subacute thyroiditis
Summary
Subacute thyroiditis (de Quervain, granulomatous, or subacute granulomatous thyroiditis) is a self-limited, post-viral inflammatory thyroid disease presenting with a painful, tender thyroid, elevated ESR, and transient thyrotoxicosis with LOW radioactive iodine uptake. It typically follows hyperthyroid → hypothyroid → euthyroid phases and is treated with NSAIDs (or prednisone if severe) plus beta-blockers for symptoms.
Detail
**Etiology/Pathophysiology:** Thought to be triggered by a viral infection (e.g., coxsackievirus, mumps, adenovirus, influenza) or post-viral inflammatory process, often preceded by an upper respiratory infection. Associated with HLA-B35. Most common in women aged 30-50. Viral-induced destruction of thyroid follicles causes release of preformed thyroid hormone (T4/T3) into the circulation, leading to thyrotoxicosis (NOT increased synthesis). TSH suppression then reduces iodine uptake.
**Histology:** Granulomatous inflammation with multinucleated giant cells, disruption of follicles, and lymphocyte/neutrophil infiltrate, followed by fibrosis. Minimal fibrosis compared with Riedel thyroiditis.
**Clinical course (4 phases):** 1. Thyrotoxic phase (weeks 2-6): painful, tender, firm, enlarged thyroid; pain may radiate to the jaw/ear; fever, malaise, palpitations, tremor, heat intolerance. 2. Hypothyroid phase (weeks to a few months): transient, as follicular stores are depleted. 3. Recovery/euthyroid phase. 4. Most patients (~90%) return to euthyroid; a minority develop permanent hypothyroidism.
**Labs/Diagnosis:** - Elevated ESR and CRP (markedly elevated ESR is classic). - Early: increased T4/T3, suppressed TSH. - LOW radioactive iodine uptake (RAIU) on scan (key discriminator from Graves disease, which shows high, diffuse uptake). - Thyroglobulin elevated; anti-TPO/TRAb typically negative or low titer (no TSH receptor antibodies). - Mild leukocytosis and mild anemia may occur.
**Management:** - Supportive: NSAIDs/aspirin for pain and inflammation. - Glucocorticoids (prednisone) for severe pain or if NSAIDs fail; rapid response supports diagnosis. - Beta-blockers (propranolol) for adrenergic symptoms of thyrotoxicosis. - Antithyroid drugs (methimazole, PTU) are NOT indicated since hormone synthesis is not increased. - Levothyroxine only if symptomatic hypothyroidism develops (often temporary).
**Differential/High-yield comparisons:** - Graves disease: painless, high RAIU, TRAb positive, exophthalmos, pretibial myxedema. - Hashimoto thyroiditis: painless, anti-TPO/antithyroglobulin antibodies, Hürthle cells, lymphocytic infiltrate with germinal centers; HLA-DR5; risk of B-cell (MALT) lymphoma. - Painless (silent/lymphocytic) thyroiditis and postpartum thyroiditis: painless, low RAIU, normal ESR, anti-TPO often positive. - Riedel thyroiditis: rock-hard, fixed "woody" thyroid due to fibrosis extending into neck structures; IgG4-related; may cause compressive symptoms. - Acute suppurative thyroiditis: bacterial infection with fever, erythema, abscess; usually normal thyroid function and normal RAIU; associated with pyriform sinus fistula (4th branchial pouch anomaly), most commonly left-sided. - Thyrotoxicosis factitia: low RAIU, low thyroglobulin. - Amiodarone-induced thyroiditis, and exogenous hormone use also cause low RAIU thyrotoxicosis.
**Pearls:** Painful thyroid + high ESR + low RAIU + thyrotoxicosis = de Quervain. Self-limited, usually resolves in 2-6 months; recurrence is uncommon.
Sources
- First Aid for the USMLE Step 1 (Endocrine chapter)
- Robbins & Cotran Pathologic Basis of Disease (Thyroid chapter)
- Harrison's Principles of Internal Medicine (Disorders of the Thyroid Gland)
- UpToDate: Subacute thyroiditis
- 2016 ATA Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis
- Pathoma (Endocrine chapter)
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