Thyroiditis

• Thyroiditis means inflammation of the thyroid gland. It is not one disease: it ranges from a painful, virus-triggered illness that resolves on its own to lifelong autoimmune destruction of the gland.
• Most inflammatory forms damage thyroid follicles and release stored hormone, producing a predictable sequence: a transient thyrotoxic phase, then a possible hypothyroid phase, then recovery.
• Pain is the clinical clue that separates subacute (de Quervain) thyroiditis from the painless forms. Suppurative thyroiditis is painful too, but it is a bacterial abscess that needs antibiotics and drainage.
• Hashimoto (chronic autoimmune) thyroiditis is the most common cause of permanent hypothyroidism in iodine-sufficient countries; it is treated with levothyroxine, not anti-inflammatory drugs.
• Radionuclide uptake is low or absent in destructive thyroiditis, whereas it is high in Graves disease. That single test resolves most diagnostic doubt.
• Most cases are managed with symptomatic care: beta blockers for thyrotoxic symptoms, anti-inflammatory treatment for the painful forms, and levothyroxine when the hypothyroid phase is symptomatic or TSH is high.

By the end of this page you should be able to:

1. Classify the main types of thyroiditis by cause, course and outcome.
2. Explain why destructive thyroiditis produces transient thyrotoxicosis followed by hypothyroidism and recovery.
3. Use pain, thyroid function, antibodies, ESR/CRP and radionuclide uptake to tell thyroiditis from Graves disease and from one another.
4. Plan management of subacute thyroiditis: when to use NSAIDs or glucocorticoids, beta blockers, levothyroxine and follow-up.
5. Recognise acute suppurative thyroiditis and Riedel thyroiditis as different, potentially dangerous entities.
6. Adapt care for low-resource settings where scans and antibody tests are limited.

The useful clinical split is between destructive and autoimmune chronic thyroiditis. Destructive forms (subacute, silent, postpartum, drug-induced) leak preformed hormone, so they cause transient thyrotoxicosis with low radionuclide uptake and usually recover. Chronic autoimmune thyroiditis (Hashimoto thyroiditis) slowly destroys the gland and is the commonest cause of permanent hypothyroidism. Acute suppurative thyroiditis is a bacterial abscess; Riedel thyroiditis is a rare fibrosing process that fixes and hardens the gland.

The table summarises the six types you must know.

• Subacute thyroiditis is the most common cause of a painful thyroid. In general endocrine practice it may account for up to 5 percent of patients seen with clinical thyroid disease. ^[1]
• Population-based cohorts suggest an annual incidence of roughly 3 to 20 cases per 100 000 depending on case definition and region, with clear female predominance and a peak in young and middle-aged adults. ^[1]
• Hashimoto thyroiditis is the most common autoimmune endocrine disease and the most frequent cause of hypothyroidism in iodine-sufficient countries. ^[2]
• Destructive thyroiditis as a group is common in iodine-replete and iodine-deficient settings alike, although the mix of causes differs: toxic nodular goitre is more prominent where iodine intake is low.

Destructive thyroiditis is not a primary autoimmune disease that perpetuates itself. The central event is destruction of thyroid follicles, with leakage of stored thyroxine (T4) and triiodothyronine (T3) into the blood.

• Subacute (de Quervain) thyroiditis is widely regarded as a post-viral, HLA-linked inflammatory illness. Many patients report an upper respiratory infection 2 to 8 weeks earlier. HLA-B35 is present in roughly two-thirds of affected patients in some cohorts, and more recent work implicates HLA-B18:01, DRB101 and C04:01. Recurrence is linked to combinations such as HLA-B35 with HLA-B*18:01. ^[1]
• SARS-CoV-2 infection and vaccination have expanded the recognised trigger list, sometimes producing painless or oligosymptomatic disease. ^[1]
• Hashimoto thyroiditis is a lymphocytic infiltration with fibrosis and atrophy. While patients may be euthyroid or even transiently thyrotoxic (hashitoxicosis), most ultimately become hypothyroid. ^[2]
• Silent and postpartum thyroiditis are also destructive forms, usually with positive thyroid peroxidase antibodies (TPOAb), suggesting an autoimmune trigger without a sustained inflammatory destructive syndrome.
• Acute suppurative thyroiditis is usually bacterial and is associated with anatomic risk factors such as a pyriform sinus fistula, especially in children and young adults, or with immunosuppression.
• Riedel thyroiditis is a rare dense fibrosing process, often associated with IgG4-related disease affecting other organs.
• Drug-induced thyroiditis is seen with amiodarone, interferon-alpha, interleukin-2, lithium and newer agents such as tyrosine kinase inhibitors and immune checkpoint inhibitors.

