Painless thyroiditis
Painless (silent) thyroiditis is a self-limited destructive thyroiditis, usually arising in patients with underlying autoimmune thyroid disease, that releases preformed hormone in a triphasic pattern of thyrotoxicosis, hypothyroidism, and recovery without a tender gland. Treatment is symptomatic, with a beta-blocker for the thyrotoxic phase and temporary levothyroxine for a symptomatic hypothyroid phase, because thionamides and radioactive iodine have no role.
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What this article covers
- Overview
A destructive, not overproductive, thyrotoxicosis: painless (silent) thyroiditis releases preformed thyroid hormone from inflamed follicles rather than increasing hormone synthesis, so it behaves…
- Epidemiology
A recognized cause of destructive thyroiditis: painless thyroiditis is grouped with postpartum and drug-induced thyroiditis as forms of destructive, low-uptake thyrotoxicosis.
- Risk factors
Preexisting thyroid autoimmunity: TPO antibody positivity or known Hashimoto thyroiditis is the strongest identifiable risk factor.
- Pathophysiology
Lymphocytic infiltration without granuloma formation: the histology resembles Hashimoto thyroiditis, with lymphocytic infiltration of the gland, but without the giant cells and granulomas of subacute granulomatous thyroiditis.
- Clinical features
Painless, non-tender goiter or normal-sized gland: the defining examination finding that separates this entity from the painful, tender gland of subacute granulomatous thyroiditis.
- Differential diagnosis
Graves disease: thyrotoxicosis with elevated (not suppressed) RAIU, positive TSH receptor antibodies, and often ophthalmopathy, unlike the low-uptake, antibody-negative-for-TRAb pattern of painless thyroiditis.
- Diagnosis
The diagnosis is established by thyrotoxicosis with a suppressed RAIU on thyroid scintigraphy, which confirms a destructive process rather than increased hormone synthesis; a compatible clinical…
- Management
First, treat thyrotoxic-phase symptoms with a beta-blocker: metoprolol tartrate 25 mg to 100 mg PO twice daily, titrated to control palpitations, tremor, and tachycardia.
- Complications
Recurrent episodes: patients who have had one bout of painless thyroiditis carry an increased risk of subsequent episodes.
- Prognosis
Favorable in most patients: the disease is self-limited, with each phase lasting up to 3 months and most patients returning to euthyroidism within about 6 to 9 months of onset.
- Prevention
No primary prevention exists for the idiopathic autoimmune form.
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Related articles
- Hashimoto thyroiditis
Hashimoto thyroiditis is a chronic autoimmune process in which lymphocytic infiltration destroys the thyroid, and is the most common cause of hypothyroidism in iodine-sufficient regions such as the United States. Diagnosis rests on an elevated thyroid-stimulating hormone with a low or normal free thyroxine, and first-line treatment is lifelong levothyroxine replacement dosed to normalize thyroid-stimulating hormone.
- Postpartum thyroiditis
Postpartum thyroiditis is a destructive, painless thyroiditis that occurs in the first year after delivery, typically following the same thyrotoxic-then-hypothyroid-then-recovery course as painless thyroiditis, and permanently affects thyroid function in about 20% of cases. Treatment is symptomatic, with a beta-blocker for thyrotoxic symptoms and levothyroxine for a symptomatic or persistent hypothyroid phase, since thionamides and radioactive iodine are not indicated.
- Subacute granulomatous thyroiditis
Subacute granulomatous (de Quervain) thyroiditis is a painful, tender destructive thyroiditis that follows a viral upper respiratory illness and produces a transient thyrotoxic phase, often followed by a hypothyroid phase, with a markedly elevated erythrocyte sedimentation rate. Treatment is symptomatic, an NSAID for mild pain or a glucocorticoid taper for moderate to severe pain, with a dramatic response within 24 to 48 hours, since thionamides and radioactive iodine have no role.
- Graves disease
Graves disease is an autoimmune disorder in which thyrotropin receptor antibodies stimulate the thyroid, causing hyperthyroidism, and is the most common cause of thyrotoxicosis in iodine-sufficient regions. Diagnosis rests on a suppressed thyroid-stimulating hormone with elevated free thyroxine and positive thyrotropin receptor antibodies, and first-line treatment is a thionamide, most often methimazole, with radioactive iodine or thyroidectomy reserved for recurrence or patient preference.