Thyroiditis
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Direct answer
Pain separates the thyroiditides at the bedside: painful subacute granulomatous (de Quervain) thyroiditis follows a viral prodrome with tender goitre, markedly raised ESR and a thyrotoxic then hypothyroid then recovery phase, whereas painless Hashimoto thyroiditis — the commonest cause of hypothyroidism in iodine-replete populations — silently enlarges the gland with lymphocytic infiltration, Hürthle cell change and anti-TPO antibodies. Between and beyond sit silent (pain-free lymphocytic) thyroiditis including postpartum thyroiditis, suppurative thyroiditis (a true infection, often left lobe in children), and Riedel thyroiditis, an IgG4-related fibrosing disease producing a rock-hard gland fixed to surrounding structures and mimicking carcinoma. Drug forms matter: amiodarone (both thyrotoxic and hypothyroid) and checkpoint inhibitors, which unmask Hashimoto-like disease.
What you must remember
- Hashimoto thyroiditis: antithyroid peroxidase antibodies (anti-microsomal) are the serological marker, often with anti-thyroglobulin; histology shows lymphocytic infiltrate with germinal centres, oxyphil Hürthle cell metaplasia, and atrophic follicles; firmly enlarged, painless gland in a middle-aged woman; carries a raised risk of B-cell lymphoma of the thyroid and, modestly, papillary carcinoma.
- Subacute granulomatous (de Quervain) thyroiditis: giant-cell granulomas around damaged follicles after viral illness (mumps, coxsackie, adenovirus quoted classically); painful gland radiating to the jaw, high ESR, low radioiodine uptake in the thyrotoxic phase; self-limiting with NSAIDs and steroids for pain; permanent hypothyroidism is uncommon.
- Painless and postpartum thyroiditis: autoimmune, painless, transient thyrotoxicosis with low uptake followed by hypothyroidism; postpartum thyroiditis occurs within roughly six months of delivery, in anti-TPO-positive women, and often recurs in subsequent pregnancies.
- Suppurative thyroiditis: bacterial abscess, usually left-sided (from fourth-pouch sinus tracts), with fever and severe pain; drainage and antibiotics.
- Riedel thyroiditis: dense fibrosis replacing the gland and invading muscle — woody, fixed, painless; part of the IgG4-related disease spectrum (with retroperitoneal fibrosis and sclerosing pancreatitis); surgery only for compression, steroids and tamoxifen described medically.
- Drug anchors: amiodarone type 1 (iodine-induced excess synthesis, treated with thionamides) versus type 2 (destructive thyroiditis, treated with steroids); lithium and interferon-alpha also induce thyroiditis; checkpoint inhibitors produce both thyrotoxicosis and permanent hypothyroidism.
- Uptake rule worth memorising: high radioiodine uptake in thyrotoxicosis means overproduction (Graves, toxic nodules); low uptake means destructive release (all thyroiditides) — the two-line discriminator the exam asks endlessly.
- Indian angle: with universal salt iodisation under the National Iodine Deficiency Disorders Control Programme, Hashimoto disease has become the dominant cause of goitre in many Indian clinics, displacing iodine-deficiency goitre — a real shift asked as a one-liner.
Bedside-to-biopsy correlation in thyroiditis
A 32-year-old woman, three months postpartum, has palpitations for four weeks: mild thyrotoxicosis, painless small goitre, low radioiodine uptake, positive anti-TPO — postpartum (painless) thyroiditis; propranolol for symptoms, no thionamides (they do not work in destructive release), and watch for the hypothyroid dip. A 40-year-old man has painful neck swelling after a flu-like illness: tender gland, ESR above 80, low uptake — de Quervain; NSAIDs, steroids if severe, and reassurance that recovery usually follows. A 50-year-old woman has a slowly firm, painless goitre with TSH of 18: Hashimoto; levothyroxine titrated to TSH, with review because a rapidly enlarging Hashimoto gland is lymphoma until biopsied. A 45-year-old with a stony-hard gland fixed to strap muscles and compressive symptoms: Riedel; check IgG4 and imaging for retroperitoneal fibrosis, and relieve compression. Each correlation shows the same logic: phase (toxic, hypothyroid, recovered), uptake (high versus low), pain (present versus absent), and antibody status — four axes that answer nearly every thyroiditis question.
Where candidates slip
The commonest error is treating destructive thyrotoxicosis with carbimazole or propylthiouracil: in de Quervain and painless thyroiditis the gland is leaking stored hormone, not synthesising, so thionamides are useless and steroids or beta-blockers are correct — the uptake test exists precisely to prevent this mistake. Second, ESR is the de Quervain marker while anti-TPO is the Hashimoto marker; candidates swap them. Third, postpartum thyroiditis is painless and thyrotoxic first — students remember only the hypothyroid phase and miss the early thyrotoxic window. Fourth, Riedel thyroiditis versus anaplastic carcinoma: both are hard fixed masses in older patients, but Riedel is fibrosis with preserved general health, while anaplastic carcinoma kills within months — biopsy is mandatory, and confusion in either direction is a viva disaster. Fifth, remember the Hashimoto-lymphoma link: the only thyroiditis that predisposes to malignancy (MALT-type B-cell lymphoma).
Frequently asked questions
Which antibody profile defines Hashimoto thyroiditis?
Anti-thyroid peroxidase antibodies, frequently with anti-thyroglobulin antibodies, accompanying a painless firm goitre and gradual hypothyroidism.
How does de Quervain thyroiditis present and resolve?
Tender goitre after viral prodrome with fever, markedly raised ESR, transient thyrotoxicosis with low radioiodine uptake, progressing through a hypothyroid phase to recovery in most patients.
Why are thionamides ineffective in thyroiditis-related thyrotoxicosis?
Destructive thyroiditis releases preformed hormone rather than synthesising new hormone, so synthesis blockers such as carbimazole have no target; beta-blockers and symptom control are used.
What distinguishes amiodarone-induced thyrotoxicosis type 1 from type 2?
Type 1 is iodine-induced hormone overproduction with high uptake (thionamide-responsive), type 2 is destructive thyroiditis with low uptake (glucocorticoid-responsive).
Which thyroiditis is linked to IgG4-related disease?
Riedel thyroiditis — dense fibrosis extending beyond the thyroid into perithyroidal tissues, associated with multifocal fibrosclerosis and elevated IgG4.