Description
De Quervain’s thyroiditis, also known as subacute granulomatous thyroiditis or giant cell thyroiditis, is a self-limiting inflammatory condition of the thyroid gland characterised by neck pain, swelling, and systemic symptoms. It is believed to be caused by a viral infection, though the exact etiology is unknown.
Pathogenesis
De Quervain’s thyroiditis is presumed to have a viral etiology, although the exact pathophysiology remains largely indeterminate. The viral insult triggers an inflammatory response in the thyroid gland, resulting in follicular cell necrosis and consequent leakage of preformed thyroid hormones into the circulation. This pathologic cascade results in a transient thyrotoxic phase (hyperthyroidism).
As the disease progresses, the depleted storage of thyroid hormones leads to a hypothyroid phase, which is typically transient. However, in a minority of patients, this may progress to become permanent. As the inflammation subsides, the thyroid gland usually recovers and resumes normal thyroid hormone production. This is often the final stage of the disease process, leading to the restoration of euthyroid status.
Epidemiology, Risk Factors & Associations
- Predominantly affects middle-aged women (female-to-male ratio about 5:1).
- Presumed viral aetiology as often follows an upper respiratory tract infection and exhibits seasonal variation.
- Geographic variation has been observed, with higher incidence rates in certain regions.
Clinical Features
- Painful, tender goitre usually extending to the jaw or ears.
- Systemic symptoms such as fatigue, malaise, anorexia, and weight loss.
- Fever may be present.
- Transient hyperthyroidism symptoms may be observed early in the disease process, including palpitations, nervousness, and heat intolerance.
Complications
- Transient hyperthyroidism: Due to the release of preformed thyroid hormone.
- Transient hypothyroidism: Occurs later in the course of the disease, as the thyroid hormone stores become depleted.
- Permanent hypothyroidism: Rare but can occur.
Pathological Features
Histopathology
- Disruption of the follicular architecture with extensive infiltration by inflammatory cells, including numerous multinucleated giant cells.
- Occasional granuloma formation.
- Variable degrees of fibrosis.
Serology
- Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).
- Early thyrotoxic phase is associated with low TSH and high free T4 and T3 levels.
- Hypothyroid phase is characterised by elevated TSH and low free T4.
Radiological Features
US
- Diffuse decrease in echogenicity or focal hypoechoic regions.
- Decreased vascularity on Doppler.
NM
- Thyroid uptake on technetium or iodine scan is usually decreased or absent, differentiating it from Graves’ disease.
Diagnosis
Diagnosis is primarily clinical and is supported by laboratory findings such as elevated ESR, and low radioiodine uptake in the setting of hyperthyroidism.
Differential Diagnosis
- Graves’ disease: Presents with similar clinical features, but usually with diffusely increased radioiodine uptake.
- Thyroid carcinoma: Presents with a thyroid mass, but usually without pain unless there is rapid growth or hemorrhage.
- Hashimoto’s thyroiditis: Chronic thyroiditis, usually painless.
Management
- Symptomatic treatment with NSAIDs or corticosteroids for severe symptoms.
- Beta-blockers for thyrotoxic symptoms.
- Thyroid hormone replacement in hypothyroid phase if symptoms are severe.
- Regular monitoring of thyroid function tests to identify and manage transient hyperthyroidism or hypothyroidism.