Thyroiditis
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Direct answer
Pain over the gland, a high ESR and a low radioiodine uptake form the signature of subacute (de Quervain) thyroiditis — a destructive, usually viral inflammation that passes through thyrotoxic, hypothyroid and recovery phases, treated with beta-blockers for symptoms, NSAIDs and, if needed, prednisolone 40 mg daily tapering over weeks. Painless, TPO-antibody-positive thyroiditis — silent or within a year of delivery (postpartum thyroiditis) — runs the same triphasic course without pain, requires no antithyroid drug (the gland is leaking, not synthesising), and leaves a fifth to a third of women permanently hypothyroid. Hashimoto disease is the chronic lymphocytic form and the commonest cause of spontaneous hypothyroidism in iodine-replete India. Amiodarone, 37 per cent iodine by weight, produces both type 1 (iodine-induced excess synthesis, treated with thionamides) and type 2 (destructive, treated with 40–60 mg prednisolone) thyrotoxicosis — the distinction being the endocrinologist's drug-side headache par excellence.
What you must remember
- Uptake divides thyrotoxicosis: low uptake — destruction (subacute, silent, postpartum, amiodarone type 2, exogenous iodine) or exogenous hormone; high uptake — synthesis (Graves, toxic nodular). One scan answers what biochemistry cannot.
- Subacute thyroiditis numbers: ESR above 50 (often over 100) with raised CRP distinguishes it from silent thyroiditis; thyrotoxic phase 4–6 weeks, transient hypothyroidism follows, and over 90 per cent recover fully.
- Postpartum thyroiditis clock: affects about 5–10 per cent of deliveries, classically thyrotoxic at 1–4 months then hypothyroid at 4–8 months; strongly TPO-associated; recurs in most subsequent pregnancies; annual TSH follow-up advised for life.
- Beta-blocker-only rule for destructive thyrotoxicosis: propranolol for palpitations; thionamides are useless — the gland is not making hormone — a perennial one-mark distinction from Graves.
- Hashimoto markers: TPO antibodies in about 90 per cent, firm painless goitre, increased risk of other autoimmunity (type 1 diabetes, coeliac, vitiligo) and of lymphoma in long-standing disease (rapidly enlarging Hashimoto goitre = biopsy).
- Amiodarone duality: type 1 (underlying nodular gland, iodine-driven synthesis — thionamides) versus type 2 (destructive thyroiditis — glucocorticoids 40–60 mg); mixed pictures exist, and both can follow treatment; hypothyroidism is the more frequent complication in iodine-replete populations.
- Riedel thyroiditis: rock-hard, painless fibrosis infiltrating beyond the capsule, associated with IgG4 disease; surgery risks structures, medical therapy (glucocorticoids, tamoxifen) often preferred.
- Iodine footnote for Indian exams: national iodisation pushed India from deficient to replete status, shifting the thyroiditis–Graves balance and making Hashimoto the dominant cause of spontaneous hypothyroidism — programme-level knowledge examiners enjoy.
Telling the thyroiditides apart at the bedside
Four patients, four calendars. A 34-year-old woman three months after delivery, palpitations and a slightly tender-free small goitre, TSH suppressed, free T4 high — postpartum (lymphocytic) thyroiditis in its thyrotoxic phase: propranolol for six weeks, no carbimazole, TSH rechecked at three-monthly intervals because the hypothyroid dip is coming; if it is symptomatic, transient levothyroxine, and if it persists beyond a year, permanent. A 45-year-old man with a fortnight of painful neck radiation to the jaw after a viral illness, ESR 96, thyrotoxic biochemistry — subacute thyroiditis: NSAIDs first, prednisolone 40 mg if pain resists, warn about the hypothyroid phase. A 28-year-old painless thyrotoxicosis with TPO strongly positive and uptake 2 per cent — silent thyroiditis, managed like postpartum disease. A 66-year-old on amiodarone for eight months, thyrotoxic without pain: measure interleukin-6? Practically, scan where feasible and colour-flow Doppler (type 1 shows increased vascularity, type 2 absent) — then commit: thionamide for type 1, prednisolone for type 2, accepting that many need both or ultimately total thyroidectomy if the arrhythmia forbids stopping amiodarone. The skill being examined is phase-thinking: which compartment is leaking, is anything being synthesised, and what will the gland do next month.
The classic confusion
Graves versus destructive thyrotoxicosis is the stem of half the questions: both arrive with suppressed TSH and high T4, but Graves has a diffuse goitre with bruit, orbitopathy and high uptake, while thyroiditis has a low uptake, short-lived thyrotoxicosis and disproportionate symptoms for the hormone level. The second confusion is antithyroid drugs written for postpartum thyroiditis — pharmacologically futile and, in a breastfeeding mother, unnecessary exposure. The third is the painless goitre labelled "subacute" without an ESR: silent thyroiditis has a normal ESR, subacute a markedly raised one; that single test reallocates the entire management. Finally, amiodarone-induced thyrotoxicosis type 2 treated with thionamides alone will smoulder for months — the destructive gland needs steroids.
Frequently asked questions
Which single test separates Graves from destructive thyroiditis?
Radioiodine uptake (or a technetium scan): high in Graves, low in all destructive thyrotoxicoses including subacute, silent, postpartum and amiodarone type 2 disease.
How is subacute thyroiditis treated?
NSAIDs for pain plus a beta-blocker for thyrotoxic symptoms; prednisolone about 40 mg daily tapering over weeks when pain is severe or resistant, with counselling about the transient hypothyroid phase.
What follow-up does postpartum thyroiditis require?
TSH at three- to six-monthly intervals through the first year, levothyroxine if the hypothyroid phase is symptomatic or persists, and lifelong annual TSH — recurrence in future pregnancies is the rule rather than the exception.
How do type 1 and type 2 amiodarone-induced thyrotoxicosis differ?
Type 1 is iodine-driven hormone synthesis in an abnormal gland (thionamides); type 2 is a destructive thyroiditis (glucocorticoids 40–60 mg); mixed forms exist, and colour-flow Doppler or scanning helps where available.
Which thyroiditis carries lymphoma risk?
Long-standing Hashimoto disease — a rapidly enlarging gland in that setting warrants ultrasound and biopsy rather than empirical levothyroxine escalation.