Understanding the why makes the whole course predictable.

1. Destruction releases hormone. Inflammatory damage ruptures follicles and proteolyses stored thyroglobulin, dumping preformed T4 and T3 into the circulation. Synthesis is not increased, so this is thyrotoxicosis without hyperthyroidism.
2. Thyrotoxic phase. TSH is suppressed, free T4 (and T3) are raised, but hormone levels are only mildly to moderately increased and T3 is not disproportionately high, unlike Graves disease.
3. Depletion and euthyroid interval. As stores empty, hormone levels fall and TSH recovers. There may be a short euthyroid interval.
4. Hypothyroid phase. With functioning tissue lost and TSH still suppressed from the previous phase, TSH rises and free T4 falls. This produces temporary hypothyroidism, often with few symptoms.
5. Recovery. Follicles regenerate, synthesis resumes and thyroid function usually returns to normal.

This sequence explains two practical rules. First, antithyroid drugs do not help in destructive thyroiditis, because hormone is leaking, not being overproduced. Second, radioiodine uptake is low or absent, because damaged tissue cannot trap iodine and TSH is suppressed.

Thyroid autoantibodies (TPOAb, thyroglobulin antibodies (TgAb)) and TSH receptor antibodies (TRAb) are usually absent or present only at low titres at presentation in subacute thyroiditis, and any rise during the hypothyroid phase is thought to be a secondary response to released antigen rather than a primary autoimmune driver. ^[1] In Hashimoto thyroiditis the picture is different: TPOAb and TgAb are usually positive and the gland is slowly destroyed. ^[2]

Patients with subacute thyroiditis classically describe:

• A viral-like prodrome with low-grade fever, myalgias and malaise for days to weeks before neck pain begins. ^[1]
• Anterior neck pain that often starts on one side and may radiate to the jaw, ears or upper chest; it is worse with swallowing, coughing or turning the head. ^[1]
• Systemic symptoms: fatigue, fever, anorexia, generalised myalgias.
• In about half of patients, mild thyrotoxic symptoms such as palpitations, heat intolerance and tremor; these are usually less prominent than the pain. ^[1]
• The pain can "migrate" from one lobe to the other (creeping thyroiditis).

Hashimoto thyroiditis presents more insidiously: a goitre, symptoms of hypothyroidism (fatigue, weight gain, cold intolerance, constipation, depression), or it is found incidentally. It is usually painless. An early hashitoxicosis can mimic hyperthyroidism transiently.

Silent and postpartum thyroiditis present with features of transient thyrotoxicosis (palpitations, heat intolerance, weight loss) without pain, often discovered on routine testing. Postpartum thyroiditis occurs within 12 months of delivery and may be mistaken for postpartum anxiety or depression.

Acute suppurative thyroiditis presents with high fever, severe unilateral neck pain, dysphagia, and a tender, red, sometimes fluctuant mass over the thyroid. It occurs mainly in children and young adults.

Riedel thyroiditis presents as a very hard, "woody", fixed goitre that may compress the trachea or oesophagus, with hoarseness or stridor; hypothyroidism is common.

Drug-induced thyroiditis may produce no symptoms, transient thyrotoxicosis, or hypothyroidism depending on the drug and timing.

