Bit · Endo
Hashimoto vs Graves vs De Quervain (subacute) thyroiditis
Three patterns of thyroid disease. Same gland, different antibody or trigger, opposite hormonal direction.
Mechanism
All three are autoimmune (or post-viral) thyroid disorders. They split on whether the gland is being destroyed (hypo) or activated (hyper):
- Hashimoto thyroiditis — chronic autoimmune destruction. Anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin antibodies. Lymphocytic infiltrate, Hürthle cells, germinal centres on biopsy. Most common cause of hypothyroidism in iodine-replete countries. Painless goiter, gradual hypothyroidism, weight gain, cold intolerance, hair loss, constipation. Increased risk of thyroid lymphoma.
- Graves disease — autoimmune activation. TSH receptor antibody (TSI / TRAb) stimulates thyroid → hyperthyroidism. Diffuse goiter, weight loss, heat intolerance, palpitations, tremor, hyperreflexia, anxiety. Distinctive features: ophthalmopathy (proptosis, lid lag, periorbital edema — from fibroblast stimulation), pretibial myxedema, thyroid acropachy. Radioactive iodine uptake: diffusely increased.
- De Quervain (subacute granulomatous) thyroiditis — post-viral, often after a URI. Tender, painful thyroid (the pivot — unlike Hashimoto and Graves, which are painless). Transient hyperthyroidism initially (release of preformed hormone) → may transition through euthyroid → hypothyroid → recovery. Low radioactive iodine uptake. ↑ ESR. Treat with NSAIDs (mild) or steroids (severe).
Differentiator Table
| Hashimoto | Graves | De Quervain (subacute) | |
| Underlying immune problem | Destructive autoimmunity (anti-TPO, anti-Tg) | TSH receptor antibody (TSI) — stimulating | Post-viral, granulomatous |
| Hormonal direction | Hypo (chronic) | Hyper (sustained) | Transient hyper → hypo → recover |
| Gland on exam | Firm, non-tender, +/- goiter | Diffuse, non-tender goiter; bruit possible | TENDER, painful gland |
| Distinctive features | Lymphocytic infiltrate with germinal centres, Hürthle cells | Ophthalmopathy, pretibial myxedema, thyroid acropachy | Pain, fever, ↑ ESR, post-viral history |
| Radioactive iodine uptake | Variable (low if late) | Diffusely INCREASED | DECREASED (gland not making new hormone) |
| Antibodies | Anti-TPO, anti-thyroglobulin | TSI / TRAb (stimulating) | Usually none specific |
| Long-term outcome | Permanent hypothyroidism — lifelong levothyroxine | Treat with antithyroid drugs (methimazole/PTU), radioactive iodine, or thyroidectomy | Usually full recovery |
| Lymphoma risk | Yes — thyroid lymphoma | No | No |
The Pivot
Three questions decide it:
- Painful, tender gland after a viral illness? → De Quervain.
- Hyperthyroidism + ophthalmopathy + pretibial myxedema? → Graves.
- Painless, gradual hypothyroidism with goiter and anti-TPO antibodies? → Hashimoto.
Radioactive iodine uptake clinches it: high in Graves, low in De Quervain, variable in Hashimoto.
NBME-Style Stem
A 32-year-old woman presents 2 weeks after a viral upper respiratory infection with anterior neck pain, fever, palpitations, and tremor. Examination shows a tender, firm thyroid. TSH is suppressed, free T4 is elevated. ESR is 78 mm/hr. Radioactive iodine uptake is markedly decreased. Which of the following is the most likely diagnosis?
Concept Anchor
Hashimoto destroys the thyroid quietly; Graves antibody-activates it loudly with eye signs; De Quervain inflames it painfully after a virus. The uptake scan and the tenderness on palpation are the two cleanest splitters.