Silent Thyroiditis

Silent thyroiditis is painless autoimmune destructive thyroiditis causing transient thyrotoxicosis, often followed by hypothyroidism and then recovery. It occurs as a sporadic form and as postpartum thyroiditis.

It accounts for a minority of thyrotoxicosis, and postpartum thyroiditis affects about 5 to 10% of women within 12 months of delivery.

Risk factors are positive thyroid peroxidase antibodies, type 1 diabetes, previous Graves disease or Hashimoto disease, and drugs such as interferon alpha, lithium, tyrosine kinase inhibitors and immune checkpoint inhibitors.

The thyrotoxic phase lasts 2 to 8 weeks, the hypothyroid phase 1 to 3 months, and euthyroidism returns by about 12 months. Permanent hypothyroidism occurs in a minority of sporadic cases and in many women with positive antibodies.

Pathophysiology.

Lymphocytic infiltration destroys follicles and releases preformed thyroid hormone, so thyrotoxicosis occurs without increased hormone synthesis. Radioiodine uptake is low.

Reserve is depleted afterwards, giving transient hypothyroidism until follicles regenerate.

• Mild to moderate thyrotoxic symptoms: palpitations, tremor, weight loss, heat intolerance and anxiety.
• Small, firm, painless goitre. No eye disease or pretibial myxoedema.

Red flags.

• Severe thyrotoxicosis, atrial fibrillation or heart failure (look for another cause such as amiodarone or Graves disease).
• Severe neck pain or tenderness (suggests subacute granulomatous thyroiditis).

• Suppressed thyroid stimulating hormone with raised free thyroxine (and often free triiodothyronine).
• Thyroid peroxidase antibodies positive in most, thyrotropin receptor antibodies negative, and normal or mildly raised ESR and CRP.
• Thyroid radioiodine or technetium uptake low (under 5% at 24 hours). Ultrasound shows a hypoechoic gland with low Doppler flow. In pregnancy and breastfeeding use ultrasound with Doppler or thyrotropin receptor antibodies, not radionuclide scanning.

Differential diagnosis.

• Graves disease (thyrotropin receptor antibodies, high uptake, eye signs).
• Subacute granulomatous thyroiditis (painful, high ESR).
• Exogenous thyroid hormone (low thyroglobulin), iodine induced thyrotoxicosis and amiodarone effect.
• Toxic nodular goitre, struma ovarii and gestational transient thyrotoxicosis.
• TSH-secreting adenoma.

• Antithyroid drugs do not help, because hormone synthesis is not increased.
• Symptomatic control: propranolol 10 to 40 mg three to four times daily (or atenolol 25 to 50 mg daily) until the thyrotoxic phase settles.
• Hypothyroid phase: levothyroxine if symptomatic, if thyroid stimulating hormone is over 10 mU/L, or if pregnancy is planned (about 1.6 micrograms/kg daily; start 25 to 50 micrograms in older adults or heart disease). After 6 to 12 months reduce the dose and recheck thyroid stimulating hormone after 6 weeks to test for recovery.

Special groups. Postpartum: propranolol is compatible with breastfeeding. Check thyroid stimulating hormone yearly for life after postpartum thyroiditis because of the high risk of permanent hypothyroidism, and again in any later pregnancy and postpartum.

Monitoring. Free thyroxine and thyroid stimulating hormone every 4 to 6 weeks until euthyroid, then at 12 months and yearly if thyroid peroxidase antibodies are positive.

Referral and escalation. Endocrinology for severe thyrotoxicosis, atrial fibrillation, diagnostic doubt or persistent hypothyroidism.