• Subacute: the thyroid is slightly to moderately enlarged, firm and very tender, sometimes asymmetric. Temperature may be raised. There are no eye signs of Graves disease and no thyroid bruit.
• Hashimoto: diffuse firm goitre with a rubbery feel; signs of hypothyroidism (dry skin, bradycardia, delayed reflexes) later in disease.
• Suppurative: erythema and tenderness over one lobe, fever, cervical lymph nodes, possible abscess.
• Riedel: extremely hard gland fixed to surrounding structures; stridor or dysphagia if compressing.

The painful and painless thyroiditides must be separated from each other and from Graves disease, toxic nodular goitre, haemorrhage into a nodule and thyroid malignancy. Key distinguishing points:

• Graves disease: painless thyrotoxicosis with a diffuse goitre and bruit, eye disease may be present, high TRAb, high radionuclide uptake, marked hypervascularity ("thyroid inferno") on Doppler; inflammatory markers normal.
• Toxic nodular goitre/adenoma: older patient, nodular gland, focal or patchy increased uptake on scan.
• Silent/postpartum thyroiditis: no pain, usually TPOAb positive, low uptake, normal inflammatory markers.
• Haemorrhage into cyst/nodule: sudden focal pain without fever, normal thyroid function generally, ultrasound shows blood; uptake shows a cold defect.
• Painful Hashimoto thyroiditis: TPOAb/TgAb positive, variable uptake, often hypothyroid rather than thyrotoxic.
• Thyroid malignancy with pain: focal lesion with suspicious features on ultrasound, FNA or core biopsy needed.

Thyroiditis is primarily a clinical diagnosis supported by tests. The aim is to confirm a destructive thyrotoxicosis and exclude mimics.

• TSH, free T4 and free T3: in destructive thyroiditis TSH is suppressed with mildly to moderately raised free T4 and T3; T3 is not disproportionately raised. ^[1] Hashimoto disease in its hypothyroid phase shows raised TSH with low free T4.
• Inflammatory markers: ESR and/or CRP are markedly raised in subacute thyroiditis and usually normal in silent and postpartum disease. ^[1]
• Full blood count: leucocytes are normal or slightly raised; marked neutrophilic leucocytosis should raise suspicion of acute suppurative thyroiditis. ^[1] Mild anaemia may occur.
• Antibodies: TRAb is negative in thyroiditis; TPOAb/TgAb are often positive in Hashimoto, silent and postpartum thyroiditis and usually absent or low in subacute disease. ^[1][2]
• Pregnancy test in women of childbearing age before imaging or radioactive iodine.

• RAIU or technetium-99m scan: low or absent uptake in destructive thyroiditis (often under 1 to 3 percent); an uptake above about 5 percent at 24 hours makes subacute thyroiditis unlikely. High diffuse uptake indicates Graves disease; focal uptake indicates a toxic nodule. ^[1]
• Ultrasound: in subacute disease shows ill-defined hypoechoic areas with blurred margins and low or normal vascularity; useful to exclude abscess, nodule or malignancy. Doppler shows no "thyroid inferno". ^[1]
• Fine-needle aspiration: not routinely needed; reserved for unilateral painful enlargement with suspicious imaging, failure to respond to anti-inflammatory treatment, suspected abscess, or suspected malignancy. Cytology in subacute disease shows giant cells, disrupted follicular cells and colloid. ^[1]

There are no universally agreed criteria, but a practical framework is:

1. Anterior neck pain and thyroid tenderness (absent in the painless forms). ^[1]
2. Biochemical thyrotoxicosis with suppressed TSH.
3. Elevated ESR and/or CRP (in the painful forms).
4. Supportive imaging: low or absent radionuclide uptake and/or hypoechoic lesions with reduced vascularity on ultrasound.
5. Exclusion of alternative causes.

A rapid and dramatic response to glucocorticoids supports the diagnosis of subacute thyroiditis.

Most patients improve with simple measures. Treatment is stepped.

