normal size. It is exquisitely tender to palpation.
• Rarely, the patient may present with a solitary nodule and tenderness.
• The gland is firm to hard in consistency. The swelling is diffuse and involves the entire gland but may involve one lobe.
• The presentation of hyperthyroidism may manifest with fever, tachycardia, and hyperreflexia.
• Orbitopathy and dermopathy, which are characteristic of Graves disease, are absent.

Causes

While most cases of subacute thyroiditis are secondary to a viral illness, other causes of subacute thyroiditis (SAT) exist and include the following:

• Subacute thyroiditis has been described in patients receiving interferon-alpha for chronic hepatitis.
• Radioiodine therapy for Graves disease can result in transient thyroidal inflammation, causing thyroiditis.
• Subacute thyroiditis also has been described following external radiation to the neck.
• Subacute thyroiditis has presented as a paraneoplastic manifestation of renal cell carcinoma.
• An association between subacute thyroiditis and febrile neutrophilic dermatoses (Sweet syndrome) has been reported.
• Concurrence of giant cell arteritis has been reported in patients with classic de Quervain thyroiditis.
• Subacute thyroiditis has been described after bone marrow transplantation for chronic granulocytic leukemia.
• Amiodarone may produce a painful thyroiditis with thyrotoxicosis.² While the major cause of amiodarone-induced thyrotoxicosis is iodine overload in a gland with underlying abnormalities, a direct toxic effect is observed in some patients.

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