1. Mild pain: NSAIDs first line. Common regimens are aspirin 2.0 to 2.6 g per day in divided doses, naproxen 500 to 1500 mg per day in two divided doses, or ibuprofen 800 to 3200 mg per day in three or four divided doses; references differ on the upper doses. Adjust for renal function and gastrointestinal risk. Improvement should be evident within 2 to 3 days; if not, stop the NSAID and use a glucocorticoid. ^[1]
2. Severe pain or systemic symptoms: glucocorticoid. Regimens differ between references (15 to 60 mg daily); a typical start is prednisone or prednisolone 30 to 40 mg daily, and 15 to 20 mg daily may suffice for milder disease. Give for 1 to 2 weeks then taper, for example by 5 to 10 mg every 5 to 7 days, over about 4 to 12 weeks. Pain relief is often within 24 to 48 hours; lack of brisk response should prompt reconsideration of the diagnosis. Recurrence during taper is managed by increasing the dose and tapering more slowly. ^[1]
3. Thyrotoxic symptoms: a beta blocker such as propranolol 40 to 120 mg per day or atenolol 25 to 50 mg per day. ^[1] Avoid high-dose beta blockers with asthma or severe bradycardia.
4. Hypothyroid phase: levothyroxine 50 to 100 micrograms per day in healthy adults if symptoms are present or TSH is at least 10 mU/L. Reassess after several weeks and withdraw once recovery is established. ^[1]
5. Avoid: antithyroid drugs, radioiodine and routine antibiotics have no role in uncomplicated subacute thyroiditis. ^[1]

Treatment is replacement when hypothyroidism develops: levothyroxine titrated to TSH. There is no evidence-based role for routine glucocorticoids or NSAIDs. Recently reported options for the small group with persistent symptoms despite biochemical euthyroidism (total thyroidectomy, combination LT4 plus T3, supplements, acupuncture) are not first-line and require specialist and shared decision-making. ^[2]

These are managed symptomatically: beta blockers during the thyrotoxic phase and levothyroxine during a symptomatic hypothyroid phase. Anti-inflammatory drugs are usually unnecessary because there is no significant pain. In postpartum disease, avoid radioactive iodine while breastfeeding and check thyroid function at 6 and 12 weeks and again at 6 to 12 months. ^[1]

This is an abscess until proven otherwise. Give intravenous antibiotics directed at usual skin and upper respiratory flora, obtain ultrasound to identify collections, and drain when an abscess is present. Look for an underlying pyriform sinus fistula, particularly in children and adolescents, because definitive treatment (fistula excision or endoscopic ablation) prevents recurrence.

First-line treatment is glucocorticoids to reduce inflammation and halt progression. Refractory cases may respond to tamoxifen or rituximab. Surgery is reserved for compressive symptoms and is technically difficult because of dense fibrosis; tracheostomy may be needed for airway compromise. Treat any coexisting IgG4-related disease systemically.

Where possible, withdraw or change the offending drug (for example, amiodarone), although this is not always safe or practical. Treat symptoms with beta blockers; use levothyroxine during prolonged hypothyroidism. For amiodarone, distinguish type 1 (iodine-induced hyperthyroidism treated with antithyroid drugs) from type 2 (destructive thyroiditis treated with glucocorticoids). Thyroid function usually recovers once the drug is stopped.

• Permanent hypothyroidism in about 5 to 15 percent of subacute cases and a substantial fraction of Hashimoto, silent and postpartum disease. ^[1]
• Recurrence of subacute thyroiditis in 10 to 20 percent of patients, sometimes years later; it often affects the other lobe and responds to the same treatment but may need a slower glucocorticoid taper. ^[1]
• Cardiac and thrombotic complications from unrecognized thyrotoxicosis: atrial fibrillation, embolic stroke, heart failure.
• Osteoporosis and fracture risk with prolonged excess thyroid hormone.
• Tracheal or oesophageal compression in Riedel disease.
• Sepsis or airway compromise in neglected suppurative thyroiditis.

The natural history of subacute thyroiditis is favourable: the full course rarely exceeds 4 to 6 months from pain onset to full recovery, and most patients regain normal thyroid function. ^[1] Roughly half of patients pass through a distinct hypothyroid phase. Long-term outcome is excellent in the majority, but permanent hypothyroidism occurs in up to 15 percent, particularly with more extensive destruction or coexisting autoimmune thyroid disease. ^[1]

Recommended follow-up:

• Recheck thyroid function after the acute illness and again at 4 to 8 weeks, then at 3 and 6 months.
• Test once more after any levothyroxine withdrawal to confirm recovery.
• In low-risk cases, annual TSH thereafter is reasonable because permanent hypothyroidism can emerge late.

For Hashimoto thyroiditis, follow-up is lifelong: TSH 6 to 8 weeks after starting or changing levothyroxine, then every 6 to 12 months. Pregnant women need more frequent monitoring.

• Children and adolescents: acute suppurative thyroiditis is relatively more common; Hashimoto disease can also present in children.
• Pregnancy: thyrotoxicosis in pregnancy has a broad differential. Subacute thyroiditis during pregnancy is harder to diagnose because fever is less prominent and the picture overlaps with hyperemesis gravidarum and gestational thyrotoxicosis. Avoid radioiodine; rely on ultrasound, TSH/free T4 and ESR/CRP. ^[1]
• Postpartum: both destructive postpartum thyroiditis and recurrence of autoimmune disease are common; advise women that hypothyroidism may be permanent and that future pregnancies or postpartum periods may re-trigger it.
• Older adults: may have fewer adrenergic symptoms and more atrial fibrillation; avoid over-replacement.

Where scans, antibody assays and radioactive uptake studies are scarce, thyroiditis remains a clinical diagnosis for most patients.

• Use pattern recognition: anterior neck pain with a tender gland, systemic symptoms and transient thyrotoxicosis points to subacute thyroiditis; its non-tender counterpart with low ESR is silent or postpartum thyroiditis.
• Basic tests go far: TSH and free T4 (when available), ESR/CRP, a pregnancy test, and a portable ultrasound if available. A blood count supports suspicion of abscess.
• Treat empirically but sensibly: NSAIDs are inexpensive and effective for subacute pain; prednisolone is widely available for severe cases; propranolol controls symptoms; levothyroxine replaces hormone when needed. Avoid unnecessary antibiotics and antithyroid drugs.
• Safety netting: patients treated for "thyroiditis" must be reviewed, because a presumed painless case may turn out to be Graves disease or a toxic nodule. Persistent focal pain, a dominant nodule, compressive symptoms or failure to respond to anti-inflammatory treatment warrants referral for ultrasound and FNA.
• Work around iodine status: in iodine-deficient settings toxic multinodular goitre is more common; uptake patterns differ from the iodine-replete world, but a very low uptake still supports destructive thyroiditis.
• Refer early for abscess, airway compromise, suspected malignancy or severe thyrotoxicosis.

• Thyroiditis is a family of inflammatory disorders with different causes and outcomes.
• Destructive forms (subacute, silent, postpartum, drug-induced) release preformed hormone: transient thyrotoxicosis with low radionuclide uptake, then possible hypothyroidism, then recovery.
• Pain distinguishes subacute from the painless destructive forms; high fever and unilateral fluctuance suggest suppurative abscess.
• Hashimoto thyroiditis is the most common cause of permanent hypothyroidism and is treated with levothyroxine.
• Subacute thyroiditis is usually post-viral and HLA-linked; about half of patients develop a hypothyroid phase and about 5 to 15 percent have permanent hypothyroidism. ^{[1] [2]}
• Radionuclide uptake is low or absent in destructive thyroiditis and high in Graves disease.
• Antithyroid drugs and radioiodine have no role in uncomplicated destructive thyroiditis.
• NSAIDs are first-line for subacute pain; glucocorticoids are reserved for severe or refractory disease.
• Beta blockers control adrenergic symptoms; levothyroxine (about 50 to 100 micrograms daily in healthy adults) is used for a symptomatic hypothyroid phase.
• Riedel thyroiditis is a rare fibrosing process with a rock-hard gland that may compress the airway.
• Low-resource care relies on clinical pattern recognition and follow-up rather than on advanced testing.

• Hyperthyroidism and thyrotoxicosis
• Hypothyroidism
• Thyroid function tests
• Goitre and thyroid nodules
• Graves disease
• Pregnancy and thyroid disease